
4 Main Types of Writing
Quiz by Cristina Barde
Customize this quiz to suit your class
Instantly translate to 100+ languages
Tag the questions with any skills you have. Your dashboard will track each student's mastery of each skill.
Give this quiz to my class
âExpository writing's main purpose is
to give information
to explainÂ
to tell
to help
âFacts and figures belong to which type of writing?
Expository writing
narrative writing
persuasive writing
descriptive writing
Expository writing's main purpose is
Facts and figures belong to which type of writing?
I would use expository writing in ________.
An example of descriptive writing is...
In persuasive writing the reader is often asked to...
Narrative writing's main purpose is to...
Descriptive writing's main purpose is...
Narrative writing has...
You can use persuasive in...
In descriptive writing, the writer uses his/her...
1. What is the main purpose of including theme and main idea questions in a text? a) To test your reading comprehension skills b) To understand the overall message or lesson of the text c) To practice identifying specific details in the text d) To improve your vocabulary and word knowledge 2. What is the purpose of finding the theme in a text? a) To summarize the main idea of the text in a few words b) To identify the specific details and examples in the text c) To understand the order of events in the text d) To analyze the author's writing style and techniques 3. Which of the following represents the theme of a text? a) A long sentence that describes the setting of the story b) A single word or short phrase that captures the main idea of the text c) A list of characters and their traits d) A detailed description of the plot and conflict in the story 4. How does identifying the main idea of a paragraph help you understand the text? a) It allows you to make connections between different parts of the text b) It helps you identify the author's purpose for writing the text c) It enables you to predict what will happen next in the story d) It helps you remember the specific details and examples in the paragraph 5. Which of the following best describes the main idea of a paragraph? a) The specific details and examples that support the theme of the text b) The order of events and actions in the paragraph c) The overall message or lesson conveyed by the paragraph d) The vocabulary words and their definitions in the paragraph 6. In a short paragraph about dogs, what could be a possible theme? a) Running and playing in the park b) Different breeds of dogs and their characteristics c) The loyalty and companionship dogs provide d) How to train a dog to do tricks 7. What might be the main idea of a paragraph about the importance of recycling? a) Recycling reduces pollution and conserves natural resources b) The process of recycling and how it works c) The different types of materials that can be recycled d) The history of recycling and its impact on society 8. Which of the following could be the theme of a paragraph about the benefits of reading? a) The importance of reading for academic success b) How to choose the right book to read c) The different genres of literature and their characteristics d) The role of libraries in promoting reading 9. If a paragraph discusses the life cycle of a butterfly, what would be the most likely main idea? a) The different colors and patterns of butterfly wings b) The stages of a butterfly's life from egg to adult c) The habitats and environments where butterflies live d) The types of plants that attract butterflies for feeding 10. What is the purpose of including vocabulary words and their meanings in context in a text? a) To test your knowledge of different words and their definitions b) To understand the specific details and examples in the text c) To improve your reading comprehension skills d) To practice using new words in your own writing
Covalent Molecules and Compounds Just as an atom is the simplest unit that has the fundamental chemical properties of an element, a molecule is the simplest unit that has the fundamental chemical properties of a covalent compound. Some pure elements exist as covalent molecules. Hydrogen, nitrogen, oxygen, and the halogens occur naturally as the diatomic (âtwo atomsâ) molecules H2, N2, O2, F2, Cl2, Br2, and I2 (part (a) in Figure 3.1.1). Similarly, a few pure elements exist as polyatomic (âmany atomsâ) molecules, such as elemental phosphorus and sulfur, which occur as P4 and S8 (part (b) in Figure 3.1.1). Each covalent compound is represented by a molecular formula, which gives the atomic symbol for each component element, in a prescribed order, accompanied by a subscript indicating the number of atoms of that element in the molecule. The subscript is written only if the number of atoms is greater than 1. For example, water, with two hydrogen atoms and one oxygen atom per molecule, is written as H2O. Similarly, carbon dioxide, which contains one carbon atom and two oxygen atoms in each molecule, is written as CO2. Covalent compounds that predominantly contain carbon and hydrogen are called organic compounds. The convention for representing the formulas of organic compounds is to write carbon first, followed by hydrogen and then any other elements in alphabetical order (e.g., CH4O is methyl alcohol, a fuel). Compounds that consist primarily of elements other than carbon and hydrogen are called inorganic compounds; they include both covalent and ionic compounds. In inorganic compounds, the component elements are listed beginning with the one farthest to the left in the periodic table, as in CO2 or SF6. Those in the same group are listed beginning with the lower element and working up, as in ClF. By convention, however, when an inorganic compound contains both hydrogen and an element from groups 13â15, hydrogen is usually listed last in the formula. Examples are ammonia (NH3) and silane (SiH4). Compounds such as water, whose compositions were established long before this convention was adopted, are always written with hydrogen first: Water is always written as H2O, not OH2. The conventions for inorganic acids, such as hydrochloric acid (HCl) and sulfuric acid (H2SO4), are described elswhere. Note! For organic compounds: write C first, then H, and then the other elements in alphabetical order. For molecular inorganic compounds: start with the element at far left in the periodic table; list elements in same group beginning with the lower element and working up. Write the molecular formula of each compound. a. The phosphorus-sulfur compound that is responsible for the ignition of so-called strike anywhere matches has 4 phosphorus atoms and 3 sulfur atoms per molecule. b. Ethyl alcohol, the alcohol of alcoholic beverages, has 1 oxygen atom, 2 carbon atoms, and 6 hydrogen atoms per molecule. c. Freon-11, once widely used in automobile air conditioners and implicated in damage to the ozone layer, has 1 carbon atom, 3 chlorine atoms, and 1 fluorine atom per molecule. Solution: a. âą A The molecule has 4 phosphorus atoms and 3 sulfur atoms. Because the compound does not contain mostly carbon and hydrogen, it is inorganic. âą B Phosphorus is in group 15, and sulfur is in group 16. Because phosphorus is to the left of sulfur, it is written first. âą C Writing the number of each kind of atom as a right-hand subscript gives P4S3 as the molecular formula. b. âą A Ethyl alcohol contains predominantly carbon and hydrogen, so it is an organic compound. âą B The formula for an organic compound is written with the number of carbon atoms first, the number of hydrogen atoms next, and the other atoms in alphabetical order: CHO. âą C Adding subscripts gives the molecular formula C2H6O. c. âą A Freon-11 contains carbon, chlorine, and fluorine. It can be viewed as either an inorganic compound or an organic compound (in which fluorine has replaced hydrogen). The formula for Freon-11 can therefore be written using either of the two conventions. âą B According to the convention for inorganic compounds, carbon is written first because it is farther left in the periodic table. Fluorine and chlorine are in the same group, so they are listed beginning with the lower element and working up: CClF. Adding subscripts gives the molecular formula CCl3F. âą C We obtain the same formula for Freon-11 using the convention for organic compounds. The number of carbon atoms is written first, followed by the number of hydrogen atoms (zero) and then the other elements in alphabetical order, also giving CCl3F. Write the molecular formula for each compound. a. Nitrous oxide, also called âlaughing gas,â has 2 nitrogen atoms and 1 oxygen atom per molecule. Nitrous oxide is used as a mild anesthetic for minor surgery and as the propellant in cans of whipped cream. b. Sucrose, also known as cane sugar, has 12 carbon atoms, 11 oxygen atoms, and 22 hydrogen atoms. c. Sulfur hexafluoride, a gas used to pressurize âunpressurizedâ tennis balls and as a coolant in nuclear reactors, has 6 fluorine atoms and 1 sulfur atom per molecule. Answer: a. N2O b. C12H22O11 c. SF6. Ionic Compounds The substances described in the preceding discussion are composed of molecules that are electrically neutral; that is, the number of positively-charged protons in the nucleus is equal to the number of negatively-charged electrons. In contrast, ions are atoms or assemblies of atoms that have a net electrical charge. Ions that contain fewer electrons than protons have a net positive charge and are called cations. Conversely, ions that contain more electrons than protons have a net negative charge and are called anions. Ionic compounds contain both cations and anions in a ratio that results in no net electrical charge. Note! Ionic compounds contain both cations and anions in a ratio that results in zero electrical charge.An ionic compound that contains only two elements, one present as a cation and one as an anion, is called a binary ionic compound. One example is MgCl2, a coagulant used in the preparation of tofu from soybeans. For binary ionic compounds, the subscripts in the empirical formula can also be obtained by crossing charges: use the absolute value of the charge on one ion as the subscript for the other ion. This method is shown schematically as follows: Crossing charges. One method for obtaining subscripts in the empirical formula is by crossing charges. When crossing charges, it is sometimes necessary to reduce the subscripts to their simplest ratio to write the empirical formula. Consider, for example, the compound formed by Mg2+ and O2â. Using the absolute values of the charges on the ions as subscripts gives the formula Mg2O2:Polyatomic Ions Polyatomic ions are groups of atoms that bear net electrical charges, although the atoms in a polyatomic ion are held together by the same covalent bonds that hold atoms together in molecules. Just as there are many more kinds of molecules than simple elements, there are many more kinds of polyatomic ions than monatomic ions. Two examples of polyatomic cations are the ammonium (NH4+) and the methylammonium (CH3NH3+) ions. P. The method used to predict the empirical formulas for ionic compounds that contain monatomic ions can also be used for compounds that contain polyatomic ions. The overall charge on the cations must balance the overall charge on the anions in the formula unit. Thus, K+ and NO3â ions combine in a 1:1 ratio to form KNO3 (potassium nitrate or saltpeter), a major ingredient in black gunpowder. Similarly, Ca2+ and SO42â form CaSO4 (calcium sulfate), which combines with varying amounts of water to form gypsum and plaster of Paris. The polyatomic ions NH4+ and NO3â form NH4NO3 (ammonium nitrate), a widely used fertilizer and, in the wrong hands, an explosive. One example of a compound in which the ions have charges of different magnitudes is calcium phosphate, which is composed of Ca2+ and PO43â ions; it is a major component of bones. The compound is electrically neutral because the ions combine in a ratio of three Ca2+ ions [3(+2) = +6] for every two ions [2(â3) = â6], giving an empirical formula of Ca3(PO4)2; the parentheses around PO4 in the empirical formula indicate that it is a polyatomic ion. Writing the formula for calcium phosphate as Ca3P2O8 gives the correct number of each atom in the formula unit, but it obscures the fact that the compound contains readily identifiable PO43â ions.Summary âą There are two fundamentally different kinds of chemical bonds (covalent and ionic) that cause substances to have very different properties. âą The composition of a compound is represented by an empirical or molecular formula, each consisting of at least one formula unit.Contributors The atoms in chemical compounds are held together by attractive electrostatic interactions known as chemical bonds. Ionic compounds contain positively and negatively charged ions in a ratio that results in an overall charge of zero. The ions are held together in a regular spatial arrangement by electrostatic forces. Most covalent compounds consist of molecules, groups of atoms in which one or more pairs of electrons are shared by at least two atoms to form a covalent bond. The atoms in molecules are held together by the electrostatic attraction between the positively charged nuclei of the bonded atoms and the negatively charged electrons shared by the nuclei. The molecular formula of a covalent compound gives the types and numbers of atoms present. Compounds that contain predominantly carbon and hydrogen are called organic compounds, whereas compounds that consist primarily of elements other than carbon and hydrogen are inorganic compounds. Diatomic molecules contain two atoms, and polyatomic molecules contain more than two. A structural formula indicates the composition and approximate structure and shape of a molecule. Single bonds, double bonds, and triple bonds are covalent bonds in which one, two, and three pairs of electrons, respectively, are shared between two bonded atoms. Atoms or groups of atoms that possess a net electrical charge are called ions; they can have either a positive charge (cations) or a negative charge (anions). Ions can consist of one atom (monatomic ions) or several (polyatomic ions). The charges on monatomic ions of most main group elements can be predicted from the location of the element in the periodic table. Ionic compounds usually form hard crystalline solids with high melting points. Covalent molecular compounds, in contrast, consist of discrete molecules held together by weak intermolecular forces and can be gases, liquids, or solids at room temperature and pressure. An empirical formula gives the relative numbers of atoms of the elements in a compound, reduced to the lowest whole numbers. The formula unit is the absolute grouping represented by the empirical formula of a compound, either ionic or covalent. Empirical formulas are particularly useful for describing the composition of ionic compounds, which do not contain readily identifiable molecules. Some ionic compounds occur as hydrates, which contain specific ratios of loosely bound water molecules called waters of hydration.
Transportation is the means of moving people, goods and services from one place to another. There are three means of transportation, that is, land, water and air. Land transportation is the means of moving from one place to another on land. The means of transportation used in Nigeria varies from one locality to another. In the riverine areas, the most widely used means of transportation is by canoe or boat. This is because the people live on the water. TYPES OF TRANSPORTATION The following are the main types of transportation: 1. Land transportation 2. Air transportation 3. Water transportation FORMS OF LAND TRANSPORTATION The forms of land transportation include: (i) Roads: This includes the use of cars, trucks, buses, motorcycles, bicycles etc. (ii) Rail: The use of trains. (iii) Trekking on foot. (iv) The use of animals like donkeys, camels, horses etc. They are called beast of burden. PROBLEMS OF LAND TRANSPORTATION The following are the problems of land transportation: 1. Transportation facilities are not sufficient for the number of people using them. 2. Too many accidents on the road. 3. The spare parts are very expensive. 4. High cost of transportation. 5. Potholes on the road, thereby causing a lot of damage to vehicles. 6. Reckless driving on the road by some drivers. SOLUTIONS TO THE PROBLEMS OF ROAD TRANSPORTATION ARE: 1. Drivers should not drink before and while driving. 2. Government should help repair damaged roads. 3. Drivers should avoid reckless driving. 4. Traffic offenders should be punished. 5. The cost of transportation should be reduced. 6. Spare parts should be made available at cheaper prices. 7. Road signs should be placed at major locations. 8. Road users should be educated on the use of the road and road signs.
Continental Drift Theory. From the discussion of the rock cycle, it has been pointed out that through Earth's external and internal processes. Earth's surface is constantly changing. However, this idea of a changing environment did not conform with the belief of earlier scientists. Rather, they thought that the geographic positions of ocean basins and continents have been static since the beginning of time. It was around the 1500s when Leonardo da Vinci, upon his discovery of fossil seashells found at the high mountains of Italy, first thought of the idea that the areas where mountains are located may have been oceans in the past. Through time, other fossils of marine organisms found far above the current sea level further supported the idea that mountains were uplifted and weathering wore them down. At around the 1800s, most scientists have accepted the idea that Earth's crust is undergoing large vertical movements or uplifting. There was also evidence of possible horizontal movements, but the scientists then were not convinced about it. Alfred Wegener showed evidence of horizontal or lateral movement of the continents in his continental drift theory. According to him, the continents have drifted around the world and have once formed a giant landmass or supercontinent called Pangaea. To support his theory, Alfred Wegener presented a set of geographical, biological, and climatic evidence.Wegener's geographical evidence included the jigsaw puzzle fit of the current continents. He pointed out that the coastlines of South America and Africa seem to fit together. He also pointed the presence of mountain ranges having similar rock types and age but separated by vast oceans, like that of the folded rocks of the Caledonian mountains. The same folded rocks run through West Africa, North America, Newfoundland, Ireland, Wales, Scotland, Greenland, and Norway, all of which are now separated by the Atlantic Ocean. A geographical evidence on the similar rock types in West Africa, North America, Greenland, and Europe is found. The biological evidence came in the discovery of similar plant and animal fossils in different continents separated by oceans. The animal fossils of Mesosaurus and Lystrosaurus indicate that they were not capable of crossing the oceans to reach the other continents. If they were, the fossils should have been more widely distributed Africa, Australia, India, and South America were too large to be carried by wind. This indicates that the areas where the fossils were found were closely linked. It has also been found out that the plant only grew in areas with subpolar climate, which would indicate that the landmasses were located near the South Pole.Lastly, for his climatic evidence, Wegener discovered that a glacial period occurred during the late Paleozoic era in Southern Africa, South America, Australia, and India. The initial explanation for this event was global cooling, but it was rejected because large tropical swamps with so much vegetation were found at the same time in the Northern Hemisphere. This further supported the idea that the supercontinent was indeed near the South Pole, and the continents in Northern Hemisphere were once near the equator. The glacial period also left glacial striations, or the scratches glaciers make as they move across on the underlying bedrock, on the aforementioned continents. For such an event to happen, the continents would have to be connected. SCIENCE PIONEER. Alfred Wegener (1880-1930). Alfred Wegener was a German polar researcher, geophysicist, and meteorologist. He was known for his work on the continental drift theory. In his effort to defend his work, he went to the Greenland ice sheet where he died.Even with all the compelling evidence, the continental drift theory hardly convinced the scientific community at that time because Wegener was unable to identify a credible mechanism that drives the continental drift. He was unable to clearly explain how the continents moved and how the larger continents broke through the ocean floor. Eventually, critics of the continental drift began to accept the theory when new evidence supporting the theory was discovered. The new evidence led to a more encompassing theory the theory of plate tectonics. This theory provided a more convincing explanation as to how the continents moved. The evidence that paved the way for the theory of plate tectonics was the idea of wandering poles. Scientists began studying volcanic rocks to determine the location of the magnetic poles. When volcanic rocks crystallize, the minerals with magnetic properties align themselves parallel to Earth's magnetic field at the time the minerals were formed. This finding allowed scientists to determine the polarity of Earth's magnetic field and the magnetic inclination that showed the location of the poles. Upon studying the paleomagnetism of the rocks, geophysicists found out that rocks from various locations point to different magnetic north poles, suggesting that the poles have wandered. Since movement of magnetic poles is very unlikely, scientists have accepted the idea that the continents are indeed moving. And if the continents are moving, scientists thought that maybe the ocean basins are moving too. They also discovered that some rocks showed magnetic reversals, which led them to believe that the magnetic north pole now was not always the magnetic north pole. Seafloor Spreading. After World War II, exploration on the ocean floor became the focus of many geologic studies. It was only then that the ocean ridge system was discovered. A geologist in Princeton University named Harry Hess, along with other scientists, studied this ocean ridge system and hypothesized that the oceanic crust was moving away from the ridge. His hypothesis, known as seafloor spreading, showed that the ocean floor is split along the ridge where the magma rises to form the new ocean floor.Because of this, rocks located near the ridge are younger than those that are located magnetic polarity of Earth is also preserved in those rocks. Withe ridge scientists were able to see the magnetic reversals in the ocean floor, and they were able to make use of information to determine that the ocean floor is moving at a rate of about 10 cm per year. Plate Tectonics. Confirmation of the seafloor spreading hypothesis proved that continents are not moving above the ocean floor. Rather, it is the fragments of the lithosphere. The lithosphere is the rigid layer that is composed of the uppermost mantle and the crust that carry the continents and the ocean basins along. These fragments of the lithosphere are called plates. Underneath the lithosphere is a weaker region in the mantle known as asthenosphere that behaves like a fluid. Thus, the lithosphere floats above the asthenosphere, making it detached and free to move. This became the basis of the theory of plate tectonics. Now that it has been made clear that it is the plates which are moving, the question as to how they move remained. Sir Arthur Holmes proposed the driving force for this plate movement in 1919. He suggested that the movement in the mantle carries the plates along. It was previously discussed that Earth's interior is very hot due to the heat produced by radioactive decay. Convection takes place in the mantle, keeping the asthenosphere hot and weak. The convection currents produced in the asthenosphere are the ones carrying the lithospheric plates and making them move. However, convection currents are not enough. Mechanisms such as ridge push and slab pull aid the convection currents to slowly move the lithospheric plates. Ridge push occurs at mid ocean ridges which are higher in elevation than the surrounding trenches and abyssal plains. The new ocean floor from the ridge is hot and relatively thin. As it moves away from the ridge, it cools down and gets denser, heavier, and thicker. Below this cooling ocean floor is the asthenosphere, which is less dense. This area becomes a massive shear zone and the new ocean floor will effectively slide down the slope of the asthenosphere. When the plate collides with another plate with lesser density, the denser plate sinks and a subduction zone is formed. When the subducting plate sinks, it pulls on the rest of the plate behind it. These mechanisms explain the movement of the plates.Earth has seven major lithospheric plates that account for 94% of Earth's surface. These are the North American Plate, South American Plate, Pacific Plate, African Plate, Eurasian Plate, Indo-Australian Plate, and Antarctic Plate. These plates are constantly moving relative to the other plates. Thus, the interaction of plates occurs mostly along the boundaries. These movements are plotted using information from earthquakes and volcanic activities. There are three main types of plate boundaries: convergent, divergent, and transform boundaries Convergent boundaries are boundaries where two plates move towards each other A convergent boundary is also known as destructive margin since this is where the collision between two plates occhins. There are three types of convergence-oceanic oceanic, oceanic-continental, and continental-continental. Trenches are features of the ocean floor that are present in both oceanic-oceanic boundary and oceanic-continental boundary. Subduction occurs at the trenches, therefore, these are characterized as the deepest parts of Earth. A divergent boundary is the opposite of convergent boundary: two plates move away from each other. Divergent boundaries create new crust; thus, they are also known as constructive margins. The ocean ridge system is a divergent boundary where new ocean floor is produced as magma rises, pushing the older rocks aside.Transform boundary is also known as conservative plate margin since two plates just move past one another, neither creating nor destroying land. Earthquake epicenters are usually detected at transform boundaries because the rocks tend to break and not fold or sink, like in convergent boundaries. Evolution of the Ocean Basins. Both the movement of the plates and seafloor are responsible for the evolution of ocean basins. Along the divergent boundary where ocean ridge systems are found, magma is released and new ocean floor is created. Along convergent boundaries, the ocean floor is being destroyed. The evolution of the ocean basins started during the time when Pangaea was still present and was surrounded by the vast ocean or superocean known as Panthalassa, also called Paleo-Pacific or "old Pacific." Upon the initial break up of Pangaea into Laurasia and Gondwanaland, the Tethys Sea began to form. Then, the Eurasian and North about, forming the North Atlantic. The South Atlantic only started to form when the African Plate and South American Plate separated. The continued movement of the plates created the Himalayas at one side and separated the Pacific Ocean and Atlantic Ocean at the other side, which consequently formed the current ocean basins. Both the movement of the plates and seafloor are responsible for the evolution of ocean basins. Along the divergent boundary where ocean ridge systems are found, magma is released and new ocean floor is created. Along convergent boundaries, the ocean floor is being destroyed. The evolution of the ocean basins started during the time when Pangaea was still present and was surrounded by the vast ocean or superocean known as Panthalassa, also called Paleo-Pacific or "old Pacific." Upon the initial break up of Pangaea into Laurasia and Gondwanaland, the Tethys Sea began to form. Then, the Eurasian and North about, forming the North Atlantic. The South Atlantic only started to form when the African Plate and South American Plate separated. The continued movement of the plates created the Himalayas at one side and separated the Pacific Ocean and Atlantic Ocean at the other side, which consequently formed the current ocean basins.Continents do not immediately end at the point where the ocean meets the land. They may extend slightly into the oceans. The portion of the continent that is submerged is called continental margin. There are two types of continental margin: passive margin and active margin. A passive continental margin consists of a continental shelf, continental slope, and continental rise. It is not associated with plate boundaries; thus, there are very little tectonic activities. An active continental margin only has a continental shelf and a continental slope. It is associated with plate boundaries; thus, a main feature of this boundary is a trench. The different features of a continental margin are the following: 1. The continental shelf is the gently-sloping submerged portion of the continent. 2. The continental slope is the steep slope after the continental shelf. It is still part of the continent. 3. The continental rise is the gently-sloping area after the continental slope and before the ocean floor. 4. The trenches are the deepest parts of the ocean. These are narrow depressions caused by the subduction of the ocean floor along the convergent boundaries. 5. The mid-oceanic ridge is the mountain range system in the ocean. It is responsible for the production of new ocean floor. This is the region where new magma constantly emerges from. SCIENCE CAREER. A scientific illustrator uses art to inform and communicate complex details and concepts of science. He/She makes use of scientifically informed observations and research along with his/her technical art and aesthetic skills to make accurate representations. In Natural History, the scientific illustrators recreate how the extinct species look like by working with scientists and fossil records. Moreover, with the advances in technology, illustrators are now into 3D modelling, animation, and video making. Earth's History. All the processes that have been discussed require long periods of time to create a noticeable change on Earth's surface. You can just imagine how long it would take to create an oceanas vast as the Pacific Ocean if the ocean floor moves only at about 10 cm/year. It is then important to know the history of Earth to learn the complexities of its past and be able to use it to understand the present. Just like learning the history of a country that requires one to read a lot of books, learning the history of Earth involves studying a lot of rocks. Rocks, especially sedimentary rocks, contain a lot of information about Earth's past. It holds the key to most of the geologic processes that happened on Earth and the key to uncovering how life on Earth evolved. But these discoveries are worthless if there is no time perspective. Thus, one of the most important contributions of geologists to mankind is the geologic time scale, which holds a history that is exceedingly long.
Lide 1: Introduction to Bioreactor A bioreactor is a vessel used for growing microorganisms, plant or animal cells Provides controlled conditions for biological reactions Maintains optimum pH, temperature, oxygen, and nutrients Widely used in fermentation, enzyme, vaccine, and antibiotic production Ensures sterile and aseptic environment Scale ranges from laboratory to industrial production Slide 2: Basic Design Requirements of a Bioreactor Must be constructed with non-toxic, corrosion-resistant materials Should allow effective mixing and mass transfer Provision for sterilization (in situ sterilization) Must maintain uniform temperature and pH Easy sampling without contamination Should support scalability and automation Slide 3: Materials Used in Bioreactor Construction Stainless steel (SS-316) for industrial bioreactors Glass for laboratory-scale bioreactors Plastic (polycarbonate) for disposable bioreactors Materials must withstand heat and pressure Should be smooth to prevent microbial attachment Resistant to chemicals and cleaning agents Slide 4: Main Parts of a Bioreactor Vessel: holds the culture medium and microorganisms Agitator (impeller): provides mixing Sparger: supplies sterile air Baffles: prevent vortex formation Sensors: monitor pH, temperature, dissolved oxygen Ports: used for inoculation, sampling, and feeding Slide 5: Agitation System Ensures uniform mixing of nutrients and cells Improves oxygen transfer rate Common impellers: Rushton turbine, marine propeller Speed controlled by motor Prevents settling of cells Affects shear stress on cells Slide 6: Aeration System Supplies oxygen for aerobic fermentation Air introduced through sparger Types of spargers: ring, nozzle, sintered Maintains dissolved oxygen concentration Air is filtered for sterility Essential for high cell density cultures Slide 7: Temperature and pH Control Temperature controlled by heating/cooling jackets pH maintained using acid or alkali addition Sensors continuously monitor parameters Automated control systems used Ensures optimal microbial growth Prevents enzyme denaturation Slide 8: Foam Control System Foam formed due to protein and agitation Excess foam reduces oxygen transfer Mechanical foam breakers used Chemical antifoam agents added Foam sensor detects foam formation Maintains efficient fermentation Slide 9: Types of Bioreactors â Based on Mode of Operation Batch bioreactor Fed-batch bioreactor Continuous bioreactor Choice depends on product type Widely used in industrial fermentation Controls productivity and yield Slide 10: Batch Bioreactor All nutrients added at the beginning No addition or removal during process Simple and easy to operate Low risk of contamination Used for antibiotics and enzymes Limited control over nutrient depletion Slide 11: Fed-Batch Bioreactor Nutrients added during fermentation Prevents substrate inhibition High product yield Widely used in industrial fermentation Allows better control of growth rate Used in insulin and enzyme production Slide 12: Continuous Bioreactor Fresh medium continuously added Culture removed at same rate Maintains steady-state conditions High productivity Risk of contamination is high Used in wastewater treatment and SCP production Slide 13: Types of Bioreactors â Based on Design Stirred tank bioreactor Airlift bioreactor Bubble column bioreactor Packed bed bioreactor Fluidized bed bioreactor Photobioreactor Slide 14: Stirred Tank Bioreactor (STR) Most commonly used bioreactor Mechanical agitation using impellers Suitable for aerobic fermentation Excellent mixing and oxygen transfer Used for bacteria and fungi Easy scale-up Slide 15: Airlift Bioreactor Mixing achieved by air circulation No mechanical agitator Low shear stress Energy efficient Suitable for shear-sensitive cells Used in wastewater treatment Slide 16: Bubble Column Bioreactor Air bubbles provide mixing Simple design and low cost No moving parts Limited mixing efficiency Used for microbial fermentation Suitable for large-scale operations Slide 17: Packed Bed Bioreactor Contains immobilized cells or enzymes Substrate flows through packed matrix High cell density Used in continuous processes Limited oxygen transfer Used in enzyme and wastewater treatment Slide 18: Fluidized Bed Bioreactor Immobilized particles kept in suspension Better mass transfer than packed bed Reduced clogging Suitable for continuous operation Used in biotransformations Higher operational complexity Slide 19: Photobioreactor Designed for photosynthetic organisms Provides light source Used for algae and cyanobacteria Controls light, COâ, and temperature Used in biofuel and pigment production Can be tubular or flat-plate design Slide 20: Applications of Bioreactors Production of antibiotics and vaccines Enzyme and organic acid production Single cell protein production Wastewater treatment Biofertilizer and biopesticide production Biopharmaceutical manufacturing
Some substances, such as macromolecules and nutrients, are too large to pass through the cell membrane by the transport processes you have studied so far. Cells employ two other transport mecha- nismsâendocytosis and exocytosisâto move such substances into or out of cells. Endocytosis and exocytosis are also used to transport large quantities of small molecules into or out of cells at a single time. Both endocytosis and exocytosis require cells to expend energy. Therefore, they are types of active transport. Endocytosis Endocytosis (EN-doh-sie-TOH-sis) is the process by which cells ingest external fluid, macromolecules, and large particles, including other cells. As you can see in Figure 5-7, these external materials are enclosed by a portion of the cellâs membrane, which folds into itself and forms a pouch. The pouch then pinches off from the cell membrane and becomes a membrane-bound organelle called a vesicle. Some of the vesicles fuse with lysosomes, and their con- tents are digested by lysosomal enzymes. Other vesicles that form during endocytosis fuse with other membrane-bound organelles. Two main types of endocytosis are based on the kind of material that is taken into the cell: pinocytosis (PIEN-oh-sie-TOH-sis) involves the transport of solutes or fluids, and phagocytosis (FAG-oh-sie-TOH-sis) is the movement of large particles or whole cells. Many unicellular organisms feed by phagocytosis. In addition, certain cells in animals use phagocytosis to ingest bacteria and viruses that invade the body. These cells, known as phagocytes, allow lysosomes to fuse with the vesicles that contain the ingested bacteria and viruses. Lysosomal enzymes then destroy the bacteria and viruses before they can harm the animal. CYTOSOL EXTERNAL ENVIRONMENT During endocytosis, the cell membrane folds around food or liquid and forms a small pouch. The pouch then pinches off from the cell membrane to become a vesicle. FIGURE 5-7 vesicle from the Latin vesicula, meaning âbladderâ or âsacâ Word Roots and Origins www.scilinks.org Topic: Endocytosis Keyword: HM60505 mb06se_homs02.qxd 5/18/07 11:03 AM Page 105 106 CHAPTER 5 1. Explain the difference between passive trans- port and active transport. 2. What functions do carrier proteins perform in active transport? 3. What provides the energy that drives the sodium-potassium pump? 4. Explain the difference between pinocytosis and phagocytosis. 5. Describe the steps involved in exocytosis. 6. How do endocytosis and exocytosis differ? How can that difference be seen? CRITICAL THINKING 7. Analyzing Information During intense exercise, potassium tends to accumulate in the fluid surrounding muscle cells. What membrane protein helps muscle cells counteract this tendency? Explain your answer. 8. Evaluating Differences How does the sodium- potassium pump differ from facilitated diffusion? 9. Relating Concepts The vesicles formed during pinocytosis are much smaller than those formed during phagocytosis. Explain. SECTION 2 REVIEW Vesicle Cell membrane EXTERNAL ENVIRONMENT CYTOSOL During exocytosis, a vesicle moves to the cell membrane, fuses with it, and then releases its contents to the outside of the cell. FIGURE 5-8 INSIDE OF CELL Vesicle OUTSIDE OF CELL Exocytosis Exocytosis (EK-soh-sie-TOH-sis) is the process by which a substance is released from the cell through a vesicle that transports the sub- stance to the cell surface and then fuses with the membrane to let the substance out of the cell. This process, illustrated in Figure 5-8, is basically the reverse of endocytosis. During exocytosis, vesi- cles release their contents into the cellâs external environment. Figure 5-8 also shows a photo of a vesicle during exocytosis. Cells may use exocytosis to release large molecules such as pro- teins, waste products, or toxins that would damage the cell if they were released within the cytosol. Recall that proteins are made on ribosomes and packaged into vesicles by the Golgi apparatus. The vesicles then move to the cell membrane and fuse with it, deliver- ing the proteins outside the cell. Cells in the nervous and endocrine systems also use exocytosis to release small molecules that control the activities of other cells.
Received: 26 November 2019 Revised: 10 January 2020 Accepted: 19 January 2020 DOI: 10.1111/obr.13005 PEDIATRICS/PHYSIOLOGY Adipokines: A gear shift in puberty DesirĂ©e Nieuwenhuis | NatĂ lia Pujol-Gualdo Amanda J. Kiliaan Department of Anatomy, Radboud university medical center, Donders Institute for Brain, Cognition and Behaviour, Preclinical Imaging Center PRIME, Nijmegen, The Netherlands Correspondence Amanda J. Kiliaan, PhD, Associate Professor, Department of Anatomy, Donders Institute for Brain, Cognition, and Behaviour, Preclinical Imaging Center PRIME, Radboud university medical center, 6500 HB Nijmegen, Geert Grooteplein 21N 6525 EZ Nijmegen, The Netherlands. Email: amanda.kiliaan@radboudumc.nl Funding information Europees Fonds voor Regionale Ontwikkeling (EFRO), Grant/Award Number: BriteN 2016 1 | INTRODUCTION The prevalence of obesity in adolescents and children is increasing in | Ilse A.C. Arnoldussen | Summary In this review, we discuss the role of adipokines in the onset of puberty in children with obesity during adrenarche and gonadarche and provide a clear and detailed overview of the biological processes of two major players, leptin and adiponectin. Adipokines, especially leptin and adiponectin, seem to induce an early onset of puberty in girls and boys with obesity by affecting the hypothalamic-pituitary- gonadal (HPG) axis. Moreover, adipokines and their receptors are expressed in the gonads, suggesting a role in sexual maturation and reproduction. All in all, adipokines may be a clue in understanding mechanisms underlying the onset of puberty in child- hood obesity and puberty onset variability. KEYWORDS adipokines, obesity, puberty 1,2 the age of 5 years were overweight or were with obesity in 2016, and 3 Obesity is defined by an excessive accumulation of white adipose tissue (WAT), and it is often indicated by a body mass index (BMI) 4 above 30. Two main types of adipose tissue were described: WAT and brown adipose tissue (BAT), which differ in morphology and func- 5-7 Ilse A.C. Arnoldussen and Amanda J. Kiliaan contributed equally to this work. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. © 2020 The Authors. Obesity Reviews published by John Wiley & Sons Ltd on behalf of World Obesity Federation Obesity Reviews. 2020;21:e13005. wileyonlinelibrary.com/journal/obr 1 of 10 https://doi.org/10.1111/obr.13005 alarming rates. Specifically, worldwide, 41 million children below this number is expected to increase to 70 million in 2025. obesity is associated with various severe health complications, includ- ing increased risk of diabetes mellitus type 2, hypertension, heart dis- eases, and disturbances in sex hormone levels. 5,6 and mitochondria and plays a role in thermogenesis. Adipocytes in tion. BAT consists of adipocytes containing multiple lipid droplets WAT contain only a few mitochondria and a single lipid droplet. Adipose tissue has several functions including the storage of energy, thermogenesis, and the production and secretion of adipokines Generally, two physiological processes, adrenarche and gonadarche, 11,24 Childhood 5,7,8 a key role in puberty onset. Puberty is known as a period through which the body changes physically, being a physiological process resulting in the maturation of children, i.e. they develop sexual characteristics and obtain reproduc- 9,11 Adipokines are involved in a number of physiological processes including blood pressure, metabo- lism, glucose, and vascular homeostasis and may play amongst others 8-10 (hormones, cytokines, and peptides). tive functions. between obesity and puberty,2,12-23 the biological mechanisms under- lying obesity and puberty onset remain unclear. Hereafter, we review in detail the role of adipokines in the onset of puberty in childhood obesity. Although many studies have shown associations 2 | INITIATION OF PUBERTY PHYSIOLOGICAL PROCESSES IN THE interact to regulate the onset of puberty. During adrenarche, the adrenal cortex secretes steroid hormones (including 2 of 10 NIEUWENHUIS ET AL. androstenedione, dehydroepiandrosterone, dehydroepiandrosterone sulfate (DHEAS), androstenedione, and cortisol), insulin-like growth factor, and growth hormone, which contribute to the pubertal insights on new genetic loci (e.g. melanocortin-4 receptor, mitochon- drial carrier 2, and mitogen-activated protein kinase 13) and on sev- eral pathways that regulate the timing of puberty; however, it partly 34 9,24,25 Both adrenarche and gonadarche are involved in the development growth spurt, body odor, skin oiliness, and skeletal maturation. explains puberty timing variation. Thereby, defining the role of 25 adipokines is of importance in elucidating the variability in puberty as the expression of adipokines is sex-specific and is altered with body composition, adiposity, and during growth spurts. Moreover, adipokines and their receptors are expressed in gonads and several brain regions suggesting involvement in the onset of puberty and sex- ual maturation. Lastly, adipokines interfere in processes regulating timing and duration of puberty, for instance in the HPA and HPG axes which are both key players during adrenarche and gonadarche. Involvement of adipokines in the onset of puberty and specifically in individuals with obesity will be further reviewed in the next 2,24 3 | Puberty onset in girls is assessed using different markers, such as thelarche (breast development), menarche (the start of of pubic hair. pituitary-gonadal (HPG) axis is activated,2,26 and several hormones have been identified to participate in the activation of the HPG axis During gonadarche (Figure 1), the hypothalamic- 2,27 Kisspeptin, neurokinin B, and dynorphin are released by specialized including kisspeptin, neurokinin B, dynorphin, leptin, and ghrelin. 28 key regulator of the pulsatile secretion of gonadotropin releasing neurons, the KNDy neurons in the hypothalamus. Kisspeptin is a 29,30 B stimulates, and dynorphin inhibits the release of kisspeptin, which hormone (GnRH) from the hypothalamus. In addition, neurokinin implies that both coordinate a pulsatile release of kisspeptin. 31 Sub- sections. sequently, the activated HPG axis induces the pituitary gland to secrete luteinising hormone (LH) and follicle stimulating hormone (FSH). As a result, gametogenesis occurs, and the gonads will release sex hormones. Consequently, secondary sex characteristics develop including breast development in girls and an increased testicular vol- 2,26,32 is possibly due to differences in levels of body fat, hypothalamic-pitui- THE ONSET OF PUBERTY IN GIRLS ume in boys. The age at puberty onset varies greatly among individuals, which 19 35 menstruation), and pubic hair development. 33 genome-wide association studies have provided important new tary-adrenal (HPA) axis activity, and genetic background. Recent The average age of However, this age differs between cultures and ethnicities, and since 1980, age at menarche is girls at start of menarche is 12.4 years. 36 significantly decreasing. 36-39 F I G U R E 1 Hormonal regulation in the initiation of puberty in boys and girls. The secretion of kisspeptin, neurokinin B, and dynorphin from KNDy neurons initiate the release of gonadotropin releasing hormone (GnRH) from the hypothalamus. This activates the pituitary gland to produce and secrete luteinising hormone (LH) and follicle stimulating hormone (FSH), which in turn stimulate the gonads to produce estrogen and testosterone in girls and boys, respectively 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 3 of 10 T A B L E 1 Summary of included studies Authors Year Country Study Design Primary Outcome Sex Sample Size (n) Age (y) Data Collection Lian et al21 2019 China Cross-sectional Puberty starts earlier in Chinese Han girls with obesity compared with Chinese Han girls with normal weight. Girls 2996 9-19 2012 and 2013 Biro et al12 Lazzeri et al20 2018 USA 2018 Italy Longitudinal Cross-sectional Body mass index had a greater effect on age at menarche than did race and ethnicity. Girls 946 6-16 2004-2014 Li et al23 2018 China Longitudinal For both, boys and girls, a higher BMI (ie, overweight and obese) is associated with earlier onset of puberty Girls Girls Boys Girls 542 Deng et al22 Flom et al15 2017 China Cross-sectional Increased BMI is associated with early timing spermarche and menarche. Boys Girls Girls 1278258 9-15 2005-2012 He et al24 Holmgren et al17 2017 China 2017 Sweden Cross-sectional Longitudinal Onset of puberty is not related to obesity in boys. Boys Boys Girls Girls 782 7-17 972 929 5839 Kelly et al19 2017 UK 2016 Brazil 2016 USA Longitudinal prospective cohort Higher BMI in girls is associated with the onset of menstruation at an earlier age. 11 10-18 11-17 Barcellos Gemelli et al25 Cross-sectional Longitudinal Excess weight is associated with early age of menarche. Girls 727 2014 2003-2009 Glass et al16 Lee et al26 In girls, but not in boys, greater adiposity is associated with the earlier onset of puberty. Boys Girls 135 Cabrera et al27 Leonibus et al14 2014 USA 2013 Italy Cross-sectional Longitudinal Thelarche occurred earlier than recently reported, while age of menarche remained unchanged. Girls 610 3-17.9 2007 2005-2012 Currie et al13 2012 Europe, USA, Canada Cross-sectional Overweight/obesity during childhood predicts the early onset of puberty in girls. Girls 20410 11, 13, 15 2005-2006 2017 USA Prospective birth cohort Overweight/obese status at the age of 7 ye was associated with increased risk of early menarche 788 From birth to menarche occurred Pregnancies 1959-1966 2016 USA Cross-sectional Boys with overweight enter puberty earlier compared with boys with normal weight or obesity, while puberty starts later in boys with obesity compared with boys with normal weight and overweight. Boys 3872 6-16 2005-2010 Overweight during childhood shows a relation with the early onset of puberty in girls. 6535 4259 695 11 15 5.8-12.2 2009/2010 2013/2014 2014-2017 Higher BMI during childhood is associated with early puberty. 2008 and 2009 2000-2002 Obesity during childhood is related to the earlier onset of puberty. Boys Girls 84 123 71 (Continues) 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 4 of 10 NIEUWENHUIS ET AL. 3.1 | Fat storage For the initiation of puberty, the timing of stimulation and/or inhibi- tion of different hormones is important, and additionally, a certain amount and distribution of body fat is needed in order to start menar- che, which emphasizes the importance of body fat. From an evolution- ary point of view, body fat increases in mammalian females during puberty onset, and it highlights the need to guarantee a healthy preg- 40 women with anorexia nervosa. particularly body fat localized predominantly on the gluteofemoral fat depots, is profoundly associated with start of menarche, more than nancy, offspring, and maternal survival. fat, sex-hormones, and neuroendocrine alterations can evolve in men- strual dysfunction, for instance, in women with severe obesity or in 41-43 44-46 to gluteofemoral fat depots suggesting that leptin may convey infor- amount of total body fat. mation on body fat distribution to the hypothalamus during puberty. An improper level of body Importantly, body fat distribution, Blood leptin levels are strongly related 45 3.2 | HPG axis The HPG axis is activated by the release of kisspeptin resulting in the release of GnRH from the hypothalamus, and LH and FSH from the pituitary gland. In girls, FSH is involved in the development of the folli- cles in the ovaries, and it promotes the secretion of estrogen. LH stim- ulates the production of androgen hormones and induces ovulation 48 9,47 the release of kisspeptin and neurokinin B, and kisspeptin thereby (Figure 1). The secretion of estrogen has an inhibitory effect on inhibits the GnRH release from the hypothalamus. pattern of GnRH is important for the regulation of the menstrual cycle. This roughly 28-day-cycle comprises several phases, including the follicular phase and luteal phase. During the follicular phase, increasing levels of FSH stimulate the maturation of follicles and the production of estrogen from the ovaries. This in turn inhibits the release of FSH from the pituitary gland. A high level of estrogen will induce the production of LH by the pituitary gland, resulting in ovula- tion. The matured follicle secretes progesterone thereby inhibiting the release of GnRH. When the corpus luteum is demolished, there is less 48 3.3 | Adipokines According to results from studies reported in Table 1, girls with obe- sity enter puberty earlier compared with girls with normal higher leptin concentrations inhibit the intake of food and increases inhibition of GnRH. As a consequence, the cycle will start again. whole process, starting from the activated HPG axis, results in the development of the secondary sex characteristics in girls including 9,47 thelarche and menarche. 13,14,16-23,49-51 weight. these girls might be found in the secretion of adipokines. For instance, leptin is positively associated with the amount of body fat. Generally, energy expenditure. 9,52-54 An explanation for the early onset of puberty in The expression This TABLE 1 (Continued) Authors Year Country Study Design Primary Outcome Sample Sex Size (n) Age (y) Data Collection Herman-Giddens et al28 2012 USA Cross-sectional Observed mean ages of beginning genital and pubic hair growth and early testicular volumes were earlier than in past studies, depending on the characteristic and race/ethnicity. Boys 4131 6-16 2005-2010 Sorensen et al29 Aksglaede et al30 2010 2009 Denmark Denmark Cross-sectional/longitudinal Longitudinal Puberty onset at earlier ages was associated with an increased BMI in boys. Boys 1528 5.8-19.9 1991-1993/2006-2008 1930-1969 Juul et al31 Ribeiro et al32 2007 2006 Denmark Portugal Retrospective cohort Cross-sectional Higher BMI is associated with early voice break. 11-15 10-15 1990-1999 Kaplowitz et al18 Abbreviation: BMI, body mass USA Cross-sectional The early onset of puberty in Caucasian girls is likely related to an increased BMI. 5-12 1992-1993 2001 index. The higher BMI in boys and girls at 7 y of age, the earlier they enter puberty. Boys 21 612 Girls 135 223 Boys 463 Boys 382 Girls 437 Girls 10 750 Early sexual maturation in boys and girls is associated with overweight. 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 5 of 10 Leptin may possibly play a role in adrenarche as its plasma level increases with higher levels of body fat and as it can modulate both girls. 33 ing adrenarche. In coherence, in children with obesity, the androgen These findings suggested that lower reproductive status was associated with higher total adiponectin concentrations and that a higher reproductive status was related to higher HMW adiponectin the HPA and HPG axes. These axes are functionally integrated dur- DHEAS was positively associated with leptin levels. Nevertheless, concentrations in girls. In addition, individuals with obesity often another study showed that enhanced adrenal androgen secretion in girls with premature adrenarche was not explained by leptin or BMI 55 ated with androgen levels in girls ; however, it was not related to levels. and IL-6. TNF-α alters, and IL-6 inhibits the expression of 56 8 In addition, the adipokine adiponectin was negatively associ- 57 differences of adiponectin seem to develop during the progression of 56 adiponectin (Figure 2). Thereby, a low level of total adiponectin and/or high levels of inflammatory cytokines in individuals with obe- sity can promote the onset of puberty. Many more adipokines are secreted by WAT including omentin, 52,65-67 9,36,62,68 adrenarche in girls with Prader-Willi syndrome. Interestingly, sex puberty. adrenarche; however, both are not required factors. Thus, leptin and adiponectin might be able to influence In gonadarche, leptin can stimulate the secretion of kisspeptin, and subsequently activation of the HPG axis, which eventually increases the expression of estrogen and androstenedione in the ova- 58 2,60 65-67 The expression of these ries (Figure 2). Ob gene in WAT, resulting in the synthesis and secretion of leptin. Thus, high levels of leptin promote onset of puberty in girls via secre- tion of kisspeptin, and estrogen stimulates leptin secretion addition- ally. Moreover, adiponectin can affect the HPG axis due to the expression of adiponectin receptors in the hypothalamus, pituitary In return, estrogen stimulates the expression of the 59 gland, and gonads. onset as it inhibits the secretion of kisspeptin and GnRH in the hypo- thalamus and the release of GH and LH in the pituitary gland, and 2,60-62 52,60 63 girls with central precocious puberty (CPP). Moreover, total adiponectin had negative correlations with progression of puberty in girls (defined by Tanner stages), whereas HMW adiponectin had FIGURE 2 Adipokinesaffectingthe initiation of puberty in girls. Leptin stimulates the release of kisspeptin in KNDy neurons, which activates the hypothalamus to produce gonadotropin releasing hormone (GnRH). In response to the release of GnRH, the pituitary gland secretes follicle stimulating hormone (FSH) and luteinising hormone (LH), which stimulates the ovaries to release estrogen resulting in the formation of secondary sex characteristics in girls. Estrogen stimulates the production of leptin. Adiponectin inhibits GnRH release resulting in reduced levels of GnRH and thereby a delayed onset of puberty. TNF- α and IL-6 inhibit the production of adiponectin and therefore stimulate the onset of puberty In detail, adiponectin is a regulator of puberty thereby inhibiting the onset of puberty (Figure 2). with obesity often have low levels of adiponectin. et al. showed that total adiponectin was significantly lower, whereas high molecular weight (HMW) adiponectin was significantly higher in ment. 55 63 develop a chronic low-grade inflammatory state, which can be indi- cated by a high level of circulating inflammatory cytokines like TNF-α 64 Individuals Sitticharoon positive associations with LH levels and the progression of puberty in 63 visfatin, resistin, and chemerin. and visfatin are expressed in the ovaries. adipokines in the ovaries suggests a role within the reproductive sys- tem; however, the exact biological processes have to be examined. Thus, specifically leptin, adiponectin, and inflammatory cytokines pro- duced by WAT could be permissive key players during an early onset of puberty in girls with obesity. As an exception, HMW adiponectin seems to have a stimulatory effect on peripheral repro- ductive function as HMW is not able to cross the blood brain 63 barrier. 4 | Markers that are used to assess puberty onset in boys are THE ONSET OF PUBERTY IN BOYS spermarche, voice break, testicular volume, and pubic hair develop- 35 spermarche develop in the early stages of puberty onset, voice In women, omentin, chemerin, While pubic hair development, larger testicular volume, and 69 testicular volume increases, which occurs at an average age of break usually appears in later stages of puberty. Generally, first 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 6 of 10 NIEUWENHUIS ET AL. 11.9 years, followed by the development of pubic hair at 12.2 years of average, and lastly, boys experience spermarche around an aver- 55 related with leptin levels. Thereby, leptin plausibly has a minor impact in adrenarche in boys. Since leptin receptors are found in the hypothalamus, pituitary gland, and testes, they might be involved in the onset of puberty by affecting the HPG axis during gonadarche. Leptin stimulates the release of kisspeptin and GnRH, and as a consequence, it accelerates the onset of puberty (Table 1, Figure 3). In contrast, adiponectin inhibits the secretion of GnRH, GH, LH, and FSH therewith delaying the onset of puberty. However, adiponectin levels are generally lower in men compared with women and even lower in men with obe- age age of 13.4 years. 70 4.1 | Fat storage Many aspects of the reproductive physiology are energetically demanding,71 and therefore, an adequate energy level is necessary. In boys, a dynamic change in body composition occurs around the age of 10 to 13 years, in which they gain approximately 40% of sity. culating inflammatory cytokines. levels can stimulate the HPG axis and therewith an early onset of puberty in boys. Nevertheless, leptin can inhibit the production of tes- 72 mostly consisting of lean mass, which causes exhaustion of most of fat. Subsequently, a growth spurt follows in which they gain tissue 72 in boys, an adequate amount of body fat is important in the onset of their body fat. These alterations in amount of body fat indicate that 4.2 | Puberty in boys is initiated by the release of kisspeptin. As mentioned before, this activates the HPG axis, resulting in the release of GnRH from the hypothalamus, and consequently the release of LH and FSH 9,74 puberty. tosterone from the testes, to estrogen (Figure 3). of the development of secondary sex characteristics in boys. Additionally, leptin can affect fertility in men as it can modulate the nutritional support of spermatogenesis, and moreover, dysfunction of spermatogenesis is associated with an increased leptin level and 73 58 2,60-62 HPG axis from the pituitary gland (Figure 1). and LH stimulates the secretion of testosterone from the testes, which inhibits the release of kisspeptin from the KNDy neurons and 9,48 in men, the release of kisspeptin is more consistent, causing a con- 29,48 subsequently GnRH from the hypothalamus. receptors expressed on KNDy neurons. In humans, KNDy neurons Contrarily to women, LH-induced testosterone levels lead to the stant release of LH. development of secondary sex characteristics in boys. differences between sexes in kisspeptin release are related to a sex- specific and sex steroid-dependent kisspeptin system as estrogen and progesterone modulate kisspeptin activity through the sex-steroid 48 in the infundibular nucleus are involved in negative and positive sex- 48 tal exposure to sex steroids and result in sex-specific differences in steroid feedbacks. kisspeptin release. These sexual dimorphisms are induced by perina- 75,76 4.3 | Adipokines The association between obesity and puberty onset in boys is rather controversial compared with findings in girls. Most studies reported an early onset of puberty in boys associated with increased ate adipose tissue from actual breast tissue. stages are more difficult to assess than female stages as boys lack a more determined marker such as menarche. Thirdly, puberty onset can be indicated by the activation of the HPG axis, and the presence of these secondary sex characteristics is the result of hormonal 2 14,17,22,23,50,51,77,78 BMI, 20,49 all while others reported no associations at Current markers used 79 16,80 or a delayed onset of puberty (Table 1). The presence of excessive adipose tissue can be involved in puberty onset in boys as the secretion of adipokines can modulate both adrenarche and gonadarche. Leptin can affect adrenarche by modulating both the HPG and HPA axes,33 and moreover, androgen levels were positively 55 nal androgen secretion in boys with premature adrenarche was not associated with plasma leptin levels. Nevertheless, enhanced adre- 9 In more detail, 61,62 adiponectin, and individuals with obesity often have high levels of cir- Moreover, inflammatory cytokines, TNF-α, and IL-6, inhibit expression of the leptin receptor in the testis. FSH induces spermatogenesis, too. function and role still have to be examined. 64 High leptin and low adiponectin and fat tissue can convert testosterone Both processes might result in the delay 29,61,79 81,82 In men, other adipokines like chemerin are found in the gonads 65 Thus, particularly high leptin and low adiponectin levels stimulate the HPG axis and thereby accelerate the onset of puberty in boys. Additionally, leptin can dysregulate the development of secondary sex characteristics and spermatogenesis by affecting testosterone levels and nutritional sup- port of spermatogenesis. 5 | LIMITATIONS AND FUTURE RESEARCH DIRECTIONS Even though multiple epidemiological studies have shown the link between puberty onset and obesity, there are some important limita- tions. Firstly, determining both the onset and stage of puberty is rather difficult. For instance, assessing the stage of breast develop- ment in girls with obesity is complicated as clinicians should differenti- 2 changes in response to the activated HPG axis. to determine the onset of puberty refer to secondary sex characteris- tics, such as testicular volume in boys and breast development in girls. A more accurate measurement of puberty onset would be to combine secondary sex characteristics with plasma or serum hormone level measurements such as LH, FSH, adipokines, e.g. leptin. Thereby, differences in puberty measurements could explain variations in the age of puberty onset between boys and girls within different Thereby, resistin is expressed in the testes of rats, but its exact 83 Secondly, male pubertal 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 7 of 10 FIGURE 3 Adipokines affecting the initiation of puberty in boys. Leptin activates kisspeptin secretion in KNDy neurons, this activates the production of gonadotropin releasing hormone (GnRH) from the hypothalamus. GnRH stimulates the pituitary gland to secrete follicle stimulating hormone (FSH) and luteinising hormone (LH), activating the production of testosterone from the testes allowing the development of secondary sex characteristics. Leptin also inhibits the production of testosterone, which may cause a delayed onset of puberty. Adiponectin inhibits GnRH release. Low levels of adiponectin, as a result of TNF-α and IL-6 expression, lead to a reduced inhibition of GnRH. In response to GnRH release, the pituitary gland will secrete FSH and LH, and the testes will produce testosterone resulting in the development of secondary sex characteristics in boys countries, and In addition, the inclusion of a of puberty. ferent time points is complicated, as subjects examined several decades ago presented pronounced differences concerning lifestyle patterns such as nutrition and exercise habits. Lastly, obesity or over- weight is often determined by BMI, a classification based on weight and height measurements. Additionally, it is important that all studies studies or across continents, ethnicities proper age range (8-16 years) is important when assessing the onset (Figure 4). 12-15,17,20-23,49,77-79,84,85 30,47 Furthermore, comparison between studies from dif- 86 Specifically in children, BMI is often dependent on age and growth use the same anthropometric standards and sex-specific cut-offs. 13,14,16-23,49-51,77-80 fat and would represent a more accurate measurement in its regard. Based on this review, several suggestions can be made for further research. Firstly, the roles of adipokines like resistin, chemerin, visfatin, and omentin in puberty onset, fertility, and sexual maturation should be examined in detail. Secondly, future research examining the onset of puberty should combine indicators of puberty onset (e.g. breast development or testicular volume) with plasma or serum hor- mone measurements such as LH, FSH, sex-steroids, adipokines (e.g. spurts. ment in case of growth spurts. distribution of body fat should be taken into account in determining puberty and obesity in children. For instance, the body adiposity index (BAI), which was introduced in 2011 by Bergman et al.,87 uses hip cir- cumference and height in order to estimate the percentage of body 87 Thereby, BMI is a less accurate measure- F I G U R E 4 87,88 Therefore, both percentage and Average age of puberty onset in Europe, China, and the United States according to several studies from Table 1. Age of puberty onset ranges from 8.47 to 13.33 years in girls and from 8.63 leptin), and body fat distribution (e.g. BAI,87 waist-hip ratio's and/or dual-energy X-ray absorptiometry (DXA)2). Additionally, defining con- sistent and general measurements of puberty in both boys and girls, combined with a proper age range (8-16 years), would facilitate the comparisons between different studies and their results. 12-15, 17, 20-23, 25-29, 31 to 13.7 years in boys. included if average age of markers used to assess puberty was not reported. Pink: girls. Blue: boys Studies (Table 1) were not 39, 56 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 8 of 10 NIEUWENHUIS ET AL. 6 | CONCLUSION In conclusion, epidemiological data regarding obesity and puberty onset in girls show similar outcomes as adiposity results in the early onset of puberty in girls. The majority of the studies examining boys with obesity indicate an early onset of puberty, while not all reported an earlier onset of puberty. In detail, high leptin, TNF-α, and IL-6 levels combined with low adiponectin levels stimulate the activation of the HPG axis in girls and boys with obesity, and 5, 45, 50, 51 REFERENCES 1. Kumar S, Kelly AS. Review of childhood obesity: from epidemiology, etiology, and comorbidities to clinical assessment and treatment. May- o Clin Proc. 2017;92(2):251-265. 2. Reinehr T, Roth CL. Is there a causal relationship between obesity and puberty? The Lancet Child & adolescent health. 2019;3(1):44-54. 3. WorldHealthOrganization. Facts and figures on childhood obesity. 2017. 4. Guglielmi V, Sbraccia P. Obesity phenotypes: depot-differences in adipose tissue and their clinical implications. Eat Weight Disord. 2018; 23(1):3-14. 5. Gomez-Hernandez A, Beneit N, Diaz-Castroverde S. Escribano O. Dif- ferential role of adipose tissues in obesity and related metabolic and vas- cular complications. 2016;2016:1-15, 1216783. 6. Zwick RK, Guerrero-Juarez CF, Horsley V, Plikus MV. Anatomical, physiological, and functional diversity of adipose tissue. Cell Metab. 2018;27(1):68-83. 7. Gulyaeva O, Dempersmier J, Sul HS. Genetic and epigenetic control of adipose development. Biochimica et Biophysica Acta (BBA)â Molecular and Cell Biology of Lipids. 2019;1864:3-12. 8. Khan M, Joseph F. Adipose tissue and adipokines: the association with and application of adipokines in obesity. Forensic Sci. 2014;2014: 711-724, 328592. 9. Alotaibi MF. Physiology of puberty in boys and girls and pathological disorders affecting its onset. J Adolesc. 2019;71:63-71. 10. Cousminer DL, Stergiakouli E, Berry DJ, et al. Genome-wide associa- tion study of sexual maturation in males and females highlights a role for body mass and menarche loci in male puberty. Hum Mol Genet. 2014;23(16):4452-4464. 11. Ahmed ML, Ong KK, Dunger DB. Childhood obesity and the timing of puberty. Trends in endocrinology and metabolism: TEM. 2009;20(5): 237-242. 12. Biro FM, Pajak A, Wolff MS, et al. Age of menarche in a longitudinal US cohort. J Pediatr Adolesc Gynecol. 2018;31(4):339-345. 13. Currie C, Ahluwalia N, Godeau E, Nic Gabhainn S, Due P, Currie DB. Is obesity at individual and national level associated with lower age at menarche? Evidence from 34 countries in the Health Behaviour in School-aged Children Study. The Journal of adolescent health: official publication of the Society for Adolescent Medicine. 2012;50(6): 621-626. 14. De Leonibus C, Marcovecchio ML, Chiavaroli V, de Giorgis T, Chiarelli F, Mohn A. Timing of puberty and physical growth in obese children: a longitudinal study in boys and girls. Pediatr Obes. 2014; 9(4):292-299. 15. Flom JD, Cohn BA, Tehranifar P, et al. Earlier age at menarche in girls with rapid early life growth: cohort and within sibling analyses. Ann Epidemiol. 2017;27(3):187-93.e2. 16. Glass NA, Torner JC, Letuchy EM, et al. The relationship between greater prepubertal adiposity, subsequent age of maturation, and bone strength during adolescence. Journal of bone and mineral research: the official journal of the American Society for Bone and Min- eral Research. 2016;31(7):1455-1465. 17. Holmgren A, Niklasson A, Nierop AF, et al. Pubertal height gain is inversely related to peak BMI in childhood. Pediatr Res. 2017;81(3): 448-454. 18. Kaplowitz PB, Slora EJ, Wasserman RC, Pedlow SE, Herman- Giddens ME. Earlier onset of puberty in girls: relation to increased body mass index and race. Pediatrics. 2001;108(2):347-353. 19. Kelly Y, Zilanawala A, Sacker A, Hiatt R, Viner R. Early puberty in 11-year-old girls: Millennium Cohort Study findings. Arch Dis Child. 2017;102(3):232-237. 20. Lazzeri G, Tosti C, Pammolli A, et al. Overweight and lower age at menarche: evidence from the Italian HBSC cross-sectional survey. BMC Womens Health. 2018;18(1):168-174. thereby an early onset of obesity. leptin can inhibit the production of testosterone in boys and subse- quently inhibit the development of secondary sex characteristics affecting spermatogenesis. for other adipokines, like resistin and omentin, are present in the testes and ovaries suggesting a role in puberty or reproduction; 58, 71 however, their plausible function is still unknown. that adipokines may be key regulators in an early onset of puberty in both girls and boys with obesity, specifically by affecting the HPG axis during gonadarche. Future research should focus on assessing puberty onset by measuring consistent puberty markers and determine the percentage of body fat and its distribution and adipokines and hormone serum levels particularly involved in the HPG axis. CONFLICTS OF INTEREST The authors declare no conflict of interest. FUNDING INFORMATION This research was funded by Europees Fonds voor Regionale Ontwikkeling (EFRO), project BriteN 2016. ORCID Ilse A.C. Arnoldussen Amanda J. Kiliaan https://orcid.org/0000-0002-7395-5284 https://orcid.org/0000-0002-2158-6210 13, 14, 16-26, 29-32 Furthermore, several receptors Nevertheless, We conclude Search strategy We searched PubMed for articles published before Novem- ber 15th, 2019 using relevant keywords, including âonset of puberty and adiposity/obesityâ, âonset of pubertyâ, âchildren with obesityâ, âadipose tissueâ, âchildhood obesityâ, âadiposityâ, âobesityâ, âadipokine(s)â, âHPG axisâ, âadipokines ovary/ova- riesâ, or âadipokines testesâ, either alone or in combination. Selection criteria used were English language, longitudinal or cross-sectional studies assessing the onset of puberty, including menarche, thelarche, spermarche, or voice break, combined with high BMI or obesity/adiposity, and articles assessing or reviewing adipokines and its effects on the reproductive system. 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License NIEUWENHUIS ET AL. 9 of 10 21. Lian Q, Mao Y, Luo S, et al. Puberty timing associated with obesity and central obesity in Chinese Han girls. BMC Pediatr. 2019; 19(1):1-7. 22. Deng Y, Liang J, Zong Y, et al. Timing of spermarche and menarche among urban students in Guangzhou, China: trends from 2005 to 2012 and association with Obesity. Sci Rep. 2018;8(1):263-270. 23. Li W, Liu Q. Association of prepubertal obesity with pubertal devel- opment in Chinese girls and boys: a longitudinal study. 2018;30: e23195. 24. Mendle J, Beltz AM, Carter R, Dorn LD. Understanding puberty and its measurement: ideas for research in a new generation. Journal of research on adolescence: the official journal of the Society for Research on Adolescence. 2019;29(1):82-95. 25. Pagani S, Meazza C, Gertosio C, Bozzola E, Bozzola M. Growth hor- mone receptor gene expression in puberty. Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme. 2015;47:581-584. 26. Abreu AP, Kaiser UB. Pubertal development and regulation. Lancet Diabetes Endocrinol. 2016;4(3):254-264. 27. Aguirre RS, Eugster EA. Central precocious puberty: from genetics to treatment. Best Pract Res Clin Endocrinol Metab. 2018;32(4): 343-354. 28. Sultan C, Gaspari L, Maimoun L, Kalfa N, Paris F. Disorders of puberty. Best Pract Res Clin Obstet Gynaecol. 2018;48:62-89. 29. Skorupskaite K, George JT, Anderson RA. The kisspeptin-GnRH path- way in human reproductive health and disease. Hum Reprod Update. 2014;20(4):485-500. 30. Dahl SK, Amstalden M, Coolen L, Fitzgerald M, Lehman M. Dynorphin immunoreactive fibers contact GnRH neurons in the human hypothal- amus. Reprod Sci. 2009;16(8):781-787. 31. Navarro VM, Gottsch ML, Chavkin C, Okamura H, Clifton DK, Steiner RA. Regulation of gonadotropin-releasing hormone secretion by kisspeptin/dynorphin/neurokinin B neurons in the arcuate nucleus of the mouse. J Neurosci. 2009;29(38):11859-11866. 32. Zhai L, Liu J, Zhao J, et al. Association of obesity with onset of puberty and sex hormones in chinese girls: a 4-year longitudinal study. PLoS ONE. 2015;10(8):1-12, e0134656. 33. Cizza G, Dorn LD, Lotsikas A, Sereika S, Rotenstein D, Chrousos GP. Circulating plasma leptin and IGF-1 levels in girls with premature adrenarche: potential implications of a preliminary study. Horm Metab Res. 2001;33(3):138-143. 34. Cousminer DL, WidĂ©n E, Palmert MR. The genetics of pubertal timing in the general population: recent advances and evidence for sex-spec- ificity. Curr Opin Endocrinol Diabetes Obes. 2016;23(1):57-65. 35. Marshall WA, Tanner JM. Variations in pattern of pubertal changes in girls. Arch Dis Child. 1969;44(235):291-303. 36. Lacroix AE, Whitten R. Physiology. Treasure Island (FL): Menarche. StatPearls. StatPearls Publishing; 2018. 37. McDowell MA, Brody DJ, Hughes JP. Has Age at Menarche Chan- ged? Results from the National Health and Nutrition Examination Sur- vey (NHANES) 1999â2004. J Adolesc Health. 2007;40(3):227-231. 38. de Muinich Keizer SM, Mul D. Trends in pubertal development in Europe. Hum Reprod Update. 2001;7(3):287-291. 39. Talma H, Schönbeck Y, van Dommelen P, Bakker B, van Buuren S, Hirasing RA. Trends in menarcheal age between 1955 and 2009 in the Netherlands. PLoS ONE. 2013;8:e60056-e60056. 40. Kaplan HS, Lancaster JB. An evolutionary and ecological analysis of human fertility, mating patterns, and parental investment. Off- spring: Human fertility behavior in biodemographic perspective. 2003;1: 170-223. 41. Mitan LA. Menstrual dysfunction in anorexia nervosa. J Pediatr Adolesc Gynecol. 2004;17(2):81-85. 42. Xu H, Li P-H, Barrow TM, et al. Obesity as an effect modifier of the association between menstrual abnormalities and hypertension in young adult women: Results from Project ELEFANT. PLoS ONE. 2018; 13(11):e0207929-e0207929. 43. Tauqeer Z, Gomez G, Stanford FC. Obesity in women: insights for the clinician. J Womens Health (Larchmt). 2018;27(4):444-457. 44. de Ridder CM, Thijssen JH, Bruning PF, Van den Brande JL, Zonderland ML, Erich WB. Body fat mass, body fat distribution, and pubertal development: a longitudinal study of physical and hormonal sexual maturation of girls. J Clin Endocrinol Metab. 1992;75(2): 442-446. 45. Lassek W, Gaulin S. Brief communication: menarche is related to fat distribution. Am J Phys Anthropol. 2007;133(4):1147-1151. 46. Loomba-Albrecht LA, Styne DM. Effect of puberty on body composi- tion. Curr Opin Endocrinol Diabetes Obes. 2009;16:10-15. 47. Simonneaux V, Bahougne T. A multi-oscillatory circadian system times female reproduction. Front Endocrinol. 2015;6:1-15. 48. Marques P, Skorupskaite K, George JT, Anderson RA. Physiology of GNRH and gonadotropin secretion. In: Feingold KR, Anawalt B, Boyce A, et al., eds. Endotext. Endotext.org: South Dartmouth (MA); 2000. 49. Barcellos Gemelli IF, Farias EDS, Souza OF. Age at menarche and its association with excess weight and body fat percentage in girls in the Southwestern Region of the Brazilian Amazon. J Pediatr Adolesc Gynecol. 2016;29(5):482-488. 50. Aksglaede L, Juul A, Olsen LW, Sorensen TI. Age at puberty and the emerging obesity epidemic. PLoS ONE. 2009;4:1-6, e8450. 51. Ribeiro J, Santos P, Duarte J, Mota J. Association between over- weight and early sexual maturation in Portuguese boys and girls. Ann Hum Biol. 2006;33(1):55-63. 52. Budak E, Fernandez Sanchez M, Bellver J, Cervero A, Simon C, Pellicer A. Interactions of the hormones leptin, ghrelin, adiponectin, resistin, and PYY3-36 with the reproductive system. Fertil Steril. 2006;85(6):1563-1581. 53. Castellano JM, Tena-Sempere M. Metabolic control of female puberty: potential therapeutic targets. Expert Opin Ther Targets. 2016; 20(10):1181-1193. 54. Venancio JC, Margatho LO, Rorato R, et al. Short-term high-fat diet increases leptin activation of CART neurons and advances puberty in female mice. Endocrinology. 2017;158(11):3929-3942. 55. l'Allemand D, Schmidt S, Rousson V, Brabant G, Gasser T, Gruters A. Associations between body mass, leptin, IGF-I and circulating adrenal androgens in children with obesity and premature adrenarche. Eur J Endocrinol. 2002;146(4):537-543. 56. Böttner A, Jr K, MĂŒller G, et al. Gender Differences of adiponectin levels develop during the progression of puberty and are related to serum androgen levels. J Clin Endocrinol Metabol. 2004;89(8):4053- 4061. 57. Unanue N, Bazaes R, Iñiguez G, Cortes F, Avila A, Mericq V. Adre- narche in Prader-Willi syndrome appears not related to insulin sensi- tivity and serum adiponectin. Horm Res. 2007;67(3):152-158. 58. Michalakis K, Mintziori G, Kaprara A, Tarlatzis BC, Goulis DG. The complex interaction between obesity, metabolic syndrome and repro- ductive axis: a narrative review. Metabolism: clinical and experimental. 2013;62(4):457-478. 59. Machinal-Quelin F, Dieudonne MN, Pecquery R, Leneveu MC, Giudicelli Y. Direct in vitro effects of androgens and estrogens on ob gene expression and leptin secretion in human adipose tissue. Endo- crine. 2002;18(2):179-184. 60. Dobrzyn K, Smolinska N, Kiezun M. Adiponectin: A new regulator of female reproductive system. Int J Endocrinol. 2018;2018:1-12, 7965071. 61. Martin LJ. Implications of adiponectin in linking metabolism to testic- ular function. Endocrine. 2014;46(1):16-28. 62. Mathew H, Castracane VD, Mantzoros C. Adipose tissue and repro- ductive health. Metabolism: clinical and experimental. 2018;86:18-32. 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are governed by the applicable Creative Commons License 10 of 10 NIEUWENHUIS ET AL. 63. Sitticharoon C, Sukharomana M, Likitmaskul S, Churintaraphan M, Maikaew P. Corrigendum to: Increased high molecular weight adiponectin, but decreased total adiponectin and kisspeptin, in central precocious puberty compared with aged-matched prepubertal girls. Reprod Fertil Dev. 2017;29:2506-2517. 64. Das UN. Is obesity an inflammatory condition? Nutrition. 2001; 17(11-12):953-966. 65. Comninos AN, Jayasena CN, Dhillo WS. The relationship between gut and adipose hormones, and reproduction. Hum Reprod Update. 2014; 20(2):153-174. 66. Singh A, Choubey M, Bora P, Krishna A. Adiponectin and chemerin: contrary adipokines in regulating reproduction and metabolic disor- ders. Reproductive sciences (Thousand Oaks, Calif). 2018;25:1462- 1473. 67. Tsatsanis C, Dermitzaki E, Avgoustinaki P, Malliaraki N, Mytaras V, Margioris AN. The impact of adipose tissue-derived factors on the hypothalamic-pituitary-gonadal (HPG) axis. Hormones (Athens). 2015; 14:549-562. 68. Kang MJ, Oh YJ, Shim YS, Baek JW, Yang S. Hwang IT. The usefulness of circulating levels of leptin, kisspeptin, and neurokinin B in obese girls with precocious puberty. 2018;34:627-630. 69. Lee J, Song J, Hootman JM, et al. Obesity and other modifiable fac- tors for physical inactivity measured by accelerometer in adults with knee osteoarthritis: data from the osteoarthritis initiative (OAI). Arthritis Care Res (Hoboken). 2012;53-61. 70. Bramswig J, Dubbers A. Disorders of pubertal development. Deutsches Arzteblatt international. 2009;106:295-303. quiz 04 71. Elias CF, Purohit D. Leptin signaling and circuits in puberty and fertil- ity. Cell Mol Life Sci. 2013;70(5):841-862. 72. Riumallo J, Durnin JV. Changes in body composition in adolescent boys. Eur J Clin Nutr. 1988;42(2):107-112. 73. Siervogel RM, Demerath EW, Schubert C, et al. Puberty and body composition. Horm Res. 2003;60(Suppl 1):36-45. 74. Zhang J. Gong M. Andrologia: Review of the role of leptin in the regu- lation of male reproductive function; 2018. 75. Kauffman AS, Gottsch ML, Roa J, et al. Sexual differentiation of Kiss1 gene expression in the brain of the rat. Endocrinology. 2007;148(4): 1774-1783. 76. Zeydabadi Nejad S, Ramezani Tehrani F, Zadeh-Vakili A. The role of kisspeptin in female reproduction. Int J Endocrinol Metab. 2017;15:1- 11, e44337. 77. Sorensen K, Aksglaede L, Petersen JH, Juul A. Recent changes in pubertal timing in healthy Danish boys: associations with body mass index. J Clin Endocrinol Metab. 2010;95(1):263-270. 78. Juul A, Magnusdottir S, Scheike T, Prytz S, Skakkebaek NE. Age at voice break in Danish boys: effects of pre-pubertal body mass index and secular trend. Int J Androl. 2007;30(6):537-542. 79. Lee JM, Wasserman R, Kaciroti N, et al. Timing of puberty in overweight versus obese boys. Pediatrics. 2016;137(2):137-146, e20150164. 80. He F, Guan P, Liu Q, Crabtree D, Peng L, Wang H. The relationship between obesity and body compositions with respect to the timing of puberty in Chongqing adolescents: a cross-sectional study. BMC Pub- lic Health. 2017;17:664-673. 81. Ishikawa T, Fujioka H, Ishimura T, Takenaka A, Fujisawa M. Expres- sion of leptin and leptin receptor in the testis of fertile and infertile patients. Andrologia. 2007;39(1):22-27. 82. Martins AD, Moreira AC, Sa R, et al. Leptin modulates human Sertoli cells acetate production and glycolytic profile: a novel mechanism of obesity-induced male infertility? Biochim Biophys Acta. 1852;2015: 1824-1832. 83. Morash BA, Willkinson D, Ur E, Wilkinson M. Resistin expression and regulation in mouse pituitary. FEBS Lett. 2002;526(1-3):26-30. 84. Cabrera SM, Bright GM, Frane JW, Blethen SL, Lee PA. Age of thelarche and menarche in contemporary US females: a cross- sectional analysis. Journal of pediatric endocrinology & metabolism: JPEM. 2014;27(1-2):47-51. 85. Herman-Giddens ME, Steffes J, Harris D, et al. Secondary sexual characteristics in boys: data from the Pediatric Research in Office Settings Network. Pediatrics. 2012;130(5):e1058-e1068. 86. WHO. Physical status: the use and interpretation of anthropometry. Report of a WHO Expert Committee. World Health Organ Tech Rep Ser. 1995;854:1-452. 87. Akin I, Tolg R, Hochadel M, et al. No evidence of âobesity paradoxâ after treatment with drug-eluting stents in a routine clinical practice: results from the prospective multicenter German DES.DE (German Drug-Eluting Stent) Registry. JACC Cardiovasc Interv. 2012;5(2): 162-169. 88. Marcovecchio ML, Chiarelli F. Obesity and growth during childhood and puberty. World Rev Nutr Diet. 2013;106:135-141. How to cite this article: Nieuwenhuis D, Pujol-Gualdo N, Arnoldussen IAC, Kiliaan AJ. Adipokines: A gear shift in puberty. Obesity Reviews. 2020;21:e13005. https://doi.org/ 10.1111/obr.13005 1467789x, 2020, 6, Downloaded from https://onlinelibrary.wiley.com/doi/10.1111/obr.13005, Wiley Online Library on [10/03/2024]. See the Terms and Conditions (https://onlinelibrary.wiley.com/terms-and-conditions) on Wiley Online Library for rules of use; OA articles are gover
1. Incisors â The main use of incisors is for biting and shearing. 2. Canine â Helps you tear into foods like meat and crunchy vegetables. 3. Premolars â It is also called bicuspids, premolars sit between your canines and your molars 4. Molars â These are the flat teeth at the rear of the mouth. 5. Uvula â Prevents food and liquid from going up your nose. 6. Tongue â It helps us taste different types of foods (Sweet, Sour, Spicy, Salty, Bitter) and also helps us so we can form words clearly when talking.