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4.RA.A.2 Solve Multi-Step Word Problems
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WHAT IS SCIENCE? - is a way in which answers related to NATURAL events are proposed. - a way in which people can learn and UNDERSTAND events in the NATURAL WORLD - based on OBSERVABLE EVENTS - a study of the NATURAL WORLD - a method of DISCOVERY and UNDERSTANDING by using a PROBLEM-SOLVING process called the?? - A systematic body of knowledge based on observation and experimentation. FOUR COMMON CHARACTERISTICS OF SCIENCE: 1. It focuses on the NATURAL WORLD. 2. Goes through experiment. 3. Relies on evidence. 4. Passes through the scientific community. WHAT IS TECHNOLOGY? Brian Arthur (2009) defined technology as: 1. a means to fulfill a human purpose 2. assemblage of practices and components 3. a collection of devices and engineering practices available to a culture. SOCIETY ST (Science Technology) would not exist without society. WHAT IS STS? Science and Technology and Society (STS) is the study of how society, politics and culture affect scientific research and technological innovation and how these, in turn affects society, politics and culture. EVENTS IN THE HISTORY OF SCIENCE AND TECHNOLOGY THAT TRANSFORMED THE SOCIETY (IN THE WORLD) ANCIENT PERIOD 3500 BC. - 500 AD EUROPE - use of fire by Homo Erectus CA 750,000 - Stone Headed Spears CA 45,000 - Wooden bow and arrow CA 20,000 - The Minoans build palaces in Crete CA 2,000 THE AMERICAS - The Folsom people living on eastern side of the Rocky Mountain developed sophisticated tools CA 8,000. - Pottery is made in South America CA 6,000 - Olmec sculpture carves figurines and giant human heads. CA 1200 ASIA AND OCEANA - Earliest known clay pots are made in Japan CA 11,000. - Bronze is first made in Thailand CA 4000 - A lunar calendar is developed in China CA 2950 - Chinese doctors begin using acupuncture CA 2500 - The Hindu calendar of 360 days was introduced in India CA 1000 AFRICA AND MIDDLE EAST - Homo erectus uses stone tools CA 1000000 - CA 15000 in Africa, bone harpoons are used for fishing. - Clay tokens are used for record keeping in Mesopotamia CA 7500 - Mesopotamian mathematicians discover the Pythagorean Theorem MEDIEVAL PERIOD CA 500 -1500 - Dark ages because few written records and evidences remained - Scholastic tradition was established by Charlemagne - Vertical windmills, spectacles, mechanical clock, water mills, gothic style were invented - Johannes Gutenberg invented the printing press RENAISSANCE PERIOD 14TH – 17TH CENTURY - Rebirth of revival - Printing with movable type allowed Bible, secular books made in large amount - Nicolas Copernicus presented a heliocentric theory - Galileo Galilei invented telescope INDUSTRIAL REVOLUTION 18TH CENTURY - Skilled workers were set aside because of the machines - Iron production, steam engine and textile flourished - Scottish James Watt improved steam engine Robert Fulton (steam boat) - The following were invented: Light bulb, telephone, first steam powered locomotive 19TH CENTURY - Age of machine and tools - Herman Helmholtz (law of conservation of energy) - James Clark Maxwell (light as electro-magnetic wave) - Henry Becquerel (radioactivity) - Marie and Pierre Curie (radium) - Hans Christian Oersted (electric current near the magnet) - Michael Faraday (magnet produces electricity) - Atomic Theory proposed by John Dalton - Electron discovered by JJ. Thomson - Telegraph developed by Samuel Morse 20TH CENTURY - Communication, transportation, military research were developed - Personal computer was created - Intel developed microprocessor - Apple was introduced by Steve Jobs and Steve Wozniak - Internet was created (ARPANET) - Henry Ford's mass production of cars - Artificial Intelligence was invented SCIENCE, TECHNOLOGY AND SOCIETY (PHILIPPINE HISTORY) Stone Age - Archeological findings show that modern man from Asian mainland first came over land on across narrow channels to live in Batangas and Palawan about 48,000 B.C. - Subsequently they formed settlement in Sulu, Davao, Zamboanga, Samar, Negros, Batangas, Laguna, Rizal, Bulacan and Cagayan. Inventions - They made simple tools and weapons of stone flakes and later developed method of sawing and polishing stones around 40,000 B.C. - By around 3,000 B.C. they were producing adzes ornaments of seashells and pottery. Pottery flourished for the next 2,000 years until they imported Chinese porcelain. Soon they learned to produce copper, bronze, iron, and gold metal tools and ornaments. Iron Age - The Iron Age lasted from the third century B.C. to 11th century A.D. During this period Filipinos were engaged in extraction smelting and refining of iron from ores, until the importation of cast iron from Sarawak and later from China. INVENTIONS AND DISCOVERIES - They learn to weave cotton, make glass ornaments, and cultivate lowland rice and dike fields of terraced fields utilizing spring water in mountain regions. - They also learned to build boats for trading purposes. - Spanish chronicles noted refined plank built warships called caracoa suited for interisland trade raids 10TH CENTURY A.D. - Filipinos from the Butuan were trading with Champa (Vietnam) and those from Ma-I (Mindoro) with China as noted in Chinese records containing several references to the Philippines. These archaeological findings indicated that regular trade relations between the Philippines, China and Vietnam had been well established from the 10th century to the 15th century A.D. TRADING - The People of Ma-I and San-Hsu (Palawan) traded bee wax, cotton, pearls, coconut heart mats, tortoise shell and medicinal betel nuts, panie cloth for porcelain, leads fishnets sinker, colored glass beads, iron pots, iron needles and tin. SOME PRESPANISH FILIPINO SCIENCE AND TECHNOLOGY - Curative values of plants extract use as medicine - Alphabet (Alibata) - Counting Methods - Weights - Measuring system (isang gatang) - Calendar based on the periods of moon - Banaue Rice Terraces SPANISH REGIME Religion the Catholic Church - The latter part of the 16th Century Development of schools: - Colegio de San Ildefonso-Cebu-1595 - Colegio de San Ignacio-Manila-1595 - Colegio De Nuestra Senora del Rosario-Manila 1597 - Colegio De San Jose-Manila-1601 Colegio De San Ildefonso De Cebu - In 1863 the colonial authorities issued a royal degree to reform the existing educational system. In 1871 the school of medicine and pharmacy were opened to UST, after 15 years it had granted the degree Of Licenciado En Medicina to 62 graduates. Medicine - Development of hospitals San Juan Lazaro hospital the oldest in the far east was founded in 1578. Roads and Bridges Among other Spanish contributions: - Arithmetic - Algebra - Geometry - Trigonometry - Physics - Hydrography - Meteorology - Navigation - Pilotage American Period and Post Commonwealth Era - BUREAU OF GOVERNMENT LABORATORIES (1901) - BUREAU OF SCIENCE (1905) - INSTITUTE OF SCIENCE (1946) RA 2067 OTHERWISE KNOWN AS THE “SCIENCE ACT OF 1958”. - This was enacted to integrate, coordinate, and intensify scientific and technological research and development and to foster invention including allocation of funds and other purposes. NATIONAL RESEARCH COUNCIL WAS ESTABLISHED ON DECEMBER 8, 1933. - Its Mandate (Nrcp) Promotes And Supports Fundamental Or Basic Research For The Continuing Total Improvement Of The Research Capability Of Individual Scientists Or Group Of Scientists; Provides Advice On Problems And Issues Of National Interest; Promotes Scientific And Technological Culture To All Sectors Of Society; And Fosters Linkages With Local And International Scientific Organizations For Enhanced Cooperation In The Development And Sharing Of Information NATIONAL RESEARCH COUNCIL WAS ESTABLISHED IN DECEMBER 8, 1933. - Its Mandate (NRCP) promotes and supports fundamental or basic research for the continuing total improvement of the research capability of individual scientists or group of scientists; provides advice on problems and issues of national interest; promotes scientific and technological culture to all sectors of society; and fosters linkages with local and international scientific organizations for enhanced cooperation in the development and sharing of information. It was during the American Period when Science was inclined towards: - Agriculture - Food Processing - Forestry - Medicine - Pharmacy - NursingCâu 1: Chất khử là A. chất nhường electron. B. chất nhận electron. C. chất nhường proton. D. chất nhận proton. Câu 2: Phản ứng oxi hóa - khử là A. phản ứng hóa học trong đó có sự chuyển proton. B. phản ứng hóa học trong đó có sự thay đổi số oxi hóa. C. phản ứng hóa học trong đó phải có sự biến đổi hợp chất thành đơn chất. D. phản ứng hóa học trong đó sự chuyển electron từ đơn chất sang hợp chất. Câu 3: Sự oxi hóa một chất là quá trình A. nhận electron của chất đó. B. làm giảm số oxi hóa của chất đó. C. nhường electron của chất đó. D. làm thay đổi số oxi hóa của chất đó. Câu 4: Phát biểu nào dưới đây không đúng? A. Sự khử là sự mất hay cho electron. B. Sự oxi hoá là sự mất electron. C. Chất khử là chất nhường electron. D. Chất oxi hoá là chất nhận electron. Câu 5: Trong các phản ứng sau, phản ứng nào là phản ứng oxi hóa - khử? A. CaCO3 CaO + CO2. B. 2KClO3 2KCl + 3O2. C. 2NaHCO3 Na2CO3 + H2O + SO2. D. 2Fe(OH)3 Fe2O3 + 3H2O. Câu 6: Cho phương trình phản ứng: Fe + CuSO4 Cu + FeSO4. Vai trò của Fe trong phản ứng là A. chất oxi hóa. B. chất bị khử. C. chất khử. D. vừa là chất khử, là chất oxi hóa. Câu 7: Cho phương trình phản ứng: Cl2 + 2H2O 2HCl + 2HClO. Vai trò của Cl2 trong phản ứng là A. chất oxi hóa. B. chất bị khử. C. chất khử. D. vừa là chất khử, là chất oxi hóa. Câu 8: Cho phương trình phản ứng: AgNO3 + HCl AgCl + HNO3. Vai trò của AgNO3 trong phản ứng là A. chất oxi hóa. B. chất bị khử. C. không là chất khử, không là chất oxi hóa. D. vừa là chất khử, là chất oxi hóa. Câu 9: Trong các phản ứng sau, phản ứng nào không phải là phản ứng oxi hóa khử? A. Fe + 2HCl FeCl2 + H2. B. Zn + CuSO4 ZnSO4 + Cu. C. CH4 + Cl2 CH3Cl + HCl. D. BaCl2 + H2SO4 BaSO4 + 2HCl. Câu 10: Trong các phản ứng sau phản ứng nào là phản ứng oxi hóa - khử? A. NaOH + HCl NaCl + H2O. B. 2Fe(OH)3 + 3H2SO4 Fe2(SO4)3 + 6H2O. C. CaCO3 + 2HCl CaCl2 + H2O + CO2. D. 2CH3COOH + Mg (CH3COO)2Mg + H2. Câu 11: Số oxi hóa của S trong SO2 bằng A. +4 B. -4 C. +2 D. -2 Câu 12: Số oxi hóa của C trong CH4 bằng A. +4 B. -4 C. +1 D. -1 Câu 13: Sơ đồ: Cu → Cu+2 + 2e biểu thị quá trình A. oxi hóa. B. nhận electron. C. phân hủy. D. khử Câu 14: Sơ đồ: N+5 + 3e → N+2 biểu thị quá trình A. oxi hóa B. khử C. nhận proton D. hóa hợp Câu 15: Sục khí SO2 vào dung dịch KMnO4 (thuốc tím), màu tím nhạt dần rồi mất màu (biết sản phẩm tạo thành là K2SO4, MnSO4, H2SO4 và H2O). Nguyên nhân là do A. SO2 đã oxi hóa KMnO4 thành MnO2. B. SO2 đã khử KMnO4 thành Mn+2. C. KMnO4 đã khử SO2 thành S+6. D. H2O đã oxi hóa KMnO4 thành Mn+2. Câu 17: Hỗn hợp tecmit dùng hàn gắn đường ray có thành phần chính là aluminium (Al) và iron (III) oxide (Fe2O3). Phản ứng xảy ra khi đung nóng hỗn hợp tecmit như sau: Fe2O3 + 2Al 2Fe + Al2O3. Phát biểu nào dưới đây là đúng? A. Al là chất bị oxi hoá. B. Fe2O3 là chất nhường electron. C. Fe2O3 là chất bị oxi hóa. D. Al2O3 là chất nhận electron. Câu 18: Phản ứng thu nhiệt là phản ứng A. giải phóng năng lượng dưới dạng nhiệt. B. hấp thu năng lượng dưới dạng nhiệt. C. cung cấp năng lượng dưới dạng nhiệt. D. hấp thu năng lượng dưới dạng hóa năng. Câu 19: Phản ứng nhiệt nhôm là phản ứng giữa bột nhôm và iron (III) oxide sinh ra một lượng nhiệt rất lớn và được ứng dụng dùng để hàn đường ray. Phản ứng nhiệt nhôm là phản ứng A. thu nhiệt. B. chưa xác định được. C. tỏa nhiệt. D. vừa thu nhiệt, vừa tỏa nhiệt. Câu 20: Phản ứng nào trong các phản ứng dưới đây là phản ứng thu nhiệt? A. Vôi sống tác dụng với nước: CaO + H2O → Ca(OH)2. B. Đốt cháy than: C + O2 CO2. C. Đốt cháy cồn: C2H5OH + 3O2 2CO2 + 3H2O. D. Nung đá vôi: CaCO3 CO2 + CaO. Câu 21: Điều kiện nào sau đây không phải là điều kiện chuẩn? A. Áp suất 1 bar và nhiệt độ 25 0C. B. Áp suất 1 bar và nhiệt độ 298 K. C. Áp suất 1 bar và nhiệt độ 25 0C hay 298 K. D. Áp suất 1 bar và nhiệt độ 25K. Câu 22: Điều kiện nào sau đây là điều kiện chuẩn? A. Áp suất 1 bar và nhiệt độ 25 K. B. Áp suất 1 bar và nhiệt độ 298 0C. C. Áp suất 1 bar và nhiệt độ 298 K. D. Áp suất 1 bar và nhiệt độ 25K. Câu 23: Nồng độ đối với chất tan trong dung dịch ở điều kiện chuẩn là? A. 0,01 mol/L. B. 0,1 mol/L. C. 1 mol/L. D. 0,5 mol/L. Câu 24: 1 mol chất khí ở điều kiện chuẩn chiếm thể tích bằng bao nhiêu? A. 24,79 lít. B. 2,479 lít. C. 22,4 lít. D. 2,24 lít. Câu 25: Kí hiệu nhiệt tạo thành chuẩn của một chất là A. . B. . C. H298.. D. . Câu 26: Số oxi hóa của một nguyên tử trong phân tử là A. điện tích quy ước của nguyên tử trong phân tử khi coi tất cả các electron liên kết đều chuyển hoàn toàn về nguyên tử của nguyên tố có độ âm điện lớn hơn. B. hóa trị của nguyên tử nguyên tố đó. C. điện tích thực của nguyên tử nguyên tố đó. D. độ âm điện của nguyên tử nguyên tố đó. Câu 27: Fe2O3 là thành phần chính của quặng hematite đỏ, dùng để luyện gang. Số oxi hoá của iron (Fe) trong Fe2O3 là A. +3. B. 3+. C. 3-. D. -3. Câu 28: Trong phản ứng oxi hóa – khử, chất nhận electron được gọi là A. chất khử. B. chất oxi hoá. C. acid. D. base. Câu 29: Các phản ứng quan trọng gắn liền với cuộc sống như sự cháy của than, củi; sự cháy của xăng, dầu trong các động cơ đốt trong,…thường thuộc loại phản ứng nào? A. Phản ứng thế. B. Phản ứng cộng. C. Phản ứng phân hủy. D. Phản ứng oxi hóa - khử. Câu 30: Enthalpy phản ứng chuẩn có kí hiệu là A. . B. . C. . D. .Âu 1: Virus là gì? A. Sinh vật đơn bào B. Tế bào nhân chuẩn C. Sinh vật không có cấu tạo tế bào D. Sinh vật có cấu tạo tế bào Câu 2: Virus nhân lên bằng cách nào? A. Phân bào B. Tự sao chép ADN C. Ký sinh nội bào bắt buộc D. Sinh sản vô tính Câu 3: Vật liệu di truyền của virus có thể là gì? A. ADN hoặc ARN B. ADN kép C. ARN kép D. Cả A và B đều đúng Câu 4: Vỏ ngoài của virus được gọi là gì? A. Capsid B. Protein C. Enzyme D. Lipid Câu 5: Virus nào sau đây gây bệnh ở người? A. Virus HIV B. Virus cúm C. Virus Ebola D. Tất cả đều đúng Câu 6: Virus cần điều kiện gì để có thể phát triển và nhân lên? A. Môi trường giàu dinh dưỡng B. Nhiệt độ thấp C. Tế bào chủ D. Môi trường nước Câu 7: Virus HIV tấn công vào tế bào nào của cơ thể người? A. Tế bào máu đỏ B. Tế bào bạch cầu T C. Tế bào da D. Tế bào thần kinh Câu 8: Virus gây ra những bệnh nào dưới đây? A. Sốt xuất huyết B. Lao C. Viêm gan B D. Cả A và C đều đúng Câu 9: Vòng đời của virus bắt đầu bằng giai đoạn nào? A. Nhân đôi vật liệu di truyền B. Gắn kết vào tế bào chủ C. Tổng hợp protein D. Giải phóng virus con Câu 10: Cơ chế phòng chống virus hiệu quả nhất là gì? A. Tiêm vắc xin B. Uống kháng sinh C. Duy trì chế độ ăn uống lành mạnh D. Giảm tiếp xúc với ánh sáng mặt trời Nếu bạn cần giải thích thêm về bất kỳ câu hỏi nào, hãy cho tôi biết nhé! ChatGPT có thể mắc lỗi. Hãy kiểm tra các thCâu 1: Đặc trưng nào sau đây là một trong những yếu tố cốt lõi của trí tuệ nhân tạo? A. Tự động hóa quy trình làm việc B. Khả năng học tập và thích nghi từ dữ liệu C. Khả năng sử dụng năng lượng hiệu quả D. Thực hiện các phép tính toán học nhanh chóng Đáp án: B. Khả năng học tập và thích nghi từ dữ liệu Câu 2: Trí tuệ nhân tạo (AI) chủ yếu được sử dụng để làm gì? A. Phân tích dữ liệu và đưa ra quyết định dựa trên dữ liệu B. Thiết kế hệ thống mạng C. Giảm lượng tiêu thụ điện năng D. Thực hiện các công việc thể chất Đáp án: A. Phân tích dữ liệu và đưa ra quyết định dựa trên dữ liệu Câu 3: Hệ thống AI được gọi là “học máy” (machine learning) khi nó có khả năng: A. Tự động sửa chữa lỗi trong phần mềm B. Tạo ra các hệ thống mạng bảo mật C. Học hỏi và cải thiện hiệu suất mà không cần lập trình rõ ràng D. Tăng tốc độ xử lý của phần cứng Đáp án: C. Học hỏi và cải thiện hiệu suất Câu 4: Khả năng học của AI liên quan đến yếu tố nào sau đây? A. Học từ kinh nghiệm và dữ liệu mới để cải thiện hiệu suất B. Ghi nhớ tất cả các lệnh do con người cung cấp C. Chạy các chương trình mà không cần cập nhật D. Sửa lỗi phần mềm một cách tự động Đáp án: A. Học từ kinh nghiệm và dữ liệu mới để cải thiện hiệu suất Câu 5: Khả năng suy luận trong AI giúp hệ thống thực hiện điều gì? A. Phát triển khả năng thể hiện cảm xúc B. Sử dụng thông tin để đưa ra các quyết định có căn cứ C. Tăng tốc độ xử lý dữ liệu D. Sao chép chính xác các hành vi của con người Đáp án: B. Sử dụng thông tin để đưa ra các quyết định có căn cứ Câu 6: Khả năng nhận thức của AI là gì? A. Khả năng tự nhận biết và điều chỉnh hành vi của nó dựa trên môi trường B. Khả năng xử lý dữ liệu với tốc độ nhanh hơn C. Khả năng làm việc liên tục không cần nghỉ D. Khả năng thu thập dữ liệu từ các cảm biến và hệ thống khác Đáp án: A. Khả năng tự nhận biết và điều chỉnh hành vi của nó dựa trên môi trường Câu 7: Khả năng hiểu ngôn ngữ tự nhiên (NLP) của AI cho phép hệ thống: A. Xử lý văn bản và ngôn ngữ giống như con người B. Dịch thuật chính xác từ ngôn ngữ này sang ngôn ngữ khác C. Thay thế hoàn toàn con người trong việc viết và giao tiếp D. Tăng cường khả năng suy nghĩ trừu tượng Đáp án: A. Xử lý văn bản và ngôn ngữ giống như con người Câu 8: AI có khả năng giải quyết vấn đề khi nào? A. Khi nó sử dụng các thuật toán để tìm ra giải pháp tối ưu cho các vấn đề phức tạp B. Khi nó thay thế toàn bộ con người trong mọi công việc C. Khi nó tự động sửa chữa các lỗi phần mềm D. Khi nó cung cấp thông tin chi tiết về dữ liệu mà không cần bất kỳ sự can thiệp nào Đáp án: A. Khi nó sử dụng các thuật toán để tìm ra giải pháp tối ưu cho các vấn đề phức tạp Câu 9: Khả năng học của AI là gì? A. AI có thể học từ dữ liệu và kinh nghiệm mới. B. AI có thể tự sửa lỗi mà không cần dữ liệu đầu vào. C. AI có thể cải thiện hiệu suất thông qua học tập. D. AI không cần cập nhật khi học tập từ dữ liệu. Đáp án: • Đúng: A, C • Sai: B, D Câu 10: Khả năng suy luận của AI giúp hệ thống thực hiện điều gì? A. AI có thể đưa ra quyết định dựa trên dữ liệu. B. AI có thể suy nghĩ giống con người mà không cần dữ liệu. C. AI sử dụng thông tin để phân tích và đưa ra lựa chọn hợp lý. D. AI tự động đưa ra quyết định mà không cần học tập trước đó. Đáp án: • Đúng: A, C • Sai: B, D Câu 11: AI có khả năng nhận thức và điều chỉnh hành vi dựa trên môi trường xung quanh không? A. AI có thể nhận biết thay đổi trong môi trường và điều chỉnh hành vi. B. AI luôn cần con người giám sát để đưa ra quyết định. C. AI tự động thay đổi mà không cần lập trình lại khi môi trường thay đổi. D. AI không có khả năng điều chỉnh theo môi trường. Đáp án: • Đúng: A, C • Sai: B, D Câu 12: Khả năng giải quyết vấn đề của AI được biểu hiện như thế nào? A. AI có thể áp dụng các thuật toán để tìm ra giải pháp tối ưu. B. AI giải quyết vấn đề mà không cần dữ liệu đầu vào. C. AI tự động phân tích và đưa ra các phương án giải quyết dựa trên dữ liệu. D. AI chỉ có thể giải quyết vấn đề khi được lập trình trước. Đáp án: • Đúng: A, C • Sai: B, DCâu 15: Sục khí SO2 vào dung dịch KMnO4 (thuốc tím), màu tím nhạt dần rồi mất màu (biết sản phẩm tạo thành là K2SO4, MnSO4, H2SO4 và H2O). Nguyên nhân là do A. SO2 đã oxi hóa KMnO4 thành MnO2. B. SO2 đã khử KMnO4 thành Mn+2. C. KMnO4 đã khử SO2 thành S+6. D. H2O đã oxi hóa KMnO4 thành Mn+2. Câu 17: Hỗn hợp tecmit dùng hàn gắn đường ray có thành phần chính là aluminium (Al) và iron (III) oxide (Fe2O3). Phản ứng xảy ra khi đung nóng hỗn hợp tecmit như sau: Fe2O3 + 2Al 2Fe + Al2O3. Phát biểu nào dưới đây là đúng? A. Al là chất bị oxi hoá. B. Fe2O3 là chất nhường electron. C. Fe2O3 là chất bị oxi hóa. D. Al2O3 là chất nhận electron. Câu 18: Phản ứng thu nhiệt là phản ứng A. giải phóng năng lượng dưới dạng nhiệt. B. hấp thu năng lượng dưới dạng nhiệt. C. cung cấp năng lượng dưới dạng nhiệt. D. hấp thu năng lượng dưới dạng hóa năng. Câu 19: Phản ứng nhiệt nhôm là phản ứng giữa bột nhôm và iron (III) oxide sinh ra một lượng nhiệt rất lớn và được ứng dụng dùng để hàn đường ray. Phản ứng nhiệt nhôm là phản ứng A. thu nhiệt. B. chưa xác định được. C. tỏa nhiệt. D. vừa thu nhiệt, vừa tỏa nhiệt. Câu 20: Phản ứng nào trong các phản ứng dưới đây là phản ứng thu nhiệt? A. Vôi sống tác dụng với nước: CaO + H2O → Ca(OH)2. B. Đốt cháy than: C + O2 CO2. C. Đốt cháy cồn: C2H5OH + 3O2 2CO2 + 3H2O. D. Nung đá vôi: CaCO3 CO2 + CaO. Câu 21: Điều kiện nào sau đây không phải là điều kiện chuẩn? A. Áp suất 1 bar và nhiệt độ 25 0C. B. Áp suất 1 bar và nhiệt độ 298 K. C. Áp suất 1 bar và nhiệt độ 25 0C hay 298 K. D. Áp suất 1 bar và nhiệt độ 25K. Câu 22: Điều kiện nào sau đây là điều kiện chuẩn? A. Áp suất 1 bar và nhiệt độ 25 K. B. Áp suất 1 bar và nhiệt độ 298 0C. C. Áp suất 1 bar và nhiệt độ 298 K. D. Áp suất 1 bar và nhiệt độ 25K. Câu 23: Nồng độ đối với chất tan trong dung dịch ở điều kiện chuẩn là? A. 0,01 mol/L. B. 0,1 mol/L. C. 1 mol/L. D. 0,5 mol/L. Câu 24: 1 mol chất khí ở điều kiện chuẩn chiếm thể tích bằng bao nhiêu? A. 24,79 lít. B. 2,479 lít. C. 22,4 lít. D. 2,24 lít. Câu 25: Kí hiệu nhiệt tạo thành chuẩn của một chất là A. . B. . C. H298.. D. . Câu 26: Số oxi hóa của một nguyên tử trong phân tử là A. điện tích quy ước của nguyên tử trong phân tử khi coi tất cả các electron liên kết đều chuyển hoàn toàn về nguyên tử của nguyên tố có độ âm điện lớn hơn. B. hóa trị của nguyên tử nguyên tố đó. C. điện tích thực của nguyên tử nguyên tố đó. D. độ âm điện của nguyên tử nguyên tố đó. Câu 27: Fe2O3 là thành phần chính của quặng hematite đỏ, dùng để luyện gang. Số oxi hoá của iron (Fe) trong Fe2O3 là A. +3. B. 3+. C. 3-. D. -3. Câu 28: Trong phản ứng oxi hóa – khử, chất nhận electron được gọi là A. chất khử. B. chất oxi hoá. C. acid. D. base. Câu 29: Các phản ứng quan trọng gắn liền với cuộc sống như sự cháy của than, củi; sự cháy của xăng, dầu trong các động cơ đốt trong,…thường thuộc loại phản ứng nào? A. Phản ứng thế. B. Phản ứng cộng. C. Phản ứng phân hủy. D. Phản ứng oxi hóa - khử. Câu 30: Enthalpy phản ứng chuẩn có kí hiệu là A. . B. . C. . D. .1. Ngày truyền thống của Hải quân nhân dân Việt Nam là ngày nào? A. 19/5 B. 7/5 C. 7/10 D. 21/6 👉 Đáp án đúng: B. 7/5 2. Ngày giải phóng Trường Sa là ngày tháng năm nào? A. 07/5/1975 B. 30/4/1975 C. 29/4/1975 D. 14/3/1975 👉 Đáp án đúng: C. 29/4/1975 3. Huyện đảo Trường Sa hiện tại có bao nhiêu đảo có cư dân sinh sống? A. 2 B. 3 C. 4. D. 5 👉 Đáp án đúng: C. 4 (Trường Sa Lớn, Song Tử Tây, Sinh Tồn, Đá Tây A) 4. Hai quần đảo Hoàng Sa và Trường Sa của Việt Nam hiện nay lần lượt thuộc đơn vị hành chính nào? A. Khánh Hòa và Đà Nẵng B. Đà Nẵng và Khánh Hòa C. Đà Nẵng và Phú Yên D. Khánh Hòa và Ninh Thuận 👉 Đáp án đúng: A. Đà Nẵng và Khánh Hòa 5. Chủ quyền biển đảo Việt Nam được khẳng định rõ ràng trong văn bản pháp lý quốc tế nào sau đây? A. Hiến chương ASEAN B. Hiệp định Paris năm 1973 C. Công ước Liên Hợp Quốc về Luật Biển năm 1982 (UNCLOS 1982) D. Hiệp định Geneva năm 1954 👉 Đáp án đúng: B. Công ước Liên Hợp Quốc về Luật Biển năm 1982 (UNCLOS 1982) 6. Sự kiện lịch sử nào của Hải quân nhân dân Việt Nam nào đã diễn ra vào ngày 14/3/1988? A. Bộ Quốc phòng ban hành Chiến dịch xây dựng quần đảo Trường Sa CQ-88 B. Hải chiến Gạc Ma C. Lễ ký Công ước Liên hợp quốc về Luật biển D. Giải phóng Trường Sa 👉 Đáp án đúng: B (Hải chiến Gạc Ma) 7. Đơn vị nào hiện nay có tiền thân là Đoàn tàu không số? A. Lữ đoàn tàu ngầm 196 B. Lữ đoàn 162 C. Lữ đoàn 955 D. Lữ đoàn 125 👉 Đáp án đúng: D. Lữ đoàn 125 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 Desirée Nieuwenhuis | Natàlia 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)— 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 ‘onset of puberty and adiposity/obesity’, ‘onset of puberty’, ‘children with obesity’, ‘adipose tissue’, ‘childhood obesity’, ‘adiposity’, ‘obesity’, ‘adipokine(s)’, ‘HPG axis’, ‘adipokines ovary/ova- ries’, or ‘adipokines testes’, 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, Widén 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) 1999–2004. 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, Müller 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 “obesity paradox” 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 goverEff..rs of ott.-PoFllat i What woLrld hoppen ro our colnrry i, it is ovetsp.pulored? When our counrry is ov€.-populdted, re @ €xp€ri.nce rh€ foll.wirg: Food is our bdsic h@d. Wh€n th€.Cs an ih.re.se ir populdtion it neans thar hore ,@d is iealed. It rheds ho .naJgh food, rrtrple irll srruggle wirh eddr oth€r in ordeLro €!'r- As o l!fllr, lhde rill be o f@d -- , ond ou, now]nert of on ihdiyiduol fron d c..tair - the move$eni o, on individudl our of o cerrain pla.e which help r€duce ihe populotion of th6t fr Arcih€. b.sic ned is w.ra. Wde. shorroge ocu.s when there is on ircreare of hu,nber of p@ple ro be $pptied. rn owr-popur.t d ore.s, woler is rdior€d, Ir rEB rhoi supplies like ti,tWSS ond ,IWSI can'i $pply enoish worer. Do you hdve enough supply of sai.. in your oreo? Aside f.om food alld worer, shelier is olso ohe o, our inportant heeds. As the populoiion ihcre.!e!, building n.w hoLr!€s or rhelt€r is limit.i. To find solulion to this prcbl€n, some goverihent og.ncies dnd orhs non{ov€Ihrehl offi.iofs (N6O) .onvefied sot@ ti.elields, du,np site. dnd nountcirlr inlo flbdivisions dnd relidentiols. Sut whot uould be ths effect o{ coMrtiig .i@fields to .6id€nri6l uits in our food supply? z , 2 Z Z :'", becouse there ore no enough space for prcpex garbage dkposol. ^s o r€sulr, sore peoPle lend to ihrow'their gorbdge onywh.f€. oorbdge baones brc{niry ond rursing ground of iEecrs and onidols ihot @se horm ro pe.ple. Dec.yiry garboge olso produces r,hpleaiant odor ard ehen burn if pmduces pois.nour qds @lled nelhohe As ihe populdtion incr€a3*, the 9d6.9e dso incraes. nris is T't ,,8 T H Wha you de living in on oa-populdi.d pla@, you moy oqaiae halrh prcblerns. Ir is be@@. the woi.r srpply is limit.d ihct will l..d you to poor hygi.ni. hobirs. In plo.4 like rhis, the surrouhdiigs naybe uniidy. o focrorthoi @uld oko cfFe.t your h4l'th. The common oilments rhot yd @uld oc$rire in ovesfDpllar€d ploces ore bEnchil is, o5l hnq. diqrrha and rube.culosis. 7,\ ,\\ \1" 6. Lnck of Herlrh sarvice llosi Pelple in 6n oM-populci€d 6ra 90 ro rubli. heilrh @trtas ond governhent hospirols be6u.e ii prcvides fr@ @Eulrorion oid los @sr rEdicdrions. A3 a ..suli, lh€s€ gow.nnenr dg€rciB b.@ne itud.4$re in mcetiig ihe n eds b..ou!€ df ihsrffici€nr funds. Lock of medicol personnel ,o odmaiisi€I is also s problen in mosr hosptols ev€n rhere or. od.audtc supply of hedicire!. 7_ Do you how wlry rhe crim€ roi€ hexs ih becdur€ fiDre pe.ple o.e fnJrrct€d d@ ro sLffici€.i naE io supp.rr their forniliG. ouf country inclY{ses? If is uh.mploym€ni dnd hdve no arinet .re u$dv gr€{rer ia dn dq-popltdled ra whq. tl, , a, v, tlr I E. Air ard Wat€r Pollutioh How dir be.o'nes pollut€d? I11€ dir b@'n€s p.llurn be.4ne of rhe hormfolgoees thot ser. produ.4 by the fdciori€s and vehicles. Itete {octories ond whi.l6 @ fuel ro run nochiB ond .JBin6. In ,h€ prc.ess, they give our Cdrboh Dioxide ond other ho.6ful gars.r such 6 Nittugei Oxide, Corbon l oioxide dnd Le.d iiio the oir. Do you know whot .ontdbute io ihe incr€asing number of whides qnd foctories? It is ihe inc.6e o, populdtion. As whdt I hove dis.!sse!, wirh a lihired sra.e 9@bd9e disposalie one of the problens thot .o!ld ise i, dh o!er-pop!,.t€d ploce. exn,jple ot thie orc rhos€ pelpl€ livi,rg oh the raverside teid 'ro ,hrou, lheir gEr&ge Hde you seen 'th. P6si9 river or the Tulyahan river? Did you {ind it Whdr do you think i! ihe eff€.t of ihis ih the.re4iures sho lives ih Ahothd f6do.s thal could.on rlbule to wdtd pollutioh dre oil s?ills, gorbqg€ fro,n boa, or ships ahd som€ ihdust.iol wosre. 9. Ite l@96f p4.enroge group. Individuols who orc this grclp. of olr popllarioh is compos.n of the working @pobla of s'rpporting ,heir fomilies nok !-up Though rhas group hol& the lojgeei percenroge of d. populaiion, rhis olso becomer one o{ oveFpopulored probl€]ns b€4use there ore rc jobs awildble fo. oll of iha10. Erergy Shortdge ltere will be on energy shortdge iJ ihe populdtion incre63"l be.dise rhe d.,nand i. €le.iriciry is high. Why is thai wh.n th. PoPqldion inclE.g, rhe d4ord in el4tricity is high? Ir B be.ouse there $,ould be 8to.e hdsat dnd blildirys to lighr ond nore el?riric oPPliohces ro run. rt.6rcznho!3.Ef+ed Whor is rhe grernho@ eff€.r? In whoi say il c.uld offect c2 6re.hhG. effed is rhe wdrniltg of rhe drltlosphee. lvhen the 5un worft rhe.nrrh s1jrf.@, sone of rhe h@r go€J bo.k ro rhe ornos?herc. Air an the dtnDsphere which is C@boi Dioxid. ,rops ihe heot 6hd it mok6 the a.th very worm. As ihe populdtion coniinuou!|,l gtol4 , the gt@rl$use etfe.t b@res no.e visible. Ir is becaosu ,hera ore mo.e focrories snd whicl.s iha, produce wdst€s ond fuma5 which cduses more C{.bo. Diodde ir the ormosphere. As a rcsutt, ,herc eiould be nore h4, ,rop in the ornosphere uhich osk6 th. @ih nuch wornerIf this will hoppen continuously, ,h€ fish ih th€ ocah *ill di€, ricerields/f@mlands will dry too due to lh€ wcm clitnole 12. Destruction of rhe Ozone Loyer A5 whot you hove l@med lrheh you de in v5-6, rhot the qzore ldver is 'the proiecrive loy€. of the olnosPhd€. ft protects us {rom the homful effects of ultrdviolei rays of the su. Do you khow ,hot our Ozore lol€t q4. dQ4tt\!ci.d? Il olreadY hod holes lhai dllow the ulrroviolet rdys to .4dt ihe @rrh. How do6 this hdpPei? Does th. in rc$e of poPuldioh h@€ sonething 'to do tr,lh ir? Yes, rhe I6i grov/irts PoPuldiion .odribuied o lot be@use 6 th' populotion incre3es, rhe u5e of refrigerd'tors, d€rosol lProvs 6nd pl4srics 6bo ihcre&s6. The sid producls coiiojn chemicol called Chlorofluorocdrbons (CFCS) which is mix wafh ihe dir in ihe ormosPher€. As o resulr. ihe hcrmfirl chernicol r€oches the Prolectiw ldver dnd lhrowh. hole in {hid ult@iolzi cahders aid cai4.ct3 ,F.*Y.iis hi!586$q€9.7,- Ho$ doas dcid rdin form? Is cid roii hdmful ro rEn? In the prcvious dis.ussions, yodt€ t.on€d rhd more vel .1e3 dnd fdctori€s or€ necded fo het the iii:.e.siry number o{ P@Pla. Lefs now fihd af hd f@tot.i€s dnd vehicle! .ontribure in the forrEtion of ocid When foctories 6nd whi.ler give off woste gd..3 ,hot will ,nix on lhe noisture i. rhe oir, it will ihen Produ.e sulPhu.i. ocld dnd Nitri. o.id. 'Ihe clol,Jd folb will ,h€h obsorb rhese ccids ond ehei ihe clold f.lls os .oin, ih. ccid is ahady Pdrr of itU/ha d.id ftin falls oh lok"!, ,46 or ocan ih€ fish sill die d.d if h fdlls oh fopnlonds,lhe pldni. together oith the soil B desrroyed. When you inhole dir with Niiric acid, your blood will los. irs @pobilily io fonspori Oxyg€h to your diff€.ai bodY Po.i3. ScieniisB include other rorns oJ dcidic pr€cipiigrion. Thes€ drc nisi, Do you krcw ihot Nuclerr power slotionr Use .adiodctive ,ndie.ials in producirE fuels, yet, rhey do and those .odioactiw rndlqlotE gi\e otf radio'ting en.rgy thoi is harmrul 'to livirq thilEs. wlren rodiotion enlert ihe body ot living things it {ill srq rhere for o lorg ,eriod of ri'ne. Exonple fhe rodiqtion vG srilled to the c.m. Then rhe @rn will be aie by rhe chicken, the .odiotion o the c.rn 'rill also 'tronsf€r to the chi.k€n. Wha on individuol als ihe nat of the chickeh sith mdiarion, helshe rill .ko oblorb ihe rodi@.tirc mtaid that will destrcy hB/her .€lls ond ruket hnn/hd si.r. Over-populoiion .on leld to food shoridg€, wdter shorroqe, housiB probl€ms, qdrbog€ probl€rs, lock of halrh sdi.e. tisa ol clit@ rote, oir ond woi€r pollution, uhanpl6ynat, eiergy 5horr69e, grenhoq3€ efreci, desrruction o( th. ozo@ lat/e?, rci.l roi. olld e.l€d. watta