
Production des pommes-chips_niveau 1 --> opérateur (AFP)
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âVous travaillez dans la plus grosse entreprise de suisse de fabrication de pommes-chips, vous ĂȘtes opĂ©rateur de ligne chez:Â



âLes suisses consomment environ 1.5kg de chips par annĂ©e, surtout au paprikas
Vous travaillez dans la plus grosse entreprise de suisse de fabrication de pommes-chips, vous ĂȘtes opĂ©rateur de ligne chez:Â
Les suisses consomment environ 1.5kg de chips par année, surtout au paprikas
Dans la pomme de terre, on retrouve principalement de l'eau et des sucres (principalement de l'amidon sous forme de granules dans leurs cellules, comme sur cette photo):
Chez Zweifel, la principale variété des pommes de terre utilisée pour les chips est la:
Séparez les paramÚtres de conservation des pommes de terre. Formez 2 groupes: paramÚtres positifs et paramÚtres négatifs
Sous quelles conditions physico-chimiques sont créés les acrylamides dans les chips? Choisissez la réponse la plus juste.
Concernant les processus industriels de fabrication des pommes chips et des frites congelées:
Associer les OU avec les bons numéros

Cette installation permet de diminuer leur formationÂ

Par rapport Ă la photo suivante, trouvez les affirmation correctes

DĂšs le dĂ©but de vos recherches, vous allez collecter, produire et exploiter des donnĂ©es. La gestion des donnĂ©es (Research Data Management - RDM) fait partie du processus de recherche. Elle concerne l'ensemble des opĂ©rations de collecte, description, stockage, traitement, analyse, archivage et mise en accĂšs des donnĂ©es. (extrait de : Passeport pour la Science Ouverte. Guide pratique pour les doctorants ) "La science ouverte est la diffusion sans entrave des publications et des donnĂ©es de la recherche. Elle sâappuie sur lâopportunitĂ© que reprĂ©sente la mutation numĂ©rique pour dĂ©velopper lâaccĂšs ouvert aux publications et â autant que possible â aux donnĂ©es de la recherche. "Les donnĂ©es de la recherche sont la matiĂšre premiĂšre de la connaissance. Les partager, c'est ouvrir de nouvelles perspectives scientifiques" Source : Plan national pour la Science ouverte - MinistĂšre ESR - Juillet 2018 Source image : https://bibliotheques.univ-tlse3.fr/file/composantes-science-ouverte Cette page est une introduction Ă la gestion des donnĂ©es de recherche. Elle prĂ©sente quelques concepts et Ă©tapes clĂ©s pour vous engager dans cette dĂ©marche. Consultez les liens pour approfondir vos connaissances. âą What are data ? DĂ©finition des donnĂ©es de recherche de lâOCDE (2007) « Enregistrements factuels (chiffres, textes, images, sons) utilisĂ©s comme source principale pour la recherche scientifique et gĂ©nĂ©ralement reconnus par la communautĂ© scientifique comme nĂ©cessaires pour valider les rĂ©sultats de la recherche. Un ensemble de donnĂ©es de recherche constitue une reprĂ©sentation systĂ©matique et partielle du sujet faisant lâobjet de la recherche ». Exemples âą les images dâune ville prĂ©historique deviennent des donnĂ©es pour un chercheur qui Ă©tudie lâhistoire de cette ville; âą les « donnĂ©es » dâun linguiste peuvent ĂȘtre des Ă©crits ou des discours, des enregistrements de locuteurs ; âą les « donnĂ©es » dâun mĂ©diĂ©viste sont des sources archivistiques, archĂ©ologiques, Ă©pigraphiques, iconographiques, littĂ©raires ; âą les « donnĂ©es » dâun gĂ©ologue rassemblent des coupes et observations de terrain consignĂ©es sur un carnet, des rĂ©sultats de carottage, des analyses dâĂ©chantillons, des donnĂ©es sismographiques⊠⹠⹠Pourquoi partager ses donnĂ©es ? "La science ouverte vise Ă construire un Ă©cosystĂšme dans lequel la science est plus cumulative, plus fortement Ă©tayĂ©e par des donnĂ©es, plus transparente, plus rapide et dâaccĂšs plus universel.La science ouverte favorise Ă©galement les avancĂ©es scientifiques, particuliĂšrement les avancĂ©es imprĂ©vues, ainsi que lâinnovation, les progrĂšs Ă©conomiques et sociaux, en France, dans les pays dĂ©veloppĂ©s et dans les pays en dĂ©veloppement. Enfin, la science ouverte constitue un levier pour lâintĂ©gritĂ© scientifique et favorise la confiance des citoyens dans la science. Elle constitue un progrĂšs scientifique et un progrĂšs de sociĂ©tĂ©." Source : Plan national pour la Science Ouverte (2018) Les enjeux de l'Open Data âą enjeux patrimoniaux o preuve et mĂ©moire (Ă©viter les pertes de donnĂ©es) âą enjeux Ă©conomiques o valeur Ă©conomique de la donnĂ©e o rĂ©utilisation gratuite ou payante des donnĂ©es, exploitation des rĂ©sultats de recherches antĂ©rieures (Ă©viter de refaire ce qui a dĂ©jĂ Ă©tĂ© validĂ©), o accĂ©lĂ©ration de l'innovation et le retour sur investissement dans la R&D âą enjeux scientifiques o de "hypothesis-driven" Ă "data-driven" o plus de visibilitĂ© pour le scientifique âą enjeux sociĂ©taux o participation des citoyens et de la sociĂ©tĂ© civile : "Citizen science" o confiance en la recherche Pour aller plus loin âą Site Doranum : https://doranum.fr/enjeux-benefices/fiche-synthetique/ âą Adopter de bonnes pratiques tout au long du cycle de vie des donnĂ©es De bonnes pratiques de gestion Ă toutes les Ă©tapes du cycle de vie de la donnĂ©e sont un prĂ©alable indispensable Ă lâouverture des donnĂ©es et Ă leur rĂ©utilisation. âą Rechercher des donnĂ©es Pour identifier des jeux de donnĂ©es (datasets) pertinents pour votre thĂšse, des outils de recherche sont disponibles. Suivez ces liens pour les dĂ©couvrir : âą Site Doranum : https://doranum.fr/acces-visualisation/rechercher-donnees/ âą Site DataCC - Vos besoins, trouver des donnĂ©es : https://www.datacc.org/vos-besoins/trouver-des-donnees/ âą Fiche CoopIST : Trouver des jeux de donnĂ©es via des bases pluridisciplinaires et des moteurs de recherche Pensez-aussi Ă consulter l'entrepĂŽt institutionnel Data INRAE Page de prĂ©sentation du portail âą Choisir les bons formats et bien organiser vos donnĂ©es ï§ Choisir des formats de fichier : https://www6.inrae.fr/datapartage/Gerer/Choisir-des-formats-de-fichier ï§ Nommer et organiser vos fichiers de donnĂ©es : https://www6.inrae.fr/datapartage/Gerer/Nommer-et-organiser-ses-fichiers-de-donnees Pour aller plus loin âą Jaouen, G.- GĂ©rer ses donnĂ©es. Pourquoi, Comment ? SĂ©minaire - Guadeloupe, du 25 au 27 Novembre 2019 â CRAG INRA âą Bien dĂ©crire et documenter ses donnĂ©es La description dâun jeu de donnĂ©es se fait Ă lâaide de mĂ©tadonnĂ©es (*) qui doivent apporter suffisamment d'Ă©lĂ©ments (sur la collecte des donnĂ©es, les unitĂ©s de mesure employĂ©es...) pour chercher et trouver le jeu de donnĂ©es, juger de sa qualitĂ©/fiabilitĂ©, et pouvoir le comprendre ou le rĂ©utiliser dans un autre contexte. (*) DĂ©finition des mĂ©tadonnĂ©es : Ensemble dâinformations structurĂ©es qui dĂ©crit, explicite, localise une ressource informationnelle, dans le but dâen faciliter la recherche, lâusage, et la gestion. Source : NISO. Understanding Metadata. 2004. Quelques liens utiles : âą Site Doranum : https://doranum.fr/metadonnees-standards-formats/ âą DataCC : https://www.datacc.org/vos-besoins/documenter-ses-donnees/metadonnees/ âą Site DataPartage INRAE : https://www6.inrae.fr/datapartage/Gerer/Documenter-les-donnees En complĂ©ment des mĂ©tadonnĂ©es, la rĂ©daction d'un fichier READ ME.txt est Ă©galement recommandĂ©e. âą Stocker, sĂ©curiser, prĂ©server ses donnĂ©es Bien diffĂ©rencier les notions de stockage et d'archivage. Anticiper pour dĂ©terminer les donnĂ©es Ă Ă©liminer et celles qui doivent ĂȘtre prĂ©servĂ©es Ă long terme. âą Dans l'environnement INRAE : https://www6.inrae.fr/datapartage/Gerer/Stocker-les-donnees âą Site Doranum : https://doranum.fr/stockage-archivage/ âą Site DataCC : https://www.datacc.org/vos-besoins/conserver-ses-donnees/ âą Partager, ne pas partager ses donnĂ©es ? Dans le cadre de la Science Ouverte, il y a de plus en plus d'incitations voire d'exigences pour rendre accessibles les donnĂ©es, en particulier les donnĂ©es liĂ©es aux publications : âą de l'Ă©dition scientifique : de plus en plus de revues adoptent une "data policy" (Ă consulter dans les instructions aux auteurs) et exigent des auteurs qu'ils fournissent les donnĂ©es associĂ©es aux publications, âą des organismes de financement (ANR, Commission EuropĂ©enne ...), âą des politiques nationale (Plan national pour la Science ouverte - MinistĂšre ESR - Juillet 2018) et institutionnelle. Mais attention, toutes les donnĂ©es ne sont pas partageables : assurez-vous que vos donnĂ©es sont bien diffusables au regard du droit et des conditions d'exercice de votre thĂšse et de son mode de financement (se reporter Ă votre contrat de thĂšse). Les donnĂ©es produites dans les organismes de recherche publics sont communicables Ă tous si elles n'entrent pas dans le cadre d'exceptions lĂ©gales (sĂ©curitĂ© dĂ©fense, sĂ©curitĂ© des populations, patrimoine scientifique et technique, donnĂ©es personnelles, donnĂ©es liĂ©es au secret, statistique, etc.) Liens utiles : âą sur le site Data Partage, la page Partager-Publier ou la page : "DonnĂ©es de la recherche : qui a les droits, qui doit partager ?" âą le site INRAE dĂ©diĂ© Ă la protection des donnĂ©es personnelles et l'application du RGPD (RĂšglement gĂ©nĂ©ral sur la protection des donnĂ©es) : https://intranet.inrae.fr/cil-dpo âą Valoriser ses donnĂ©es Voici les principales voies de diffusion âą ï§ Partager ses donnĂ©es en les dĂ©posant dans un entrepĂŽt ï§ Choisir un entrepĂŽt ï§ DĂ©poser dans Data INRAE ï§ Partager ses donnĂ©es comme matĂ©riel supplĂ©mentaire d'un article (Ă la demande de l'Ă©diteur) ï§ Publier un Data Paper (article de donnĂ©es) : la meilleure voie en terme de visibilitĂ© des donnĂ©es, et pour faciliter leur rĂ©utilisation. Pour aller plus loin âą Site Doranum o DĂ©pĂŽts et entrepĂŽts. Comment et oĂč dĂ©poser mes donnĂ©es ? o Data papers et Data journals. Comment publier mes donnĂ©es comme un article scientifique ? âą Site DataCC o Valoriser ses donnĂ©es âą Site CoopIST o DĂ©poser des donnĂ©es de recherche dans un entrepĂŽt o RĂ©diger et publier un data paper dans une revue scientifique A tĂ©lĂ©charger : SynthĂšse du processus de rĂ©daction d'un article avec des donnĂ©es associĂ©es âą Pourquoi ne pas rĂ©diger un plan de gestion de donnĂ©es (PGD) pour votre thĂšse ? La thĂšse peut ĂȘtre assimilĂ©e Ă un projet et certaines universitĂ©s au Royaume Uni, aux Pays-Bas et plus rĂ©cemment en France prĂ©conisent la rĂ©daction d'un plan de gestion associĂ© Ă la thĂšse. Le PGD (ou DMP = Data Management Plan) est un outil de planification qui peut vous aider Ă anticiper et bien gĂ©rer toutes les Ă©tapes du cycle de vie de vos donnĂ©es, Ă limiter les risques de perte ou corruption de donnĂ©es, Ă adopter de bonnes pratiques de gestion, pour in fine produire des donnĂ©es respectueuses des principes FAIR, adoptĂ©s aujourd'hui par l'ensemble des acteurs de la recherche. Il est dĂ©sormais exigĂ© par la plupart des financeurs de la recherche (Commission EuropĂ©enne et ANR ...) dans le cadre de projets financĂ©s. RĂ©diger un PGD pour votre thĂšse, peut ĂȘtre un bon exercice pour vous prĂ©parer Ă la future rĂ©daction de rĂ©ponses Ă des appels d'offre. Comment faire en pratique ? âą Site DataPartage : Pourquoi et comment rĂ©diger un plan de gestion de donnĂ©es ? âą Site Doranum : https://doranum.fr/plan-gestion-donnees-dmp/, La minute vidĂ©o PGD âą Site DataCC : https://www.datacc.org/bonnes-pratiques/adopter-un-plan-de-gestion-des-donnees/ âą Suivre une classe virtuelle INRAE : Open Class "RĂ©daction d'un PGD" âą Produire des donnĂ©es FAIR ! Favoriser la production de donnĂ©es FAIR (Findable - Accessible - Interoperable - Reusable) est aujourd'hui un objectif soutenu par l'ensemble des acteurs de la recherche. Source : https://open-science-training-handbook.gitbook.io/book/ Si vous suivez les conseils et recommandations de cette page, vous avez toutes les chances d'avoir produit des donnĂ©es de qualitĂ©. Si vous prĂ©fĂ©rez une version illustrĂ©e : "Pensez FAIR" - https://datapartage.inrae.fr/Gerer/Cycle-de-la-donnee Affiche cycle de vie des donnĂ©es rĂ©alisĂ©e dans le cadre des Missions QualiNous & RGPD, INRAE-ACT Vous pouvez tester le niveau de "Fairification" de vos donnĂ©es grĂące Ă ces outils : ï§ ARDC : https://ardc.edu.au/resources/working-with-data/fair-data/fair-self-assessment-tool âą D'autres ressources pour se former ou s'autoformer En interne INRAE âą Formation Ă la science ouverte OSCAR - Module "Gestion et partage des donnĂ©es" âą Le site "Gestion et partage des donnĂ©es" âą Des classes virtuelles d'environ 2h (Open Class) sont rĂ©guliĂšrement proposĂ©es sur : o la rĂ©daction des plans de gestion de donnĂ©es, o le dĂ©pĂŽt et la description d'un jeu de donnĂ©es dans Data INRAE, o la rĂ©daction et la publication de data papers, Sites externes âą Le site DORANUM (DonnĂ©es de la Recherche : Apprentissage NUMĂ©rique Ă la gestion et au partage) propose un dispositif de formation Ă distance intĂ©grant de nombreuses ressources dâauto-formation dĂ©clinĂ©es sur diffĂ©rents supports (textes, infographies, vidĂ©os) et sur 9 thĂ©matiques. o Parcours interactif sur la gestion des donnĂ©es de la recherche (2020) o âą Le site DataCC. Accompagnement Ă la gestion des donnĂ©es de recherche en physique et en chimie : https://www.datacc.org/ o Data Stories : https://www.datacc.org/reseau-datacc/data-stories/ o âą Le dossier "Open Access & Open Data" rĂ©alisĂ© par l'Ecole des Ponts - ParisTech âą âą The Open Science Training Handbook : https://www.ouvrirlascience.fr/the-open-science-training-handbook/
I DĂ©finition La proposition commerciale est une offre adressĂ©e Ă un client ou prospect suite Ă sa demande. Le commercial doit donc veiller Ă soigner sa prĂ©sentation, car la proposition commerciale est la vitrine de lâentreprise La proposition commerciale est le support de la relation entre lâentreprise et le client/prospect. II La finalitĂ© dâune proposition commerciale La proposition commerciale permet de rĂ©pondre prĂ©cisĂ©ment aux attentes du client qui souhaite passer une commande. Dans cette optique, la proposition doit ĂȘtre : - claire, - personnalisĂ©e - diffĂ©renciĂ©e de celles de la concurrence. La proposition commerciale permet Ă©galement de renseigner le client non pas uniquement sur les prestations proposĂ©es mais aussi sur lâentreprise elle-mĂȘme grĂące Ă son numĂ©ro dâidentification (SIRET) dĂ©livrĂ© par lâINSEE III Le systĂšme dâinformation client Pour rĂ©aliser la proposition commerciale, le commercial doit collecter des informations sur la clientĂšle, sur les produits mais Ă©galement sur lâenvironnement commercial. Elle consulte donc le systĂšme dâinformation client dont lâacronyme est SIC. Il est constituĂ© de fichiers commerciaux utilisables par tous les collaborateurs de lâentreprise afin dâamĂ©liorer la connaissance de la clientĂšle et des propsects. Son contenu est le suivant : IV Les logiciels pour prĂ©parer une proposition commerciale. Il est possible de prĂ©parer les propositions commerciales sur un texteur, un tableur, un logiciel spĂ©cialisĂ© en gestion commerciale ou un progiciel de gestion intĂ©grĂ© : Logiciels pouvant ĂȘtre utilisĂ©s Traitement de texte (Word, Open Writer, etc.) Tableur (Excel, Open Calc, etc.) Logiciel de gestion commerciale (EBP, Ciel, etc.) PGI (Cegid, Sage, EBP) Si lâentreprise possĂšde un PGI ou un logiciel de gestion commerciale, la proposition commerciale sera effectuĂ©e sur ce type de logiciel. Dans le cas contraire, il est recommandĂ© dâutiliser le tableur. Le progiciel est lâoutil privilĂ©giĂ© par les entreprises car il regroupe un ensemble de logiciels (modules) intĂ©grant les principales fonctions nĂ©cessaire Ă la gestion des flux monĂ©taires et physiques de lâentreprise. Tous ces modules accĂšdent Ă des ressources communes, stockĂ©es dans une base de donnĂ©es unique. Les modules les plus courants sont : Ainsi, le PGI permet dâĂ©viter les saisies redondantes, qui sont sources dâerreurs et de perte de temps. V Distinguer devis et proposition commerciale 1. Le devis Câest une offre adressĂ©e Ă un client ou un prospect destinĂ©e Ă rĂ©pondre Ă son besoin suite Ă la demande du client. Son contenu se limite souvent Ă la rĂ©fĂ©rence des produits et leurs prix. Le devis est donc un engagement de lâentreprise pour rĂ©aliser une prestation ou pour dĂ©livrer un produit au prix indiquĂ© et dans les dĂ©lais annoncĂ©s. Seules la signature du client et la date donnent au devis la valeur juridique dâun contrat. Il peut donc ajouter « Lu et acceptĂ© » ou encore « bon pour travaux » par exemple. 2. La proposition commerciale Par rapport au devis, la proposition commerciale nĂ©cessite une analyse plus poussĂ©e des besoins du client, un chiffrage de lâoffre plus complexe et un document plus personnalisĂ© VI Les Ă©tapes pour rĂ©aliser une offre commerciale Les Ă©tapes de la mise en Ćuvre dâune proposition commerciale sont : â lâanalyse des besoins du client ; â la recherche des informations qui permettent dâĂ©tablir lâoffre correspondant aux besoins du client (prix, dĂ©lai de livraison, planning de production, etc.) ; â la mise en forme de la proposition : On peut donc la schĂ©matiser ainsi : VII Les mentions obligatoires Ă faire figurer sur la proposition commerciale VIII Les sanctions en cas de non respect des mentions obligatoires Tout manquement peut aboutir Ă une contravention pouvant aller jusquâĂ 1500 ⏠dâamende.
News Opinion Sport Culture Lifestyle Show more Books Music TV & radio Art & design Film Games Classical Stage âHollywood doesnât do very much of that business, they have the nice sign, and everythingâs good, but they donât do very much,â said Trump. View image in fullscreen âHollywood doesnât do very much of that business, they have the nice sign, and everythingâs good, but they donât do very much,â said Trump. Photograph: Lucy Nicholson/Reuters Film âIâm not trying to hurt the industryâ: Trump softens tone on movie tariffs California governor Gavin Newsom announces a $7.5bn tax incentive scheme as Trumpâs announcement of 100% tariffs on films âproduced in foreign landsâ is mocked by Jimmy Kimmel and Fallon Andrew Pulver Tue 6 May 2025 11.24 BST Share Donald Trump appears to be softening his tone after widespread dismay in Hollywood and further afield at his bombshell announcement of 100% tariffs on films âproduced in foreign landsâ, saying he was ânot looking to hurt the industryâ. In remarks reported by CNBC, Trump said he was planning to discuss the plan with film industry leaders. âIâm not looking to hurt the industry, I want to help the industry.â He added: âSo weâre going to meet with the industry. I want to make sure theyâre happy with it because weâre all about jobs.â Trump also took aim again at California state governor Gavin Newsom, saying the film industry âhas been decimated by other countries taking them out, and also by incompetence, like in Los Angeles, the governor [Gavin Newsom] is a grossly incompetent man, heâs just allowed it to be taken away fromâ. Trump added: âHollywood doesnât do very much of that business, they have the nice sign, and everythingâs good, but they donât do very much.â Trumpâs talk of film tariffs makes no sense, but itâs already doing damage â to Hollywood Peter Bradshaw Peter Bradshaw Read more Newsom responded with a statement saying: âGovernor Newsom continues to champion Californiaâs iconic film and television industry â recognising it as a cornerstone of the stateâs economy, one that sustains hundreds of thousands of good-paying jobs across every sector around the state.â âHis plan to more than double the stateâs film and television tax credit reflects a commitment to keeping production here at home, supporting workers and maintaining Californiaâs global leadership in entertainment. If the President announces a proposal with more details, we will review it.â Newsom had earlier responded to Trumpâs announcement by proposing a $7.5bn federal tax incentive scheme, saying in a statement to Variety: âBuilding on our successful state program, weâre eager to partner with the Trump administration to further strengthen domestic production.â Tax incentive schemes in the US currently operate on a state-by-state basis, and Newsom had announced a plan in April to boost Californiaâs to $750m. California senator Adam Schiff also condemned Trumpâs tariff proposal while backing calls for a federal tax credit scheme, saying in a statement: âBlanket tariffs on all films would have unintended and potentially damaging impacts, [but] we have an opportunity to work together to pass a major federal film tax credit to re-shore American jobs in the industry.â Late night TV hosts Jimmy Kimmel and Jimmy Fallon also joined the chorus of dismay and bafflement at Trumpâs plan. Commenting that Trump was ânow aiming his wrecking ball at Hollywoodâ, Kimmel questioned whether foreign-made movies were a ânational security threatâ as Trump claimed. âI donât care where theyâre made. I really donât. I guess itâs what the late, great Hannibal Lecter wouldâve wanted. Sonic, the illegal immigrant hedgehog, is a national security threat and he must be stopped!â Kimmel also mocked actor Jon Voightâs role in Trumpâs thinking, saying: âThis is where he reportedly got the tariff movies idea â from Angelina Jolieâs 86-year-old father she wonât talk to. What a great idea. Next year, The White Lotus is gonna be set at a Hampton Inn.â Fallon also took aim at Trumpâs implication that foreign locations were somehow taboo, saying: âGonna be fun seeing the next Lord of the Rings filmed in Bayonne, New Jersey,â adding: âIf you donât like that, you can also watch Emily in Des Moines [instead of Emily in Paris]. Itâs just as charming.â Explore more on these topics Film Film industry Donald Trump Trump tariffs Gavin Newsom Jimmy Kimmel Jimmy Fallon news Share Reuse this content Most viewed Live German parliament votes again on Merzâs bid to be chancellor after humiliating first round â Europe live Trump and Carney to meet at White House in closely watched encounter Mushroom lunchâs sole surviving guest details deadly meal and its aftermath as trial of Erin Patterson continues âItâs the misogyny slop ecosystem!â How Candace Owens and the American right declared war on Blake Lively Wisconsin woman missing for more than 60 years found âalive and wellâ
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
Confidentialité et protection des données
Voici le vocabulaire essentiel extrait des 4 leçons, organisĂ© par thĂ©matique pour faciliter votre rĂ©vision. ### đ Leçon 1 : IdentitĂ© NumĂ©rique & SĂ©curitĂ© Cette leçon porte sur la protection de votre accĂšs et la distinction entre vie privĂ©e et vie scolaire. * **IdentitĂ© NumĂ©rique Scolaire :** Votre "passeport" pour l'Ă©cole. L'identifiant est au format `prenom.nom@studentfr.ch`. * **Session Locale vs Web Personnel :** La distinction importante entre l'environnement de l'Ă©cole (scolaire) et votre navigation privĂ©e Ă la maison. * **MFA (Double Authentification) :** Le "verrou supplĂ©mentaire". SystĂšme de sĂ©curitĂ© qui demande deux preuves d'identitĂ© (le mot de passe + une validation sur tĂ©lĂ©phone). * **Microsoft Authenticator :** L'application mobile requise pour valider votre identitĂ© via la double authentification. * **Mot de passe fort :** Un code d'accĂšs qui respecte 4 rĂšgles (8 caractĂšres min., 1 majuscule, 1 chiffre, 1 symbole). --- ### đŹ Leçon 2 : Teams (Communication) Le vocabulaire ici concerne la navigation dans votre "salle de classe virtuelle". * **Ăquipes :** ReprĂ©sente une classe virtuelle ou une matiĂšre (ex: "EPAI-Bureautique"). * **Canal "GĂ©nĂ©ral" :** Le tableau d'affichage officiel oĂč le professeur publie les annonces importantes pour toute la classe. * **Canal (Public) :** Espace de discussion visible par toute la classe. * **Conversation (PrivĂ©) :** Messages directs visibles uniquement par les participants (comme un SMS/chat). * **Onglet "Fichiers" :** La bibliothĂšque de la classe oĂč sont rangĂ©s les documents de cours (PDF, supports). --- ### đ Leçon 3 : Rangement NumĂ©rique Les termes techniques pour organiser efficacement vos documents sur un ordinateur. * **Arborescence :** La structure d'organisation des dossiers, visualisĂ©e comme les branches d'un arbre. * **Racine :** Le dossier principal qui contient tous les autres (le point de dĂ©part, ex: `2025_PRENOM_NOM`). * **Sous-dossiers :** Dossiers créés Ă l'intĂ©rieur de la racine (ex: "01_Administratif", "02_Cours"). * **CaractĂšres interdits :** Symboles qu'il ne faut jamais utiliser pour nommer un fichier (ex: `/ \ : * ? " < > |`). * **Cycle de vie d'un fichier :** Les 3 Ă©tapes Ă maĂźtriser : CrĂ©er â Nommer â Enregistrer. --- ### âïž Leçon 4 : Cloud, Partage & IA Comprendre le stockage moderne et les nouveaux outils d'assistance. * **Cloud (Nuage) / OneDrive :** Espace de stockage en ligne ("clĂ© USB invisible"). Accessible partout avec internet, contrairement au Disque Dur Local. * **Disque Dur Local (C:) :** Stockage physique sur l'ordinateur. Les donnĂ©es ne sont accessibles que sur cet appareil prĂ©cis. * **Partage de lien :** MĂ©thode moderne d'envoi de fichier (plus lĂ©ger et sĂ»r qu'une piĂšce jointe) permettant de travailler sur une version unique du document. * **IA (Intelligence Artificielle) :** Outil assistant (comme ChatGPT ou Gemini) qui rĂ©pond Ă des instructions. * **Prompt :** L'instruction ou la question prĂ©cise que l'on donne Ă une IA pour obtenir une rĂ©ponse.
1. Laquelle des formes juridiques suivantes offre la meilleure protection du patrimoine personnel de l'entrepreneur ? a) Entreprise individuelle b) SociĂ©tĂ© c) Association de fait d) Aucune de ces rĂ©ponses 2. Quel est l'inconvĂ©nient majeur de l'entreprise individuelle ? a) DifficultĂ© de crĂ©ation b) RĂ©gime fiscal complexe c) ResponsabilitĂ© illimitĂ©e de l'entrepreneur d) ImpossibilitĂ© d'avoir des employĂ©s 3. Laquelle des affirmations suivantes concernant la sociĂ©tĂ© est vraie ? a) Elle n'a pas d'existence juridique propre. b) Le patrimoine des associĂ©s est confondu avec celui de la sociĂ©tĂ©. c) Elle peut poursuivre ses activitĂ©s mĂȘme aprĂšs le dĂ©cĂšs d'un associĂ©. d) Elle est toujours soumise Ă l'impĂŽt sur le revenu des personnes physiques. 4. Dans une association de fait, que se passe-t-il en cas de mauvaise gestion financiĂšre de l'un des associĂ©s ? a) Seul l'associĂ© responsable est tenu de rembourser les dettes. b) Tous les associĂ©s sont solidairement responsables des dettes. c) L'association est automatiquement dissoute. d) Un tribunal dĂ©signe un administrateur judiciaire pour gĂ©rer les finances. 5. Lequel des Ă©lĂ©ments suivants est un avantage de la sociĂ©tĂ© par rapport Ă l'entreprise individuelle ? a) SimplicitĂ© de crĂ©ation et de gestion b) ResponsabilitĂ© limitĂ©e des associĂ©s c) ContrĂŽle total et dĂ©cisions unilatĂ©rales d) FiscalitĂ© moins avantageuse 6. Qu'est-ce qu'une personne morale ? a) Un individu exerçant une activitĂ© commerciale en son nom propre b) Une entitĂ© juridique distincte de ses membres, dotĂ©e de droits et d'obligations c) Un contrat par lequel deux personnes s'engagent Ă mettre en commun des biens ou leur travail d) Une forme d'entreprise rĂ©servĂ©e aux professions libĂ©rales 7. Laquelle des affirmations suivantes est vraie concernant l'association de fait ? a) Elle nĂ©cessite la crĂ©ation d'une personne morale. b) Elle offre une protection du patrimoine personnel des participants. c) Elle peut ĂȘtre considĂ©rĂ©e comme une entreprise si elle verse des bĂ©nĂ©fices Ă ses membres. d) Elle est soumise aux mĂȘmes obligations comptables que les sociĂ©tĂ©s. 8. Quel est l'un des avantages de la sociĂ©tĂ© en matiĂšre de continuitĂ© d'activitĂ© ? a) Elle est dissoute automatiquement au dĂ©cĂšs de son fondateur. b) Elle peut ĂȘtre facilement transmise aux hĂ©ritiers en cas de dĂ©cĂšs d'un associĂ©. c) Elle cesse son activitĂ© si un associĂ© dĂ©cide de se retirer. d) Elle doit ĂȘtre liquidĂ©e en cas d'incapacitĂ© de travail d'un associĂ©. 9. Lequel des critĂšres suivants peut influencer le choix entre une entreprise individuelle et une sociĂ©tĂ© ? a) Le montant du capital initial b) Le nombre d'employĂ©s c) Le secteur d'activitĂ© d) La volontĂ© de protĂ©ger son patrimoine personnel 10. Quel est l'un des risques majeurs liĂ©s Ă l'absence de sĂ©paration des patrimoines dans l'entreprise individuelle ? a) La responsabilitĂ© limitĂ©e de l'entrepreneur b) La saisie du patrimoine personnel en cas de dettes de l'entreprise c) L'impossibilitĂ© de dĂ©duire les charges professionnelles de ses revenus d) La difficultĂ© d'obtenir un financement bancaire
Le vieillissement est lâensemble des processus physiologiques et psychologiques qui modifient la structure et les fonctions de lâorganisme Ă partir de lâĂąge mĂ»r. Il rĂ©sulte des effets combinĂ©s de facteurs gĂ©nĂ©tiques et environnementaux auxquels est soumis lâorganisme tout au long de sa vie. Il sâagit dâun processus lent et progressif qui est la consĂ©quence de lâaction du temps sur les fonctions de lâorganisme. La sĂ©nescence est le processus de vieillissement biologique, la suite des changements irrĂ©versibles dans un organisme qui conduisent Ă la mort. Ce processus physiologique dĂ©bute aprĂšs la phase de maturitĂ© et se traduit par la dĂ©gradation progressive et inĂ©luctable des fonctions vitales : reproduction, motricitĂ©, systĂšme immunitaire, etc. La sĂ©nilitĂ© est la dĂ©tĂ©rioration pathologique (liĂ©e Ă une maladie) des facultĂ©s physiques et mentales dâun individu ĂągĂ©. Il existe trois modalitĂ©s diffĂ©rentes de vieillissement : le vieillissement rĂ©ussi, avec une absence ou une atteinte minime des fonctions physiologiques et une absence de pathologies ; le vieillissement habituel, avec des atteintes considĂ©rĂ©es comme physiologiques, liĂ©es Ă lâĂąge, de certaines fonctions, mais sans pathologies invalidantes ; le vieillissement pathologique liĂ© Ă des maladies sĂ©vĂšres Ă©volutives ou compliquĂ©es et responsable le plus souvent dâune dĂ©pendance importante. Ă ces trois notions, il est important dâajouter la notion de fragilitĂ© qui correspond Ă un Ă©tat dâĂ©quilibre prĂ©caire avec lâimpossibilitĂ© de rĂ©pondre de façon adaptĂ©e Ă un stress quâil soit mĂ©dical, psychologique ou social. AprĂšs 65 ans, 10 Ă 20% des personnes peuvent ĂȘtre considĂ©rĂ©es comme fragiles et jusquâĂ 50% aprĂšs 85 ans. Il sâagit de personnes Ă haut risque dâhospitalisation, dâinstitutionnalisation et de dĂ©cĂšs. Les psychologues dĂ©crivent 5 grands types de personnalitĂ© liĂ©s au vieillissement, plus ou moins prĂ©sents chez chacun : le mature est actif, tolĂ©rant et il sâadapte parfaitement Ă son Ă©volution ; le pantouflard est passif, indulgent envers lui-mĂȘme et il utilise son Ăąge pour valoriser son inactivitĂ© ; le blindĂ© est mentalement rigide, il a peur de la dĂ©chĂ©ance et sâenferme dans ses souvenirs de jeunesse ; le mĂ©content est amer, intolĂ©rant et pessimiste, anxieux face Ă la mort ; il en veut au monde entier de son Ă©tat et de ses Ă©checs ; le dĂ©prĂ©ciĂ© est dĂ©pressif, insatisfait de sa vie, sans estime de soi et envahi de regrets sur le passĂ© ; il envisage la mort comme une dĂ©livrance ou une finalitĂ©. La solitude a un effet important sur la santĂ©. Si nous comparons des personnes ĂągĂ©es qui conservent un vaste rĂ©seau de relations sociales Ă dâautres qui sont isolĂ©es, ces derniĂšres auraient un risque supĂ©rieur de mort prĂ©maturĂ©e. Parler et Ă©changer avec les autres est essentiel au bien-ĂȘtre. Stimuler la mĂ©moire dâune personne ĂągĂ©e lui permettra de conserver son autonomie et de retarder la dĂ©pendance. Pour rester en forme, le cerveau doit travailler de maniĂšre complĂšte. Plusieurs activitĂ©s peuvent donc permettre Ă la personne dĂ©pendante de garder une bonne mĂ©moire le plus longtemps possible : tenir un agenda, rĂ©diger un journal, jouer Ă des jeux ou encore pratiquer des activitĂ©s de crĂ©ation. Pour stimuler lâactivitĂ© sociale dâune personne ĂągĂ©e, faire des rencontres est le meilleur moyen de rester en forme : rencontrer des personnes, poursuivre les activitĂ©s quâon aime, se servir du tĂ©lĂ©phone et mĂȘme dâinternet si possible. Il y a des personnes ĂągĂ©es qui ne parlent Ă personne pendant des semaines. Pour dâautres, le contact se limite aux relations avec les caissiĂšres des supermarchĂ©s. Avec lâĂąge, certains de nos aĂźnĂ©s sont murĂ©s dans le silence. Pas par choix. Mais parce que les liens familiaux se sont distendus ou nâexistent plus. Ils se retrouvent alors seuls, sans Ă©change, sans partage et sans affection. Un des grands dĂ©fis Ă relever pour lâavenir est la lutte contre la solitude des personnes ĂągĂ©es. Il faut savoir que la solitude est dĂ©sormais considĂ©rĂ©e comme un facteur de risque de la maladie dâAlzheimer. Lutter contre la solitude, câest prĂ©venir lâexclusion, la pauvretĂ© et la perte dâautonomie. Quel est le secret pour prĂ©server son corps malgrĂ© les annĂ©es ? Un peu dâactivitĂ© physique et des repas Ă©quilibrĂ©s ! Pour lutter contre lâapparition des rides ou la chute des cheveux et conserver ses capacitĂ©s physiques et cognitives, mieux vaut surveiller son assiette. Inutile dâaller chercher des produits miracles pour rester jeune : il faut commencer par manger mieux! Car en fonction des aliments quâon choisit, on prĂ©serve son capital santĂ© et on garde la forme durant de longues annĂ©es. Les problĂšmes alimentaires spĂ©cifiques au vieillissement apparaissent Ă des Ăąges variables et sont beaucoup plus marquĂ©s aprĂšs 85 ans. Une bonne nutrition a un rĂŽle de prĂ©vention de mieux en mieux connu sur les pathologies liĂ©es Ă lâĂąge. Un bon rĂ©gime pour un senior comprend beaucoup de fruits et de lĂ©gumes, du pain, du riz, des pĂątes et des fibres. Il ne faut pas oublier le poisson, surtout le thon, le saumon et les sardines, et limiter les viandes rouges, en prĂ©fĂ©rant le poulet, la dinde ou le lapin. Il faut aussi rĂ©duire le sel et le sucre, et tous les aliments riches en graisses comme les frites, les fritures ou les gĂąteaux. Lâeau est trĂšs importante, mais on peut aussi boire du thĂ©, des jus de fruits sans sucre ou du lait Ă©crĂ©mĂ© ou demi â Ă©crĂ©mĂ©. Il faut aussi de la vitamine D pour garder les os en bonne santĂ©. On peut la trouver dans le poisson, la margarine et les cĂ©rĂ©ales du petit dĂ©jeuner. Le corps produit tout seul la vitamine D quand il est exposĂ© au soleil, il est donc conseillĂ© de profiter du soleil de temps en temps avec de la protection pour aider le corps Ă produire cette vitamine. Ătape naturelle de la vie dâune femme, la mĂ©nopause mĂ©rite quelques attentions sur le plan nutritionnel Ă cause de la modification du statut hormonal. Beaucoup de femmes prennent du poids Ă la cinquantaine. Souvent tout simplement parce que leur mode de vie change, avec moins de dĂ©penses physiques et plus de temps pour apprĂ©cier les plaisirs de la table ! Mais aussi parce que les transformations hormonales de la mĂ©nopause vont favoriser la mise en rĂ©serve de graisses. Le premier antidote contre ce risque de surpoids est une activitĂ© physique suffisante et, en complĂ©ment, une alimentation allĂ©gĂ©e grĂące Ă lâĂ©limination des calories «inutiles». Ă Ă©viter ou Ă consommer avec beaucoup de modĂ©ration : les boissons sucrĂ©es comme les sodas, les bonbons, les biscuits salĂ©s ou sucrĂ©s, lâalcool sous toutes ses formes, les glaces et les pĂątisseries, les plats riches en graisses, les frites et les fritures, les sauces classiques, la mayonnaise, les sauces barbecue et tous les laitages au lait entier. Les modifications hormonales et la diminution de lâactivitĂ© physique ont Ă©galement pour consĂ©quence une âfonteâ progressive de la masse musculaire. Pour lutter contre ce phĂ©nomĂšne, il y a une seule solution : bouger !