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Obesity II: Establishing causal links between chemical exposures and obesity
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SYSNO ASEP 0558379 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Obesity II: Establishing causal links between chemical exposures and obesity Author(s) Heindel, J. J. (US)
Howard, S. (US)
Agay-Shay, K. (FR)
Arrebola, J. (FR)
Audouze, K. (FR)
Babin, P. (US)
Barouki, R. (US)
Bansal, A. (FR)
Blanc, E. (US)
Cave, M. (US)
Chatterjee, S. (IT)
Chevalier, N. (US)
Choudhury, M. (IE)
Collier, D. (GB)
Connolly, L. (IL)
Coumoul, X. (FR)
Garruti, G. (ES)
Gilbertson, M. (AU)
Hoepner, L. (US)
Holloway, A. K. (US)
Howell Iii, G. (US)
Kassotis, C. (US)
Kay, M. (US)
Kim, M. (US)
Lagadic-Gossmann, D. (FR)
Langouet, S. (FR)
Legrand, A. (FR)
Li, Z. (US)
Le Mentec, H. (FR)
Lind, A. L. (US)
Vondráček, Jan (BFU-R) RID, ORCIDNumber of authors 43 Article number 115015 Source Title Biochemical Pharmacology. - : Elsevier - ISSN 0006-2952
Roč. 199, MAY 2022 (2022)Number of pages 49 s. Publication form Online - E Language eng - English Country US - United States Keywords endocrine-disrupting chemicals ; persistent organic pollutants ; ambient air-pollution ; organophosphate flame-retardants ; activated-receptor-gamma ; aryl-hydrocarbon receptor Subject RIV FR - Pharmacology ; Medidal Chemistry OECD category Pharmacology and pharmacy R&D Projects GA21-00533S GA ČR - Czech Science Foundation (CSF) Method of publishing Limited access Institutional support BFU-R - RVO:68081707 UT WOS 000800429000001 EID SCOPUS 85129395591 DOI https://doi.org/10.1016/j.bcp.2022.115015 Annotation Obesity is a multifactorial disease with both genetic and environmental components. The prevailing view is that obesity results from an imbalance between energy intake and expenditure caused by overeating and insufficient exercise. We describe another environmental element that can alter the balance between energy intake and energy expenditure: obesogens. Obesogens are a subset of environmental chemicals that act as endocrine disruptors affecting metabolic endpoints. The obesogen hypothesis posits that exposure to endocrine disruptors and other chemicals can alter the development and function of the adipose tissue, liver, pancreas, gastrointestinal tract, and brain, thus changing the set point for control of metabolism. Obesogens can determine how much food is needed to maintain homeostasis and thereby increase the susceptibility to obesity. The most sensitive time for obesogen action is in utero and early childhood, in part via epigenetic programming that can be transmitted to future generations. This review explores the evidence supporting the obesogen hypothesis and highlights knowledge gaps that have prevented widespread acceptance as a contributor to the obesity pandemic. Critically, the obesogen hypothesis changes the narrative from curing obesity to preventing obesity. Workplace Institute of Biophysics Contact Jana Poláková, polakova@ibp.cz, Tel.: 541 517 244 Year of Publishing 2023 Electronic address https://www.sciencedirect.com/science/article/pii/S0006295222001095?via%3Dihub
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