Obesity II: Establishing causal links between chemical exposures and obesity.
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Author
Heindel, Jerrold JHoward, Sarah
Agay-Shay, Keren
Arrebola, Juan P
Audouze, Karine
Babin, Patrick J
Barouki, Robert
Bansal, Amita
Blanc, Etienne
Cave, Matthew C
Chatterjee, Saurabh
Chevalier, Nicolas
Choudhury, Mahua
Collier, David
Connolly, Lisa
Coumoul, Xavier
Garruti, Gabriella
Gilbertson, Michael
Hoepner, Lori A
Holloway, Alison C
Howell, George
Kassotis, Christopher D
Kay, Mathew K
Kim, Min Ji
Lagadic-Gossmann, Dominique
Langouet, Sophie
Legrand, Antoine
Li, Zhuorui
Le Mentec, Helene
Lind, Lars
Monica Lind, P
Lustig, Robert H
Martin-Chouly, Corinne
Munic Kos, Vesna
Podechard, Normand
Roepke, Troy A
Sargis, Robert M
Starling, Anne
Tomlinson, Craig R
Touma, Charbel
Vondracek, Jan
Vom Saal, Frederick
Blumberg, Bruce
Journal title
Biochemical pharmacologyDate Published
2022-04-05Publication Volume
199Publication Begin page
115015
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Show full item recordAbstract
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.Citation
Heindel JJ, Howard S, Agay-Shay K, Arrebola JP, Audouze K, Babin PJ, Barouki R, Bansal A, Blanc E, Cave MC, Chatterjee S, Chevalier N, Choudhury M, Collier D, Connolly L, Coumoul X, Garruti G, Gilbertson M, Hoepner LA, Holloway AC, Howell G 3rd, Kassotis CD, Kay MK, Kim MJ, Lagadic-Gossmann D, Langouet S, Legrand A, Li Z, Le Mentec H, Lind L, Monica Lind P, Lustig RH, Martin-Chouly C, Munic Kos V, Podechard N, Roepke TA, Sargis RM, Starling A, Tomlinson CR, Touma C, Vondracek J, Vom Saal F, Blumberg B. Obesity II: Establishing causal links between chemical exposures and obesity. Biochem Pharmacol. 2022 May;199:115015. doi: 10.1016/j.bcp.2022.115015. Epub 2022 Apr 5. Erratum in: Biochem Pharmacol. 2022 Aug;202:115144. PMID: 35395240; PMCID: PMC9124454.DOI
10.1016/j.bcp.2022.115015ae974a485f413a2113503eed53cd6c53
10.1016/j.bcp.2022.115015
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- Creative Commons
Except where otherwise noted, this item's license is described as Copyright © 2022 Elsevier Inc. All rights reserved.
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