2022
Heindel, Jerrold J.; Howard, 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.; 3rd Howell, George; Kassotis, Christopher D.; Kay, Mathew K.; Kim, Min Ji; Lagadic-Gossmann, Dominique; Langouet, Sophie; Legrand, Antoine; Li, Zhuorui; Mentec, Helene Le; Lind, Lars; Lind, P. Monica; Lustig, Robert H.; Martin-Chouly, Corinne; Kos, Vesna Munic; Podechard, Normand; Roepke, Troy A.; Sargis, Robert M.; Starling, Anne; Tomlinson, Craig R.; Touma, Charbel; Vondracek, Jan; Saal, Frederick Vom; Blumberg, Bruce
Obesity II: Establishing causal links between chemical exposures and obesity. Journal Article
In: Biochemical pharmacology, vol. 199, pp. 115015, 2022, ISSN: 1873-2968 0006-2952, (Place: England).
Abstract | Links | BibTeX | Tags: *Endocrine Disruptors/toxicity, Adipocyte differentiation, Adipogenesis, Adipose Tissue, Child, Endocrine disruptor, Environmental Exposure/adverse effects, Humans, Obesity, Obesity/etiology, Obesogen, Preschool, Weight Gain
@article{heindel_obesity_2022,
title = {Obesity II: Establishing causal links between chemical exposures and obesity.},
author = {Jerrold J. Heindel and Sarah Howard and Keren Agay-Shay and Juan P. Arrebola and Karine Audouze and Patrick J. Babin and Robert Barouki and Amita Bansal and Etienne Blanc and Matthew C. Cave and Saurabh Chatterjee and Nicolas Chevalier and Mahua Choudhury and David Collier and Lisa Connolly and Xavier Coumoul and Gabriella Garruti and Michael Gilbertson and Lori A. Hoepner and Alison C. Holloway and George 3rd Howell and Christopher D. Kassotis and Mathew K. Kay and Min Ji Kim and Dominique Lagadic-Gossmann and Sophie Langouet and Antoine Legrand and Zhuorui Li and Helene Le Mentec and Lars Lind and P. Monica Lind and Robert H. Lustig and Corinne Martin-Chouly and Vesna Munic Kos and Normand Podechard and Troy A. Roepke and Robert M. Sargis and Anne Starling and Craig R. Tomlinson and Charbel Touma and Jan Vondracek and Frederick Vom Saal and Bruce Blumberg},
doi = {10.1016/j.bcp.2022.115015},
issn = {1873-2968 0006-2952},
year = {2022},
date = {2022-05-01},
journal = {Biochemical pharmacology},
volume = {199},
pages = {115015},
abstract = {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.},
note = {Place: England},
keywords = {*Endocrine Disruptors/toxicity, Adipocyte differentiation, Adipogenesis, Adipose Tissue, Child, Endocrine disruptor, Environmental Exposure/adverse effects, Humans, Obesity, Obesity/etiology, Obesogen, Preschool, Weight Gain},
pubstate = {published},
tppubtype = {article}
}
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.
Lustig, Robert H.; Collier, David; Kassotis, Christopher; Roepke, Troy A.; Kim, Min Ji; Blanc, Etienne; Barouki, Robert; Bansal, Amita; Cave, Matthew C.; Chatterjee, Saurabh; Choudhury, Mahua; Gilbertson, Michael; Lagadic-Gossmann, Dominique; Howard, Sarah; Lind, Lars; Tomlinson, Craig R.; Vondracek, Jan; Heindel, Jerrold J.
Obesity I: Overview and molecular and biochemical mechanisms. Journal Article
In: Biochemical pharmacology, vol. 199, pp. 115012, 2022, ISSN: 1873-2968 0006-2952, (Place: England).
Abstract | Links | BibTeX | Tags: *Leptin/metabolism, *Obesity/metabolism, Adipocytes/metabolism, Adipose Tissue, Adipose Tissue/metabolism, Energy balance, Energy Metabolism/physiology, Hormone receptors, Humans, Insulin/metabolism, metabolism, Microbiome, Obesity
@article{lustig_obesity_2022,
title = {Obesity I: Overview and molecular and biochemical mechanisms.},
author = {Robert H. Lustig and David Collier and Christopher Kassotis and Troy A. Roepke and Min Ji Kim and Etienne Blanc and Robert Barouki and Amita Bansal and Matthew C. Cave and Saurabh Chatterjee and Mahua Choudhury and Michael Gilbertson and Dominique Lagadic-Gossmann and Sarah Howard and Lars Lind and Craig R. Tomlinson and Jan Vondracek and Jerrold J. Heindel},
doi = {10.1016/j.bcp.2022.115012},
issn = {1873-2968 0006-2952},
year = {2022},
date = {2022-05-01},
journal = {Biochemical pharmacology},
volume = {199},
pages = {115012},
abstract = {Obesity is a chronic, relapsing condition characterized by excess body fat. Its prevalence has increased globally since the 1970s, and the number of obese and overweight people is now greater than those underweight. Obesity is a multifactorial condition, and as such, many components contribute to its development and pathogenesis. This is the first of three companion reviews that consider obesity. This review focuses on the genetics, viruses, insulin resistance, inflammation, gut microbiome, and circadian rhythms that promote obesity, along with hormones, growth factors, and organs and tissues that control its development. It shows that the regulation of energy balance (intake vs. expenditure) relies on the interplay of a variety of hormones from adipose tissue, gastrointestinal tract, pancreas, liver, and brain. It details how integrating central neurotransmitters and peripheral metabolic signals (e.g., leptin, insulin, ghrelin, peptide YY(3-36)) is essential for controlling energy homeostasis and feeding behavior. It describes the distinct types of adipocytes and how fat cell development is controlled by hormones and growth factors acting via a variety of receptors, including peroxisome proliferator-activated receptor-gamma, retinoid X, insulin, estrogen, androgen, glucocorticoid, thyroid hormone, liver X, constitutive androstane, pregnane X, farnesoid, and aryl hydrocarbon receptors. Finally, it demonstrates that obesity likely has origins in utero. Understanding these biochemical drivers of adiposity and metabolic dysfunction throughout the life cycle lends plausibility and credence to the "obesogen hypothesis" (i.e., the importance of environmental chemicals that disrupt these receptors to promote adiposity or alter metabolism), elucidated more fully in the two companion reviews.},
note = {Place: England},
keywords = {*Leptin/metabolism, *Obesity/metabolism, Adipocytes/metabolism, Adipose Tissue, Adipose Tissue/metabolism, Energy balance, Energy Metabolism/physiology, Hormone receptors, Humans, Insulin/metabolism, metabolism, Microbiome, Obesity},
pubstate = {published},
tppubtype = {article}
}
Obesity is a chronic, relapsing condition characterized by excess body fat. Its prevalence has increased globally since the 1970s, and the number of obese and overweight people is now greater than those underweight. Obesity is a multifactorial condition, and as such, many components contribute to its development and pathogenesis. This is the first of three companion reviews that consider obesity. This review focuses on the genetics, viruses, insulin resistance, inflammation, gut microbiome, and circadian rhythms that promote obesity, along with hormones, growth factors, and organs and tissues that control its development. It shows that the regulation of energy balance (intake vs. expenditure) relies on the interplay of a variety of hormones from adipose tissue, gastrointestinal tract, pancreas, liver, and brain. It details how integrating central neurotransmitters and peripheral metabolic signals (e.g., leptin, insulin, ghrelin, peptide YY(3-36)) is essential for controlling energy homeostasis and feeding behavior. It describes the distinct types of adipocytes and how fat cell development is controlled by hormones and growth factors acting via a variety of receptors, including peroxisome proliferator-activated receptor-gamma, retinoid X, insulin, estrogen, androgen, glucocorticoid, thyroid hormone, liver X, constitutive androstane, pregnane X, farnesoid, and aryl hydrocarbon receptors. Finally, it demonstrates that obesity likely has origins in utero. Understanding these biochemical drivers of adiposity and metabolic dysfunction throughout the life cycle lends plausibility and credence to the "obesogen hypothesis" (i.e., the importance of environmental chemicals that disrupt these receptors to promote adiposity or alter metabolism), elucidated more fully in the two companion reviews.