2022
Bernal, Kévin; Touma, Charbel; Erradhouani, Chedi; Boronat-Belda, Talía; Gaillard, Lucas; Kassir, Sara Al; Mentec, Hélène Le; Martin-Chouly, Corinne; Podechard, Normand; Lagadic-Gossmann, Dominique; Langouet, Sophie; Brion, François; Knoll-Gellida, Anja; Babin, Patrick J.; Sovadinova, Iva; Babica, Pavel; Andreau, Karine; Barouki, Robert; Vondracek, Jan; Alonso-Magdalena, Paloma; Blanc, Etienne; Kim, Min Ji; Coumoul, Xavier
Combinatorial pathway disruption is a powerful approach to delineate metabolic impacts of endocrine disruptors. Journal Article
In: FEBS letters, vol. 596, no. 24, pp. 3107–3123, 2022, ISSN: 1873-3468 0014-5793, (Place: England).
Abstract | Links | BibTeX | Tags: *Endocrine Disruptors/toxicity, *Metabolic Syndrome, appetite, bisphenol, dioxin, Humans, Inflammation, insulin resistance, microbiota, Obesity/chemically induced, perfluorinated compounds, Phenols, phthalate, TBT
@article{bernal_combinatorial_2022,
title = {Combinatorial pathway disruption is a powerful approach to delineate metabolic impacts of endocrine disruptors.},
author = {Kévin Bernal and Charbel Touma and Chedi Erradhouani and Talía Boronat-Belda and Lucas Gaillard and Sara Al Kassir and Hélène Le Mentec and Corinne Martin-Chouly and Normand Podechard and Dominique Lagadic-Gossmann and Sophie Langouet and François Brion and Anja Knoll-Gellida and Patrick J. Babin and Iva Sovadinova and Pavel Babica and Karine Andreau and Robert Barouki and Jan Vondracek and Paloma Alonso-Magdalena and Etienne Blanc and Min Ji Kim and Xavier Coumoul},
doi = {10.1002/1873-3468.14465},
issn = {1873-3468 0014-5793},
year = {2022},
date = {2022-12-01},
journal = {FEBS letters},
volume = {596},
number = {24},
pages = {3107–3123},
abstract = {The prevalence of metabolic diseases, such as obesity, diabetes, metabolic syndrome and chronic liver diseases among others, has been rising for several years. Epidemiology and mechanistic (in vivo, in vitro and in silico) toxicology have recently provided compelling evidence implicating the chemical environment in the pathogenesis of these diseases. In this review, we will describe the biological processes that contribute to the development of metabolic diseases targeted by metabolic disruptors, and will propose an integrated pathophysiological vision of their effects on several organs. With regard to these pathomechanisms, we will discuss the needs, and the stakes of evolving the testing and assessment of endocrine disruptors to improve the prevention and management of metabolic diseases that have become a global epidemic since the end of last century.},
note = {Place: England},
keywords = {*Endocrine Disruptors/toxicity, *Metabolic Syndrome, appetite, bisphenol, dioxin, Humans, Inflammation, insulin resistance, microbiota, Obesity/chemically induced, perfluorinated compounds, Phenols, phthalate, TBT},
pubstate = {published},
tppubtype = {article}
}
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}
}