2022
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.