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Obesity I: Overview and molecular and biochemical mechanisms
RH. Lustig, D. Collier, C. Kassotis, TA. Roepke, MJ. Kim, E. Blanc, R. Barouki, A. Bansal, MC. Cave, S. Chatterjee, M. Choudhury, M. Gilbertson, D. Lagadic-Gossmann, S. Howard, L. Lind, CR. Tomlinson, J. Vondracek, JJ. Heindel
Jazyk angličtina Země Velká Británie
Typ dokumentu časopisecké články, přehledy, Research Support, N.I.H., Extramural, práce podpořená grantem
Grantová podpora
P30 ES025128
NIEHS NIH HHS - United States
P30 ES030283
NIEHS NIH HHS - United States
P30 ES005022
NIEHS NIH HHS - United States
P01 ES028942
NIEHS NIH HHS - United States
T32 ES011564
NIEHS NIH HHS - United States
R21 ES031510
NIEHS NIH HHS - United States
R01 ES032189
NIEHS NIH HHS - United States
P20 GM103641
NIGMS NIH HHS - United States
P01 AT003961
NCCIH NIH HHS - United States
R01 MH123544
NIMH NIH HHS - United States
R00 ES030405
NIEHS NIH HHS - United States
R35 ES028373
NIEHS NIH HHS - United States
P42 ES023716
NIEHS NIH HHS - United States
- MeSH
- energetický metabolismus fyziologie MeSH
- inzulin metabolismus MeSH
- leptin * metabolismus MeSH
- lidé MeSH
- obezita * metabolismus MeSH
- tuková tkáň metabolismus MeSH
- tukové buňky metabolismus MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- přehledy MeSH
- Research Support, N.I.H., Extramural MeSH
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 YY3-36) 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.
Brody School of Medicine East Carolina University Greenville NC 27834 United States
College of Health and Medicine Australian National University Canberra Australia
College of Pharmacy Texas A and M University College Station TX 77843 United States
Department of Biochemistry and Toxicology University of Paris INSERM U1224 75006 Paris France
Department of Medical Sciences University of Uppsala Uppsala Sweden
Healthy Environment and Endocrine Disruptor Strategies Commonweal Bolinas CA 92924 United States
Sorbonne Paris Nord University Bobigny INSERM U1124 Paris France
Univ Rennes INSERM EHESP IRSET UMR_S 1085 35000 Rennes France
Citace poskytuje Crossref.org
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- $a 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 YY3-36) 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.
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