Document Detail

Neuroendocrine body weight regulation: integration between fat tissue, gastrointestinal tract, and the brain.
MedLine Citation:
PMID:  20464707     Owner:  NLM     Status:  MEDLINE    
Human body weight is maintained at a fairly stable level regardless of changes in energy intake and energy expenditure. Compensatory mechanisms within the central nervous system (CNS), which regulate food intake and energy expenditure, are triggered by other central and peripheral signals. Peripherally, the main sources of those signals are the adipose tissue, gastrointestinal tract, and pancreas. The main signal originating from the adipose tissue is leptin, which promotes the activation of anorexigenic pathways in the CNS. Similarly, the central action of insulin also reduces food intake and stimulates catabolic pathways. The gastrointestinal tract contributes with several peptides that influence food intake, such as ghrelin, glucagon-like peptide 1 (GLP-1), peptide YY (PYY), oxyntomodulin (OXM), and cholecystokinin (CCK). Other substances secreted by the pancreas, such as pancreatic polypeptide (PP) and amylin, a hormone co-secreted with insulin, also affect energy balance. More recently, the endocannabinoid system has also been identified as a contributor in the maintenance of energy balance. Better understanding of these mechanistic systems involved in the regulation of energy metabolism will hopefully lead to the development of new therapeutic approaches against obesity, metabolic syndrome, and other nutritional disorders.
César Luiz Boguszewski; Gilberto Paz-Filho; Licio A Velloso
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Endokrynologia Polska     Volume:  61     ISSN:  0423-104X     ISO Abbreviation:  Endokrynol Pol     Publication Date:    2010 Mar-Apr
Date Detail:
Created Date:  2010-05-13     Completed Date:  2010-08-31     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0370674     Medline TA:  Endokrynol Pol     Country:  Poland    
Other Details:
Languages:  eng     Pagination:  194-206     Citation Subset:  IM    
Department of Internal Medicine, Endocrine Division (SEMPR), Federal University of Paraná, Curitiba, Brazil.
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MeSH Terms
Adipose Tissue / metabolism*
Body Weight / physiology*
Brain / metabolism
Endocannabinoids / metabolism*
Energy Metabolism / physiology*
Gastrointestinal Tract / metabolism*
Insulin / metabolism
Leptin / metabolism
Melanocortins / metabolism*
Metabolic Syndrome X / physiopathology
Neuropeptide Y / metabolism*
Obesity / physiopathology
Pancreas / metabolism
Reg. No./Substance:
0/Endocannabinoids; 0/Leptin; 0/Melanocortins; 0/Neuropeptide Y; 11061-68-0/Insulin

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