Literature DB >> 17021376

Gut peptide signaling in the controls of food intake.

Timothy H Moran1.   

Abstract

During a meal and after a meal, ingested nutrients alter the release of a variety of gut peptides that have the potential to modulate food intake. Such feedback peptide signaling can be conceptualized as having three outcomes: meal termination, inhibitory modulation of intake in subsequent meals, and orexigenic modulation. Cholecystokinin, pancreatic glucagons, and amylin are examples of peptides involved in meal termination. They are released rapidly with the onset of feeding and have short durations of action. Peptide YY(3-36) and glucagon-like peptide 1 are peptides for which longer-term feeding inhibitory actions have been proposed. They are released from the distal intestine and have longer durations of actions. Ghrelin is a gastric peptide that stimulates food intake after its exogenous administration. Plasma ghrelin levels fall with feeding and rise with food deprivation. All of these gut peptides have vagal or dorsal hindbrain mediation. Their potential as targets for the development of anti-obesity treatments is under study.

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Year:  2006        PMID: 17021376     DOI: 10.1038/oby.2006.318

Source DB:  PubMed          Journal:  Obesity (Silver Spring)        ISSN: 1930-7381            Impact factor:   5.002


  38 in total

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5.  Hindbrain GLP-1 receptor-mediated suppression of food intake requires a PI3K-dependent decrease in phosphorylation of membrane-bound Akt.

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Review 7.  Hindbrain neurons as an essential hub in the neuroanatomically distributed control of energy balance.

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Review 8.  Leptin and the systems neuroscience of meal size control.

Authors:  Harvey J Grill
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9.  Association of beta2-adrenergic receptor and insulin receptor substrate-1 polymorphisms with obesity in a Northern Indian population.

Authors:  Neena Srivastava; B R Achyut; Jai Prakash; C G Agarwal; D C Pant; Balraj Mittal
Journal:  Indian J Hum Genet       Date:  2008-05

10.  Sensitivity to the satiating effects of exendin 4 is decreased in obesity-prone Osborne-Mendel rats compared to obesity-resistant S5B/Pl rats.

Authors:  S D Primeaux; M J Barnes; H D Braymer; G A Bray
Journal:  Int J Obes (Lond)       Date:  2010-04-20       Impact factor: 5.095

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