Document Detail


Hypothalamic leptin regulation of energy homeostasis and glucose metabolism.
MedLine Citation:
PMID:  17584844     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Growing evidence suggests that food intake, energy expenditure and endogenous glucose production are regulated by hypothalamic areas that respond to a variety of peripheral signals. Therefore, in response to a reduction in energy stores or circulating nutrients, the brain initiates responses in order to promote positive energy balance to restore and maintain energy and glucose homeostasis. In contrast, in times of nutrient abundance and excess energy storage, key hypothalamic areas activate responses to promote negative energy balance (i.e. reduced food intake and increased energy expenditure) and decreased nutrient availability (reduced endogenous glucose production). Accordingly, impaired responses or 'resistance' to afferent input from these hormonal or nutrient-related signals would be predicted to favour weight gain and insulin resistance and may contribute to the development of obesity and type 2 diabetes.
Authors:
Gregory J Morton
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review     Date:  2007-06-21
Journal Detail:
Title:  The Journal of physiology     Volume:  583     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2007 Sep 
Date Detail:
Created Date:  2007-09-03     Completed Date:  2007-11-20     Revised Date:  2013-06-06    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  437-43     Citation Subset:  IM    
Affiliation:
Department of Medicine, Harbourview Medical Center, University of Washington, Seattle, WA 98104, USA. gjmorton@u.washington.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Diabetes Mellitus, Type 2 / metabolism,  physiopathology
Eating
Energy Metabolism*
Feedback, Physiological
Glucose / metabolism*
Homeostasis
Humans
Hypothalamus / metabolism*
Insulin Resistance
Leptin / metabolism*
Liver / metabolism*
Obesity / metabolism,  physiopathology
Signal Transduction*
Weight Gain
Chemical
Reg. No./Substance:
0/Leptin; 50-99-7/Glucose
Comments/Corrections
Comment In:
J Physiol. 2007 Sep 1;583(Pt 2):423   [PMID:  17766646 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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