| Hypothalamic leptin regulation of energy homeostasis and glucose metabolism. | |
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MedLine Citation:
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PMID: 17584844 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Gregory J Morton |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Review Date: 2007-06-21 |
Journal Detail:
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Title: The Journal of physiology Volume: 583 ISSN: 0022-3751 ISO Abbreviation: J. Physiol. (Lond.) Publication Date: 2007 Sep |
Date Detail:
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Created Date: 2007-09-03 Completed Date: 2007-11-20 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 0266262 Medline TA: J Physiol Country: England |
Other Details:
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Languages: eng Pagination: 437-43 Citation Subset: IM |
Affiliation:
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Department of Medicine, Harbourview Medical Center, University of Washington, Seattle, WA 98104, USA. gjmorton@u.washington.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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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:
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0/Leptin; 50-99-7/Glucose |
| Comments/Corrections | |
Comment In:
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J Physiol. 2007 Sep 1;583(Pt 2):423
[PMID:
17766646
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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