Document Detail


Role of hypothalamic AMP-kinase in food intake regulation.
MedLine Citation:
PMID:  18725075     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Adenosine monophosphate-activated protein kinase (AMPK) functions as a cellular fuel gauge that regulates metabolic pathways in nutrient metabolism. Recent studies have strongly implicated that AMPK in the hypothalamus regulates energy metabolism by integrating inputs from multiple hormones, peptides, neurotransmitters, and nutrients. Leptin is an adipocyte hormone that regulates food intake and energy expenditure in peripheral tissues. Leptin inhibits AMPK activity in the arcuate and paraventricular hypothalamus, and its inhibition is necessary for the anorexic effect of leptin. Alteration of hypothalamic AMPK activity is sufficient to change food intake and body weight. Furthermore, fasting/refeeding, glucose, and melanocortin receptor alter AMPK activity in the hypothalamus. Adiponectin has also been shown to increase food intake by activating AMPK in the arcuate hypothalamus. Recent data have shown that acetyl-coenzyme A carboxylase/malonyl-coenzyme A/carnitine palmitoyltransferase-1/fatty acid oxidation and mammalian target of rapamycin signalings are putative downstream pathways for food intake regulation in response to hypothalamic AMPK. Thus, these results suggest that food intake and nutrient metabolism are coordinately regulated by the common signaling pathway of AMPK in the hypothalamus.
Authors:
Yasuhiko Minokoshi; Tetsuya Shiuchi; Suni Lee; Atsushi Suzuki; Shiki Okamoto
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Nutrition (Burbank, Los Angeles County, Calif.)     Volume:  24     ISSN:  0899-9007     ISO Abbreviation:  Nutrition     Publication Date:  2008 Sep 
Date Detail:
Created Date:  2008-08-26     Completed Date:  2009-01-28     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8802712     Medline TA:  Nutrition     Country:  United States    
Other Details:
Languages:  eng     Pagination:  786-90     Citation Subset:  IM    
Affiliation:
Division of Endocrinology and Metabolism, National Institute for Physiological Sciences, Aichi, Japan. minokosh@nips.ac.uk
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MeSH Terms
Descriptor/Qualifier:
Adenylate Kinase / metabolism*
Animals
Body Weight / physiology
Eating / physiology
Energy Metabolism / drug effects,  physiology
Feeding Behavior / drug effects,  physiology*
Hormones / metabolism
Hypothalamus / enzymology*,  metabolism,  physiology*
Leptin / metabolism
Mice
Signal Transduction / physiology
Chemical
Reg. No./Substance:
0/Hormones; 0/Leptin; EC 2.7.4.3/Adenylate Kinase

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


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