Document Detail


Detection of extracellular glucose by GLUT2 contributes to hypothalamic control of food intake.
MedLine Citation:
PMID:  20179244     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The sugar transporter GLUT2, present in several tissues of the gut-brain axis, has been reported to be involved in the control of food intake. GLUT2 is a sugar transporter sustaining energy production in the cell, but it can also function as a receptor for extracellular glucose. A glucose-signaling pathway is indeed triggered, independently of glucose metabolism, through its large cytoplasmic loop domain. However, the contribution of the receptor function over the transporter function of GLUT2 in the control of food intake remains to be determined. Thus, we generated transgenic mice that express a GLUT2-loop domain, blocking the detection of glucose but leaving GLUT2-dependent glucose transport unaffected. Inhibiting GLUT2-mediated glucose detection augmented daily food intake by a mechanism that increased the meal size but not the number of meals. Peripheral hormones (ghrelin, insulin, leptin) were unaffected, leading to a focus on central aspects of feeding behavior. We found defects in c-Fos activation by glucose in the arcuate nucleus and changes in the amounts of TRH and orexin neuropeptide mRNA, which are relevant to poorly controlled meal size. Our data provide evidence that glucose detection by GLUT2 contributes to the control of food intake by the hypothalamus. The sugar transporter receptor, i.e., "transceptor" GLUT2, may constitute a drug target to treat eating disorders and associated metabolic diseases, particularly by modulating its receptor function without affecting vital sugar provision by its transporter function.
Authors:
Emilie Stolarczyk; Christophe Guissard; Aur?lien Michau; Patrick C Even; Alexandra Grosfeld; Patricia Serradas; Anne Lorsignol; Luc P?nicaud; Edith Brot-Laroche; Armelle Leturque; Maude Le Gall
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-02-23
Journal Detail:
Title:  American journal of physiology. Endocrinology and metabolism     Volume:  298     ISSN:  1522-1555     ISO Abbreviation:  Am. J. Physiol. Endocrinol. Metab.     Publication Date:  2010 May 
Date Detail:
Created Date:  2010-04-14     Completed Date:  2010-05-03     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100901226     Medline TA:  Am J Physiol Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  E1078-87     Citation Subset:  IM    
Affiliation:
Unit? Mixte de Recherche (UMR) S872, Centre de Recherche des Cordeliers, 15 rue de l'Ecole de m?decine, Paris, F-75006 France.
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MeSH Terms
Descriptor/Qualifier:
Analysis of Variance
Animals
Biological Transport / physiology
Body Weight / physiology
Cell Count
Eating / physiology*
Energy Metabolism
Feeding Behavior / physiology
Ghrelin / blood
Glucose / metabolism*
Glucose Transporter Type 2 / genetics,  metabolism*
Homeostasis / physiology
Hypothalamus / metabolism*
Immunohistochemistry
Insulin / blood
Intracellular Signaling Peptides and Proteins / genetics,  metabolism
Leptin / blood
Mice
Mice, Transgenic
Neuropeptides / genetics,  metabolism
Proto-Oncogene Proteins c-fos / metabolism
RNA, Messenger / genetics,  metabolism
Reverse Transcriptase Polymerase Chain Reaction
Signal Transduction / physiology
Statistics, Nonparametric
Thyrotropin-Releasing Hormone / genetics,  metabolism
Chemical
Reg. No./Substance:
0/Ghrelin; 0/Glucose Transporter Type 2; 0/Intracellular Signaling Peptides and Proteins; 0/Leptin; 0/Neuropeptides; 0/Proto-Oncogene Proteins c-fos; 0/RNA, Messenger; 0/orexins; 11061-68-0/Insulin; 24305-27-9/Thyrotropin-Releasing Hormone; 50-99-7/Glucose

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


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