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Jejunum inflammation in obese and diabetic mice impairs enteric glucose detection and modifies nitric oxide release in the hypothalamus.
MedLine Citation:
PMID:  20879900     Owner:  NLM     Status:  In-Process    
Abstract/OtherAbstract:
Intestinal detection of nutrients is a crucial step to inform the whole body of the nutritional status. In this paradigm, peripheral information generated by nutrients is transferred to the brain, which in turn controls physiological functions, including glucose metabolism. Here, we investigated the effect of enteric glucose sensors stimulation on hypothalamic nitric oxide (NO) release in lean or in obese/diabetic (db/db) mice. By using specific NO amperometric probes implanted directly in the hypothalamus of mice, we demonstrated that NO release is stimulated in response to enteric glucose sensors activation in lean but not in db/db mice. Alteration of gut to hypothalamic NO signaling in db/db mice is associated with a drastic increase in inflammatory, oxidative/nitric oxide (iNOS, IL-1β), and endoplasmic reticulum stress (CHOP, ATF4) genes expression in the jejunum. Although we could not exclude the importance of the hypothalamic inflammatory state in obese and diabetic mice, our results provide compelling evidence that enteric glucose sensors could be considered as potential targets for metabolic diseases.
Authors:
Thibaut Duparc; Damien Naslain; André Colom; Giulio G Muccioli; Nicolas Massaly; Nathalie M Delzenne; Philippe Valet; Patrice D Cani; Claude Knauf
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-09-29
Journal Detail:
Title:  Antioxidants & redox signaling     Volume:  14     ISSN:  1557-7716     ISO Abbreviation:  Antioxid. Redox Signal.     Publication Date:  2011 Feb 
Date Detail:
Created Date:  2011-01-05     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100888899     Medline TA:  Antioxid Redox Signal     Country:  United States    
Other Details:
Languages:  eng     Pagination:  415-23     Citation Subset:  IM    
Affiliation:
Institut National de la Santé et de la Recherche Médicale (INSERM), Toulouse, France.
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