Document Detail


NOS2 deficiency increases intestinal metabolism both in nonstimulated and endotoxemic mice.
MedLine Citation:
PMID:  14656712     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Animal studies have suggested that nitric oxide (NO) synthases (NOS) play a role in the regulation of protein metabolism in endotoxemia. We therefore investigated the role of inducible NOS (NOS2) on intestinal protein and neuronal NOS (NOS1) and endothelial NOS (NOS3) on amino acid metabolism. Three groups of mice were studied: 1) wild-type (WT), 2) NOS2 knockout (NOS2-KO), and 3) NOS2-KO + N(omega)-nitro-l-arginine methyl ester (NOS2-KO + l-NAME), both in nonstimulated and LPS-treated conditions. By infusion of the stable isotopes l-[phenyl-(2)H(5)]Phe, l-[phenyl-(2)H(2)]Tyr, l-[guanidino-(15)N(2)]Arg, and l-[ureido-(13)C; (2)H(2)]citrulline (Cit), intestinal protein, amino acid, and Arg/NO metabolism were studied on the whole body level and across intestine. In nonstimulated situations, NOS2 deficiency increased whole body protein turnover and intestinal Gln uptake and Cit production. In NOS2-KO + l-NAME, the above-mentioned changes were reversed. After LPS in WT, whole body NO and Cit production increased. In contrast to this, LPS decreased net intestinal Gln uptake, whole body NO, and Cit production in NOS2-KO mice. Treatment of NOS2-KO + l-NAME with LPS was lethal in eight of eleven mice (73%). The surviving mice in this group showed a major drop in intestinal protein breakdown and synthesis to almost zero. Thus both in baseline conditions and during endotoxemia, the absence of NOS2 upregulated NOS1 and/or NOS3, which increased intestinal metabolism. The drop in intestinal protein metabolism in the endotoxemic NOS2-KO + l-NAME group might play a role in mortality in that group.
Authors:
Yvonne L J Vissers; Marcella M Hallemeesch; Peter B Soeters; Wouter H Lamers; Nicolaas E P Deutz
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2003-12-04
Journal Detail:
Title:  American journal of physiology. Gastrointestinal and liver physiology     Volume:  286     ISSN:  0193-1857     ISO Abbreviation:  Am. J. Physiol. Gastrointest. Liver Physiol.     Publication Date:  2004 May 
Date Detail:
Created Date:  2004-04-07     Completed Date:  2004-05-21     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  100901227     Medline TA:  Am J Physiol Gastrointest Liver Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  G747-51     Citation Subset:  IM    
Affiliation:
Dept. of Surgery, Maastricht Univ., PO Box 616, NL-6200 MD Maastricht, The Netherlands.
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MeSH Terms
Descriptor/Qualifier:
Animals
Citrulline / metabolism
Endotoxemia / metabolism*
Enzyme Inhibitors / pharmacology
Glutamine / metabolism
Intestines / drug effects,  metabolism*
Lipopolysaccharides / pharmacology
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
NG-Nitroarginine Methyl Ester / pharmacology
Nitric Oxide Synthase / deficiency,  physiology*
Nitric Oxide Synthase Type I
Nitric Oxide Synthase Type II
Nitric Oxide Synthase Type III
Proteins / metabolism
Chemical
Reg. No./Substance:
0/Enzyme Inhibitors; 0/Lipopolysaccharides; 0/Proteins; 372-75-8/Citrulline; 50903-99-6/NG-Nitroarginine Methyl Ester; 56-85-9/Glutamine; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.13.39/Nitric Oxide Synthase Type I; EC 1.14.13.39/Nitric Oxide Synthase Type II; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.14.13.39/Nos1 protein, mouse; EC 1.14.13.39/Nos2 protein, mouse; EC 1.14.13.39/Nos3 protein, mouse

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