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NOS2 deficiency increases intestinal metabolism both in nonstimulated and endotoxemic mice.
Am J Physiol Gastrointest Liver Physiol. 2004 May; 286(5):G747-51.AJ

Abstract

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+Show Affiliations

Dept. of Surgery, Maastricht Univ., PO Box 616, NL-6200 MD Maastricht, The Netherlands.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

14656712

Citation

Vissers, Yvonne L J., et al. "NOS2 Deficiency Increases Intestinal Metabolism Both in Nonstimulated and Endotoxemic Mice." American Journal of Physiology. Gastrointestinal and Liver Physiology, vol. 286, no. 5, 2004, pp. G747-51.
Vissers YL, Hallemeesch MM, Soeters PB, et al. NOS2 deficiency increases intestinal metabolism both in nonstimulated and endotoxemic mice. Am J Physiol Gastrointest Liver Physiol. 2004;286(5):G747-51.
Vissers, Y. L., Hallemeesch, M. M., Soeters, P. B., Lamers, W. H., & Deutz, N. E. (2004). NOS2 deficiency increases intestinal metabolism both in nonstimulated and endotoxemic mice. American Journal of Physiology. Gastrointestinal and Liver Physiology, 286(5), G747-51.
Vissers YL, et al. NOS2 Deficiency Increases Intestinal Metabolism Both in Nonstimulated and Endotoxemic Mice. Am J Physiol Gastrointest Liver Physiol. 2004;286(5):G747-51. PubMed PMID: 14656712.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - NOS2 deficiency increases intestinal metabolism both in nonstimulated and endotoxemic mice. AU - Vissers,Yvonne L J, AU - Hallemeesch,Marcella M, AU - Soeters,Peter B, AU - Lamers,Wouter H, AU - Deutz,Nicolaas E P, Y1 - 2003/12/04/ PY - 2003/12/6/pubmed PY - 2004/5/22/medline PY - 2003/12/6/entrez SP - G747 EP - 51 JF - American journal of physiology. Gastrointestinal and liver physiology JO - Am J Physiol Gastrointest Liver Physiol VL - 286 IS - 5 N2 - 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. SN - 0193-1857 UR - https://www.unboundmedicine.com/medline/citation/14656712/NOS2_deficiency_increases_intestinal_metabolism_both_in_nonstimulated_and_endotoxemic_mice_ DB - PRIME DP - Unbound Medicine ER -