Lack of inducible nitric oxide synthase does not prevent aging-associated insulin resistance

Title
Lack of inducible nitric oxide synthase does not prevent aging-associated insulin resistance
Author(s)
박소영차혜나김용운김종연김용대송인환김기남[김기남]
Keywords
NECROSIS-FACTOR-ALPHA; IN-VIVO; GLUCOSE-TOLERANCE; SKELETAL-MUSCLE; WISTAR RATS; OBESE MICE; TNF-ALPHA; FAT; EXPRESSION; LIVER
Issue Date
201009
Publisher
PERGAMON-ELSEVIER SCIENCE LTD
Citation
EXPERIMENTAL GERONTOLOGY, v.45, no.9, pp.711 - 718
Abstract
Inducible nitric oxide synthase (iNOS) is involved in obesity-induced insulin resistance. Since aging is accompanied by increased iNOS expression, the effect of iNOS gene deletion on aging-associated insulin resistance was investigated in 7-month-old (adult) and 22-month-old (old) iNOS knockout and wild-type mice using the hyperinsulinemic-euglycemic clamp. While body weight and fat mass were increased, muscle mass was reduced with aging in wild-type mice. However, body composition was not changed with aging in iNOS knockout mice due to increased locomotor activity. NO metabolites in plasma, and protein levels of iNOS and nitrotyrosine in skeletal muscle increased with aging in wild-type mice. Deletion of iNOS gene attenuated NO metabolites and nitrotyrosine with aging in iNOS knockout mice. Glucose uptake in whole body and skeletal muscle was reduced with aging in both wild-type and iNOS knockout mice and there was no difference between two groups. Plasma level of tumor necrosis factor-et and gene expression of proinflammatory cytokines in peripheral tissues were increased with aging in both groups, and that was more heightened in iNOS knockout mice. These results suggest that lack of iNOS does not prevent aging-associated insulin resistance in mice and heightened production of proinflammatory cytokines may be involved. (C) 2010 Elsevier Inc. All rights reserved.
URI
http://hdl.handle.net/YU.REPOSITORY/23705http://dx.doi.org/10.1016/j.exger.2010.05.004
ISSN
0531-5565
Appears in Collections:
의과대학 > 생리학교실 > Articles
의과대학 > 이비인후과학교실 > Articles
의과대학 > 해부학교실 > Articles
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