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

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-alpha 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.

journal_name

Exp Gerontol

journal_title

Experimental gerontology

authors

Cha HN,Kim YW,Kim JY,Kim YD,Song IH,Min KN,Park SY

doi

10.1016/j.exger.2010.05.004

subject

Has Abstract

pub_date

2010-09-01 00:00:00

pages

711-8

issue

9

eissn

0531-5565

issn

1873-6815

pii

S0531-5565(10)00193-2

journal_volume

45

pub_type

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