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Glucose uptake during contraction in isolated skeletal muscles from neuronal nitric oxide synthase μ knockout mice

Citation

Hong, YH and Frugier, T and Zhang, X and Murphy, RM and Lynch, GS and Betik, AC and Rattigan, S and McConell, GK, Glucose uptake during contraction in isolated skeletal muscles from neuronal nitric oxide synthase μ knockout mice, Journal of Applied Physiology, 118, (9) pp. 1113-1121. ISSN 8750-7587 (2015) [Refereed Article]

Copyright Statement

Copyright 2015 the American Physiological Society

DOI: doi:10.1152/japplphysiol.00056.2015

Abstract

Inhibition of nitric oxide synthase (NOS) significantly attenuates the increase in skeletal muscle glucose uptake during contraction/exercise, and a greater attenuation is observed in individuals with Type 2 diabetes compared with healthy individuals. Therefore, NO appears to play an important role in mediating muscle glucose uptake during contraction. In this study, we investigated the involvement of neuronal NOSμ (nNOSμ), the main NOS isoform activated during contraction, on skeletal muscle glucose uptake during ex vivo contraction. Extensor digitorum longus muscles were isolated from nNOSμ−/− and nNOSμ+/+ mice. Muscles were contracted ex vivo in a temperature-controlled (30C) organ bath with or without the presence of the NOS inhibitor NG-monomethyl-L-arginine (L-NMMA) and the NOS substrate L-arginine. Glucose uptake was determined by radioactive tracers. Skeletal muscle glucose uptake increased approximately fourfold during contraction in muscles from both nNOSμ−/− and nNOSμ+/+ mice. L-NMMA significantly attenuated the increase in muscle glucose uptake during contraction in both genotypes. This attenuation was reversed by L-arginine, suggesting that L-NMMA attenuated the increase in muscle glucose uptake during contraction by inhibiting NOS and not via a nonspecific effect of the inhibitor. Low levels of NOS activity (∼4%) were detected in muscles from nNOSμ−/− mice, and there was no evidence of compensation from other NOS isoform or AMP-activated protein kinase which is also involved in mediating muscle glucose uptake during contraction. These results indicate that NO regulates skeletal muscle glucose uptake during ex vivo contraction independently of nNOSμ.

Item Details

Item Type:Refereed Article
Research Division:Medical and Health Sciences
Research Group:Clinical Sciences
Research Field:Endocrinology
Objective Division:Health
Objective Group:Clinical Health (Organs, Diseases and Abnormal Conditions)
Objective Field:Diabetes
Author:Rattigan, S (Professor Stephen Rattigan)
ID Code:100898
Year Published:2015
Web of Science® Times Cited:5
Deposited By:Menzies Institute for Medical Research
Deposited On:2015-06-03
Last Modified:2016-02-17
Downloads:0

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