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Publication : Skeletal muscle glucose uptake during treadmill exercise in neuronal nitric oxide synthase-μ knockout mice.

First Author  Hong YH Year  2016
Journal  Am J Physiol Endocrinol Metab Volume  310
Issue  10 Pages  E838-45
PubMed ID  27006199 Mgi Jnum  J:237085
Mgi Id  MGI:5810850 Doi  10.1152/ajpendo.00513.2015
Citation  Hong YH, et al. (2016) Skeletal muscle glucose uptake during treadmill exercise in neuronal nitric oxide synthase-mu knockout mice. Am J Physiol Endocrinol Metab 310(10):E838-45
abstractText  Nitric oxide influences intramuscular signaling that affects skeletal muscle glucose uptake during exercise. The role of the main NO-producing enzyme isoform activated during skeletal muscle contraction, neuronal nitric oxide synthase-mu (nNOSmu), in modulating glucose uptake has not been investigated in a physiological exercise model. In this study, conscious and unrestrained chronically catheterized nNOSmu(+/+) and nNOSmu(-/-) mice either remained at rest or ran on a treadmill at 17 m/min for 30 min. Both groups of mice demonstrated similar exercise capacity during a maximal exercise test to exhaustion (17.7 +/- 0.6 vs. 15.9 +/- 0.9 min for nNOSmu(+/+) and nNOSmu(-/-), respectively, P > 0.05). Resting and exercise blood glucose levels were comparable between the genotypes. Very low levels of NOS activity were detected in skeletal muscle from nNOSmu(-/-) mice, and exercise increased NOS activity only in nNOSmu(+/+) mice (4.4 +/- 0.3 to 5.2 +/- 0.4 pmol.mg(-1).min(-1), P < 0.05). Exercise significantly increased glucose uptake in gastrocnemius muscle (5- to 7-fold) and, surprisingly, more so in nNOSmu(-/-) than in nNOSmu(+/+) mice (P < 0.05). This is in parallel with a greater increase in AMPK phosphorylation during exercise in nNOSmu(-/-) mice. In conclusion, nNOSmu is not essential for skeletal muscle glucose uptake during exercise, and the higher skeletal muscle glucose uptake during exercise in nNOSmu(-/-) mice may be due to compensatory increases in AMPK activation.
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