Cited by 4Metabolism, Diabetes, and CancerAdipose Tissue and MetabolismNitric Oxide and Endothelin Effects

Nitric oxide increases Insulin sensitivity in skeletal muscle by improving mitochondrial function and insulin signaling

Open access
Lee, Woo Je, Kim, Hyoun Sik, Park, Hye-Sun, Kim, Mi-Ok, Kim, Mina, Yun, Ji-Young, Kim, Eun Hee, Lee, Sang Ah +4 more·2009·Korean Diabetes Journal

Abstract

Background: Accumulating evidence has suggested that nitric oxide (NO) is involved in the regulation of insulin sensitivity in skeletal muscle.Recent studies also suggested NO as an important molecule regulating mitochondrial biogenesis.This study examined the effect of the NO donor, 3-morpholinosydnonimine (SIN-1), on glucose metabolism in skeletal muscle and tested the hypothesis that NO's effect on glucose metabolism is mediated by its effect on mitochondrial function. Methods:In Sprague-Dawley (SD) rats treated with SIN-1 for 4 weeks, insulin sensitivity was measured by a glucose clamp study.Triglyceride content and fatty acid oxidation were measured in the skeletal muscle.In addition, mitochondrial DNA content and mRNA expression of mitochondrial biogenesis markers were assessed by real-time polymerase chain reaction and expression of insulin receptor substrate (IRS)-1 and Akt were examined by Western blot analysis in skeletal muscle.In C2C12 cells, insulin sensitivity was measured by 2-deoxyglucose uptake and Western blot analysis was used to examine the expression of IRS-1 and Akt. Results: SIN-1 improved insulin sensitivity in C2C12 cells and skeletal muscles of SD rats.In addition, SIN-1 decreased triglyceride content and increased fatty acid oxidation in skeletal muscle.Mitochondrial DNA contents and biogenesis in the skeletal muscle were increased by SIN-1 treatment.Moreover, SIN-1 increased the expression of phosphor-IRS-1 and phosphor-Akt in the skeletal muscle and muscle cells.Conclusion: Our results suggest that NO mediates glucose uptake in skeletal muscle both in vitro and in vivo by improving mitochondrial function and stimulating insulin signaling pathways.(Korean Diabetes J 33:198-205, 2009

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Crossref · 10.4093/kdj.2009.33.3.198

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  • Insulin resistance is improved by NO at various levels including insulin secretion, mitochondrial function, modulation of inflammation, insulin signaling, and glucose uptake.

    “Insulin resistance is improved by NO at various levels including insulin secretion [54,55], mitochondrial function [56], modulation of inflammation [57], insulin signaling [58] and glucose uptake [59].”

    From NO-Rich Diet for Lifestyle-Related Diseases (2015) · cites this paper as [56]

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Authors
Lee, W. J., Kim, H. S., Park, H.-S., Kim, M.-O., Kim, M., Yun, J.-Y., Kim, E. H., Lee, S. A., Lee, S. H., Koh, E. H., Park, J.-Y., & Lee, K.-U.
Affiliations
University of Ulsan (KR)
Venue
Korean Diabetes Journal
Published
2009
Volume
33
Issue
3
Pages
198
ISSN
1976-9180 (ISSN-L)
OpenAlex
W2118831075
Cited by
4
References
27
Citations by year
2022: 1 · 2015: 2
FWCI
0.13
Type
journal article
Language
en
Open access
Locations
Korean Diabetes Journal (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
Keywords
nitric oxide, insulin sensitivity, skeletal muscle, mitochondrial function, mitochondrial biogenesis, SIN-1, glucose metabolism, glucose uptake, insulin signaling, IRS-1, Akt, fatty acid oxidation, triglyceride content, mitochondrial DNA

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