Diabetes & Metabolism Journal

Original Articles

Nitric Oxide Increases Insulin Sensitivity in Skeletal Muscle by Improving Mitochondrial Function and Insulin Signaling.: Woo Je Lee, Hyoun Sik Kim, Hye Sun Park, Mi Ok Kim, Mina Kim, Ji Young Yun, Eun Hee Kim, Sang Ah Lee, Seung Hun Lee, Eun Hee Koh, Joong Yeol Park, Ki Up Lee; Korean Diabetes J. 2009;33(3):198-205. Published online June 1, 2009; DOI: https://doi.org/10.4093/kdj.2009.33.3.198

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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.

Citations

Citations to this article as recorded by

NO-Rich Diet for Lifestyle-Related Diseases
Jun Kobayashi, Kazuo Ohtake, Hiroyuki Uchida
Nutrients.2015; 7(6): 4911. CrossRef
Metformin Activates AMP Kinase through Inhibition of AMP Deaminase
Jiangyong Ouyang, Rahulkumar A. Parakhia, Raymond S. Ochs
Journal of Biological Chemistry.2011; 286(1): 1. CrossRef

A Study on Insulin action using fibroblast of leprechaunism patients.: Si Whan Koh, Yoo Joung Oh, Mi Koung Chang, Yun Soo Bae, Dong Kyu Jin; Korean Diabetes J. 2006;30(1):39-46. Published online January 1, 2006; DOI: https://doi.org/10.4093/jkda.2006.30.1.39

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Abstract PDF: BACKGROUND
Leprechaunism, which is caused by insulin receptor defect, is clinically characterized by hyperinsulinemia, stunted growth, dysmorphic somatic abnormalities, lipodystrophy and early death around 2-3 years of age. METHODS: In this study we describe 2 cases of Korean leprechaunism patients. In addition, the disturbed insulin induced effects such as glucose uptake, insulin binding assay, thymidine uptake and PDGF stimulated phosphorylation change were investigated using the fibroblasts from 1 Korean patient and those from 4 foreign leprechaunism patients. RESULTS: The morphologic study of fibroblasts derived from patient suggests that the fibroblasts of patient are less differentiated than the fibroblasts of control. Moreover, insulin induced pathways as well as PDGF stimulated phosphorylation change were disturbed in the fibroblasts of the patient. CONCLUSION: Our results suggest that the signal transduction in the fibroblasts of leprechaunism is reduced not only by insulin stimuli but also by other growth factors like PDGF.

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