Skip Navigation
Skip to contents

Diabetes Metab J : Diabetes & Metabolism Journal



Page Path
HOME > Diabetes Metab J > Volume 24(3); 2000 > Article
Original Article Metabolic Phenotype of Glycogen Synthase Gene Inhibition in Human Skeletal Muscle Cells.
Jae Joon Koh, Kyong Soo Park, Jeong Mi Kim, Seong Yeon Kim, Hong Kyu Lee, Theodore P Ciaraldi, Robert R Henry
Diabetes & Metabolism Journal 2000;24(3):331-339
Published online: January 1, 2001
  • 16 Download
  • 0 Crossref
  • 0 Scopus
1Department of Internal Medicine, Seoul National University College of Medicine.
2The Institute of Endocrinology, Nutrition and Metabolism, Seoul National University Medical Research Center.
3Department of Medicine, University of California San Diego.

Glycogen synthase (GS) is the rate-limiting enzyme controlling non-oxidative glucose disposal in skeletal muscle. Reduction in GS activity and impaired insulin responsiveness are characteristic features of skeletal muscle in type 2 diabetes that contribute to glucose intolerance. These properties also exist in human skeletal muscle cell cultures from type 2 diabetic subjects. The aim of study is to determine the effect of an isolated reduction in GS on glucose metabolism and if this change can generate a diabetes-like state. METHODS: Cultured skeletal muscle cells from non-diabetic subjects were treated with antisense oligodeoxynucleotides (ODN) to GS to interfere with expression of the gene for 6 days. GS activity, protein expression, glycogen synthesis and cellular glycogen content were measured. RESULTS: Treatment with antisense ODN reduced GS protein expression by 70% compared to control (scrambled) ODN (p<0.01). Both total GS activity and that measured at 0.1 mM G-6-P were reduced by antisense ODN treatment. Insulin responsiveness of GS was also halved. Basal GS FV0.1 was decreased in both antisense ODN and control ODN treated cells and antisense treated cells did not show increase in GS FV0.1 in response to insulin stimulation. Glucose incorporation into glycogen under basal conditions was unaltered after antisense ODN treatment, though no further stimulation in response to insulin was observed. Yet both cellular glycogen content and glycogen synthesis were lower in antisense ODN treated cells compared to control ODN treated cells. CONCLUSIONS: Reduction in GS expression in human skeletal muscle cell impair GS activity and insulin responsiveness but does not replicate the abnormalities of glycogen synthesis found in cultured diabetic skeletal muscle cells.

  • Cite
    export Copy
    Download Citation
    Download a citation file in RIS format that can be imported by all major citation management software, including EndNote, ProCite, RefWorks, and Reference Manager.

    • RIS — For EndNote, ProCite, RefWorks, and most other reference management software
    • BibTeX — For JabRef, BibDesk, and other BibTeX-specific software
    • Citation for the content below
    Metabolic Phenotype of Glycogen Synthase Gene Inhibition in Human Skeletal Muscle Cells.
    Korean Diabetes J. 2000;24(3):331-339.   Published online January 1, 2001
Related articles
Koh JJ, Park KS, Kim JM, Kim SY, Lee HK, Ciaraldi TP, Henry RR. Metabolic Phenotype of Glycogen Synthase Gene Inhibition in Human Skeletal Muscle Cells.. Diabetes Metab J. 2000;24(3):331-339.

Diabetes Metab J : Diabetes & Metabolism Journal
Close layer