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3 "Glycogen synthase"
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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
Korean Diabetes J. 2000;24(3):331-339.   Published online January 1, 2001
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BACKGROUND
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.
Effect of Troglitazone on Glycogen synthase Activity in Human skeletal Muscle Culture from Obese Non-Diabetic and Obese Non-insulin Dependent Diabetes Mellitus.
Leslie Abrams Carter, Theodore Ciaraldi, Robert R Henry, Kyong Soo Park, Hong Kyu Lee
Korean Diabetes J. 1997;21(3):254-261.   Published online January 1, 2001
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BACKGROUND
Skeletal muscle is the principal tissue of insulin resistance in obese and non-insulin dependent diabetic(NIDDM) subjects. Troglitazone, a member of thiazolidinedione class of compounds, has been shown to improve glucose tolerance in insulin resistant state. At the cellular level, troglitazone has been shown to improve insulin action in skeletal muscle, liver and adipose tissue. However, there has been no direct assessment of mechanism of this drug in insulin resistant human skeletal muscle from obese and obese NIDDM subjects. METHODS: To determine the effect of troglitzone on skeletal muscle glycogen synthase(GS) activity in insulin resistant human skeletal muscle, muscle cultures from 7 obese non-diabetic and 8 obese NIDDM subjects were grown for 4 weeks and then fused for 4 days either with or without troglitzone(0~5ug/mL) and harvested for GS activity and protein measurement. GS activity was measured by enzymatic method and protein expression was measured by Western blot using polyclonal antibody specific for C-terminal end of GS protein, RESULTS: Troglitzone increased GS activity(GS activity at 0.1 mM G6P and fractional velocity) dose-dependently in both obese non-diabetic and type II diabetes and the increased GS activity by troglitzone was mostly basal rather than insulin-stimulated. Basal fractional velocity of GS increased 2.8+/-0.7 and 3.7 +/-1.2 fold in obese non-diabetic and type II diabetes respectively. There was no changes in GS total activity and GS protein expression in either group with troglitzone treatment.. CONCLUSION: Troglitazone has effects to improve glycogen synthase activity in skeletal tnuscle of obese and obese NIDDM subjects.
Mechanism of Insulin Resistance : Time Dependence of the Development of Insulin Resistance in High Fat Fed Rats.
Kyong Soo Park, Ki Up Lee, Sung Woo Park, Hong Kyu Lee, Hun Ki Min
Korean Diabetes J. 1997;21(2):168-175.   Published online January 1, 2001
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BACKGROUND
Increased FFA availability is known to induce insulin resistance by decrease in peripheral glucose utilization and increase in hepatic glucose procluction. However, there are conflicting results about the time dependence of the developrnent of insulin resistance with increased availability of FFA. METHODS: To elucidate the time dependence of the development of insulin resistance associated with increased availability of FFA, peripheral glucose utilization rate and hepatic glucose production rate were measured by euglycemic hyperinsulinemic clamp with 3-3H glucose infusion in rats fed high fat diet (1 week or 3 weeks) or control diet(ordinary chow diet). RESULTS: Basal plasrna FFA levels and steady state plasma insulin levels increased after high fat diet. After 1 week of high fat diet, suppressibility of hepatic glucose production rate by insulin was impaired(p<0.05 vs control). Insulin sensitivity index(glucose utilization rates/steady state plasma insulin concentrmtions X100) was decreased only after 3 weeks of high fat diet(p<0.05 vs control) which was accompanied by decreased glycogen synthase activity. CONCLUSION: High fat diet induces hepatic insulin resistance before peripheral insulin resistance and decreased glycogen synthase activity may contribute to the development of peripheral insulin resistance in rats fed high fat diet.

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