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GYS1  -  glycogen synthase 1 (muscle)

Macaca mulatta

Synonyms: GYS, GYS2
 
 
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Disease relevance of GYS

 

High impact information on GYS

 

Chemical compound and disease context of GYS

  • We conclude that NIDDM is accompanied by low glycogen content in the muscle, and that some clinically normal monkeys have an alteration in insulin action on muscle GS, GP, and whole-body glucose disposal rates that may precede the development of hyperinsulinemia [5].
 

Biological context of GYS

  • Neither GS protein expression nor GS gene expression was affected by insulin or by K-111 treatment [6].
  • Reduced insulin action on skeletal muscle glycogen synthase activity and reduced whole-body insulin-mediated glucose disposal rates in insulin-resistant subjects may be associated with an alteration in muscle glucose transport (or phosphorylation) or with a defect distal to glucose 6-phosphate [2].
  • To determine the effects of insulin on glycogenolysis in rhesus monkeys, GP and glycogen were determined in muscle samples obtained under basal fasting and insulin-stimulated conditions during a euglycemic hyperinsulinemic clamp in a group of 27 monkeys ranging from normal to overtly diabetic (NIDDM) and compared to GS activity previously examined [5].
 

Anatomical context of GYS

 

Associations of GYS with chemical compounds

  • We conclude that under euglycaemic/hyperinsulinaemic conditions, a defect distal to glucose 6-phosphate is a major contributor to reduced whole-body insulin-mediated glucose disposal rates and to reduced insulin action on glycogen synthase in insulin-resistant and diabetic monkeys [2].
  • The regulation of glycogen synthase (GS) and glycogen phosphorylase (GP) activity by phosphorylation/ dephosphorylation has been proposed to be via changes in activities of several different protein (serine/threonine) phosphatases and kinases, including protein phosphatase (PP) 1/2A, PP2C, and cAMP-dependent protein kinase (PKA) [4].
  • The administration of a single oral dose of DDT (150 mg/kg body wt.) to rhesus monkey elevated the hepatic glycogen and glycogen synthase activity but depressed the glycogen phosphorylase activity [7].
  • A thiazolidinedione improves in vivo insulin action on skeletal muscle glycogen synthase in insulin-resistant monkeys [8].
  • Insulin increased the activities of liver glycogen synthase (P < 0.05) and decreased the activities of liver glycogen phosphorylase (P 0.001) [9].
 

Analytical, diagnostic and therapeutic context of GYS

  • GS and glycogen were present in all fractions obtained by differential centrifugation, except for the cytosolic fraction, under both basal and insulin-stimulated conditions [6].
  • We conclude that insulin during a euglycemic clamp activates liver GS while inhibiting liver GP and that insulin action on liver GS is positively related to whole body insulin-mediated glucose disposal rates in lean young adult rhesus monkeys [10].

References

  1. Adipose tissue glycogen synthase activation by in vivo insulin in spontaneously insulin-resistant and type 2 (non-insulin-dependent) diabetic rhesus monkeys. Ortmeyer, H.K., Bodkin, N.L., Hansen, B.C. Diabetologia (1993) [Pubmed]
  2. Relationship of skeletal muscle glucose 6-phosphate to glucose disposal rate and glycogen synthase activity in insulin-resistant and non-insulin-dependent diabetic rhesus monkeys. Ortmeyer, H.K., Bodkin, N.L., Hansen, B.C. Diabetologia (1994) [Pubmed]
  3. In vivo insulin regulation of skeletal muscle glycogen synthase in calorie-restricted and in ad libitum-fed rhesus monkeys. Ortmeyer, H.K. J. Nutr. (2001) [Pubmed]
  4. Relationship of glycogen synthase and glycogen phosphorylase to protein phosphatase 2C and cAMP-dependent protein kinase in liver of obese rhesus monkeys. Ortmeyer, H.K. Obes. Res. (1997) [Pubmed]
  5. Glycogen phosphorylase activity and glycogen concentration in muscle of normal to overtly diabetic rhesus monkeys. Ortmeyer, H.K., Bodkin, N.L., Varghese, S.S., Hansen, B.C. Int. J. Obes. Relat. Metab. Disord. (1996) [Pubmed]
  6. Skeletal muscle glycogen synthase subcellular localization: effects of insulin and PPAR-alpha agonist (K-111) administration in rhesus monkeys. Ortmeyer, H.K., Adall, Y., Marciani, K.R., Katsiaras, A., Ryan, A.S., Bodkin, N.L., Hansen, B.C. Am. J. Physiol. Regul. Integr. Comp. Physiol. (2005) [Pubmed]
  7. Acute exposure of rhesus monkeys to DDT: effect on carbohydrate metabolism. Dudeja, P.K., Sanyal, S.N., Agarwal, N., Rao, T.N., Subrahmanyam, D., Khuller, G.K. Chem. Biol. Interact. (1980) [Pubmed]
  8. A thiazolidinedione improves in vivo insulin action on skeletal muscle glycogen synthase in insulin-resistant monkeys. Ortmeyer, H.K., Bodkin, N.L., Haney, J., Yoshioka, S., Horikoshi, H., Hansen, B.C. Int. J. Exp. Diabetes Res. (2000) [Pubmed]
  9. Lack of defect in insulin action on hepatic glycogen synthase and phosphorylase in insulin-resistant monkeys. Ortmeyer, H.K., Bodkin, N.L. Am. J. Physiol. (1998) [Pubmed]
  10. Insulin regulates liver glycogen synthase and glycogen phosphorylase activity reciprocally in rhesus monkeys. Ortmeyer, H.K., Bodkin, N.L., Hansen, B.C. Am. J. Physiol. (1997) [Pubmed]
 
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