Regulation of hepatic glycogen metabolism: effects of diabetes, insulin infusion, and pancreatic islet transplantation.
Insulin-deficient diabetes mellitus results in diminished capacity of the liver to accumulate glycogen. One site of metabolic lesion in the diabetic liver is at the level of the synthase-activating enzyme, synthase phosphatase. This activity is progressively diminished with increasing severity of chemically induced diabetes in both soluble and smooth endoplasmic reticulum (SER) associated subfractions. Insulin administration via an implanted miniosmotic pump or via intrahepatic islet transplantation increased synthase phosphatase activity, particularly in SER. Hepatic glycogen synthesis and accumulation was enhanced as well. The data support a role for insulin in maintenance of the ability of the liver to synthesize and accumulate glycogen mediated either directly or indirectly through SER-synthase phosphatase activity.
D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism* / Q000628:therapy; D003922:Diabetes Mellitus, Type 1 / Q000378:metabolism* / Q000628:therapy; D004721:Endoplasmic Reticulum / Q000201:enzymology; D006006:Glycogen Synthase / Q000378:metabolism; D006007:Glycogen-Synthase-D Phosphatase / Q000378:metabolism; D007328:Insulin / Q000627:therapeutic use*; D007332:Insulin Infusion Systems; D016381:Islets of Langerhans Transplantation; D008099:Liver / Q000201:enzymology; D008112:Liver Glycogen / Q000378:metabolism*; D008297:Male; D006005:Phosphorylases / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains
D007328:Insulin; D008112:Liver Glycogen; D006005:Phosphorylases; D006006:Glycogen Synthase; D006007:Glycogen-Synthase-D Phosphatase