Control mechanisms in the acceleration of hepatic glycogen degradation during hypoxia.
Hepatic glycogen metabolism in aerobic and hypoxic conditions has been assessed with respect to glycogenolysis, phosphorylase alpha activity and nucleotide content. Insulin did not inhibit glycogen breakdown nor stimulate lipogenesis in the aerobic perfused liver. Partial ischaemia induced glycogen breakdown, release of glucose and changes in nucleotide content in the perfused liver. Phosphorylase alpha content increased within 2 min in response to total ischaemia, in vivo and in the perfused liver. This change was paralleled by an increase in hepatic AMP. Glycogen synthase alpha activity decreased, as did the hepatic content of both cyclic AMP and cyclic GMP.
D000227:Adenine Nucleotides / Q000378:metabolism; D000332:Aerobiosis / Q000187:drug effects; D000818:Animals; D050260:Carbohydrate Metabolism; D000242:Cyclic AMP / Q000378:metabolism; D006152:Cyclic GMP / Q000378:metabolism; D006006:Glycogen Synthase / Q000378:metabolism; D000860:Hypoxia / Q000378:metabolism*; D066298:In Vitro Techniques; D007511:Ischemia / Q000378:metabolism; D008112:Liver Glycogen / Q000502:physiology*; D008297:Male; D010762:Phosphorylase a / Q000378:metabolism; D051381:Rats
D000227:Adenine Nucleotides; D008112:Liver Glycogen; D000242:Cyclic AMP; D010762:Phosphorylase a; D006006:Glycogen Synthase; D006152:Cyclic GMP