Glycogen metabolism in phosphorus-depleted rats.
Glycogen content as well as the enzymes of glycogenolysis and glycogen synthesis were examined in myocardium, skeletal muscle, liver and kidneys of rats with dietary phosphorus deprivation. Myocardial glycogen content was decreased and this was accompanied by activation of the enzymes of glycogenolysis and inhibition of the enzymes of glycogen synthesis. Beta blockade (nadolol) abolished the effect of phosphorus depletion (PD) on myocardial glycogen metabolism, documenting that the effect of PD is mediated, at least in part, by increased sympathetic activity. Furthermore, administration of insulin caused a marked increase of glycogen content in the heart of both control and phosphorus-depleted (PD) animals. There was no change of glycogen content or the activities of enzymes of glycogen metabolism in skeletal muscle or kidney, but a decrease of glycogen content of the liver was observed in PD animals.
D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D005947:Glucose / Q000494:pharmacology; D006003:Glycogen / Q000378:metabolism*; D006006:Glycogen Synthase / Q000378:metabolism; D007328:Insulin / Q000494:pharmacology; D008099:Liver / Q000378:metabolism; D008297:Male; D009132:Muscles / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D009248:Nadolol; D010758:Phosphorus / Q000172:deficiency*; D010762:Phosphorylase a / Q000378:metabolism; D010763:Phosphorylase b / Q000378:metabolism; D011412:Propanolamines / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains
D000319:Adrenergic beta-Antagonists; D007328:Insulin; D011412:Propanolamines; D010758:Phosphorus; D009248:Nadolol; D006003:Glycogen; D010762:Phosphorylase a; D010763:Phosphorylase b; D006006:Glycogen Synthase; D005947:Glucose