Glycogen repletion in different skeletal muscles from diabetic rats.
It was hypothesized that chronically untreated streptozotocin-diabetic rats may compensate for the detrimental effect of insulin deficiency on glycogen restoration following muscular work. Glycogen concentration ([GLY]) was reduced by in situ stimulation of the sciatic nerve of anesthetized normal (N) and diabetic (D) Sprague-Dawley albino rats. Glycogen repletion occurred most rapidly within 30 min after stimulation. By 2 h all N muscles returned to basal [GLY]. D muscles repleted glycogen at a rate 45-75% of normal and not all of the D muscle returned to basal [GLY] by 8 h poststimulation. Neither the partial reduction in diabetic hyperglycemia by using phlorizin nor the acute further lowering of diabetic hypoinsulinemia by using insulin antibody affected glycogen restoration in D muscles. Acute insulin replenishment resulted in restoration of normal [GLY] in D muscles within 2 h poststimulation. These findings are not consistent with the proposed hypothesis and indicate insulin is necessary to have normal rates of glycogen restoration following muscular activity.
D000818:Animals; D000906:Antibodies / Q000276:immunology; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D006003:Glycogen / Q000378:metabolism*; D007328:Insulin / Q000097:blood / Q000276:immunology / Q000494:pharmacology; D008297:Male; D009132:Muscles / Q000378:metabolism*; D010695:Phlorhizin / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013311:Streptozocin; D013997:Time Factors
D000906:Antibodies; D007328:Insulin; D013311:Streptozocin; D006003:Glycogen; D010695:Phlorhizin