Abstract
The effects of insulin and thyroid hormone treatments on cardiac sarcoplasmic reticular function were investigated in chronic streptozotocin-induced diabetes in rats. ATP-dependent Ca super(2+) transport and Ca super(2+)-stimulated ATPase activities were depressed in microsomal samples from diabetic rats in comparison with control. The results provide evidence that the depression in cardiac sarcoplasmic reticular calcium accumulation during diabetes is a consequence of insulin deficiency and associated chronic metabolic changes but the hypothyroid condition that accompanies experimental diabetes dose not appear to play any role in this defect.