Regulation of glucose uptake by muscle. 8. Effects of fatty acids, ketone bodies and pyruvate, and of alloxan-diabetes and starvation, on the uptake and metabolic fate of glucose in rat heart and diaphragm muscles

Abstract

In alloxan-diabetes in the rat the uptake of glucose by heart and diaphragm muscle in vitro is impaired both in the absence and in the presence of insulin. The defect in glucose uptake in the absence of the hormone has been explained by the low rate of membrane transport of glucose in the insulin- deficient tissue (insulin accelerates the membrane transport of glucose); the defect in the membrane transport of glucose may be corrected by the addition of high concentrations of insulin in vitro but not by hypophysectomy or adrenalectomy (see Morgan, Cadenas, Regen & Park, 1961 b; Morgan, Regen, Henderson, Sawyer & Park, 1961 c; Kipnis, 1959). Two other defects cannot be ex- plained in this way: first, an impaired ability of low concentrations of insulin to stimulate membrane transport of glucose; and, secondly, a decreased rate of phosphorylation of glucose. These defects are corrected by hypophysectomy or adrenalectomy or by treatment of the diabetic rat -with insulin (Morgan et al. 1961b, c; Park et al. 1961; Kipnis, 1959; Riddick, Reisler & Kipnis, 1962); they can be restored in muscles of hypo--physectomized diabetic rats by treatment, of the animals with growth hormone and corticosteroids. The development of these defects in glucose meta- bolism in muscle in diabetes is thus favoured by a deficiency of circulating insulin together with a sufficiency of growth hormone and corticosteroids.