Effect of Insulin on Carbohydrate Metabolism and on Potassium in the Forearm of Man*

Abstract

We have described a technique for quantifying skeletal muscle metabolism in man in. situ by measing blood flow through the forearm and appropriate arteriovenous differences in concentration of selected metabolites ( 1 ). The technique lends itself to analysis of local effects of hormones and other possibly potent agents. The agent can be injected into the brachial artery at constant rate with the solution of Evans blue dye used to measure blood flow. The quantity of the agent injected can be sufficiently large to exert a measurable effect in the forearm but sufficiently small so that, upon approximately 100-fold dilution when forearm venous effluent mixes with blood in the heart and great vessels, there is no measurable systemic effect. There are, therefore, no detectable systemic counter-regulatory processes set in motion by the agent to complicate the primary response of the forearm to the agent itself.It is the purpose of this report to describe the effects on forearm muscle metabolism of insulin administered in this fashion. We sought information concerning the following two problems. 1) Only a minor fraction of oxygen consumed by forearm muscle at rest can be accounted for by dissimilation of glucose abstracted from arterial blood (1). Is this because resting muscle is so poorly permeable to glucose? If glucose uptake is increased, say by exhibition of insulin, is oxidation of glucose enhanced necessarily?2) Do the temporal and molar relations between glucose uptake and potassium uptake by muscle in response to insulin suggest that insulin-induced * These studies were aided by Contract Nonr-248 (34) potassium movement is or is not secondary to the effect of insulin on glucose? METHODS Net uptake (or output) of a metabolite by forearm tissues was calculated by the equation 0 = F(A-V), where 0 is uptake (or output) of the metabolite in units of mass per minute per 100 ml of forearm, F is blood (or plasma) flow through the forearm in units of ml per minute per 100 ml of forearm, and A and V are concentrations of the metabolite in arterial and in venous blood (or plasma), respectively, in units of mass per milliliter. The technique was as described previously (1). Briefly, a double-lumen needle was inserted into the brachial artery. A polyethylene catheter was threaded into an antecubital vein and passed distally and deeply so that it sampled blood draining muscle but also, undoubtedly, adipose tissue interspersed among muscle. A second catheter was threaded into a more superficial vein, sampling mainly from skin and subcutaneous adipose tissue. Blood flow was measured by the indicator-dilution method in which Evans blue dye was injected continuously at constant rate into the brachial artery (2).Ten young adult subjects, 6 men and 4 women, were studied. All were medical students or laboratory personnel in good health and near ideal body weight. Dietary history of carbohydrate intake was normal. No food was taken after 7 p.m. on the evening preceding the experiment. The first blood samples were obtained betwee...

Comparison of Insulin Action on Glucose versus Potassium Uptake in Humans

“…Potassium and sodium movement in the isolated diaphragm in response to insulin occurs in the absence of glucose (27). There is temporal separation of potassium and glucose uptake (28,29), and insulin stimulates potassium uptake in doses at which there is no appreciable glucose flux (30). Rats fed a high-fat diet developed slower uptake of glucose and potassium, creating an apparent view of concordant regulation (31).…”

Dynamics of blood electrolytes in repeated hyper- and/or hypoglycaemic events in patients with type 1 diabetes

“…Insulin plays an important part in ionic regulation by its stimulatory effect [11][12][13] on the Na + /K + pump. The increase in the K + levels during hyperglycaemia in protocol 1 may thus be explained by the withdrawal of that insulin, which was given to keep the study participants euglycaemic at baseline.…”

“…Experimental work on many different tissues in vitro has shown that insulin has a stimulating effect on the Na + /K + pump [8][9][10]. In vivo, in studies in humans, this stimulatory effect on the Na + /K + pump is active at baseline insulin levels [11], and has been shown to be the cause of insulin-induced decreases in plasma K + after local perfusion of the forearm with insulin [12,13]. The stimulatory effect of insulin on the Na + /K + pump is also widely believed to underlie the hypoglycaemia-induced hypokalaemia [6,7].…”

The effect of residual neurological deficit on oral glucose tolerance in persons with chronic spinal cord injury

“…In subjects with paraplegia, the contributions of innervated upper extremity or denervated lower extremity muscle to the insulin resistant state is unknown; selective glucose extraction across the arm or leg muscle beds during a hyperinsulinemic eugycemic clamp study should provide such information. 26,27 An association between obesity and hyperuricemia in the able-bodied population has been reported. 28 Zhong et al 5 reported that in subjects with chronic SCI, the level of serum uric acid and serum triglycerides in the subgroup with hyperinsulinemia was signi®cantly higher than in subjects with normal plasma insulin levels.…”