J. Dupré

Inhibition of actions of glucagon in adipocytes by gastric inhibitory polypeptide

Possible interactions between gastric inhibitory polypeptide (GIP) and glucagon were investigated in rat adipocytes. GIP was nonlipolytic and inhibited lipolysis stimulated by glucagon but not that stimulated by secretin or vasoactive intestinal polypeptide (VIP). GIP competed with 125I-glucagon for binding to adipocyte receptors, and at physiologic concentrations inhibited the stimulation of AMP produced by glucagon. Thus GIP acts as an inhibitor of actions of glucagon on adipocytes and may be a physiologic modulator of effects of glucagon.

Effects of portacaval anastomosis on glucose tolerance in the dog: Evidence of an interaction between the gut and the liver in oral glucose disposal

Continuous infusions of glucose (90 min duration) were given into the duodenum (ID), or the portal vein (IP), or a peripheral vein (IV) in conscious dogs, intact dogs, or dogs with portacaval anastomoses. In intact animals ID glucose tolerance was better than IV glucose tolerance, but IP glucose tolerance was not significantly different from IV glucose tolerance. Thus, the superiority of tolerance to ID glucose was not accounted for by relatively high levels of glucose in portal blood. IV glucose tolerance was not significantly affected by protacaval anastomosis with ligation of the portal vein, but ID glucose tolerance was markedly impaired. Disproportionate impairment in tolerance to enterically administered glucose in dogs with portacaval shunts, and the similarity of IP and IV glucose tolerance in intact dogs, suggest that both liver and the gut are important in determination of oral glucose tolerance through mechanisms that have little or no effect on responses to parenterally administered glucose. The results also suggest that the hepatic contribution is not dependent upon portal venous perfusion of the liver, and that a humoral interaction between the gut and the liver is involved which is not simply dependent on endocrine responses of the pancreas.

Interaction of Secretin and Insulin on Human Forearm Metabolism

Abstract. The effect of secretin on forearm metabolism (muscle compartment) was examined in the presence of low and high concentrations of insulin. Continuous infusions (30 min. duration) of secretin 12 ng/min. (SEC), insulin 160 ng/min. (INS) or these doses of insulin and secretin together (INS + SEC) were delivered into the brachial arteries of normal volunteers. SEC alone was without significant effect on forearm metabolism. INS as previously reported, stimulated glucose and potassium uptake and inhibited the output of some amino acids from the deep venous bed. The two hormones together (INS + SEC) increased maximum lactate (p < 0. 025) and alanine output (p < 0. 005) beyond that observed with INS alone. A marked calcium output occurred (p < 0. 001) with the combined infusion which was not observed with either hormone alone. Potassium metabolism with INS + SEC was similar to that observed with INS alone. These results suggest that these two hormones, acting in concert, stimulate glycolysis and net calcium efflux. This joint action of insulin and secretin may have a physiological role in the immediate postprandial period.

Conversion of glucose to lipid by human adipose tissue in vitro

Abstract The rates of incorporation in vitro of glucose carbons into carbon dioxide and glyceride-glycerol and fatty acids by specimens of omental adipose tissue obtained from patients undergoing elective surgery were studied in the absence and presence of insulin. The basal (absence of insulin) activity for each parameter of glucose metabolism in the individual specimens correlated significantly with the insulin-stimulated increments. The glucose metabolism of specimens of subcutaneous adipose tissue, obtained under local anesthesia from normal volunteers in the fasting state and after ingestion of a standard breakfast, was also studied. In the absence of added insulin the incorporation of the glucose carbons into glyceride-fatty acids was consistently greater in specimens obtained after feeding, but incorporation into carbon dioxide and glyceride-glycerol was not significantly increased. In the presence of maximally effective amounts of insulin, there was no significant difference between the elevated rates of incorporation of glucose carbons into carbon dioxide and glyceride-glycerol and fatty acids between the specimens obtained before and after feeding. It was concluded that feeding did not enhance the maximal capacity for lipogenesis in adipose tissue. The modest increase in glyceride-fatty acid production in specimens obtained after feeding was probably due to effects of endogenous insulin. A hypothetical rate of lipogenesis from glucose derived from these data suggests that the production of fatty acids from glucose in human adult adipose tissue occurs on a very small scale relative to the intake of carbohydrate in normal man.