The ability of various sugars and closely related substances to stimulate insulin secretion was studied by means of pancreatic-femoral cross-circulation experiments between hepatectomized donor dogs and normal recipients. In other experiments, the test substance was injected directly into the pancreatic artery of normal dogs. The administration of d-glucose, d-galactose or d-ribose was followed by a prompt hypoglycemia, suggesting insulin secretion; d-arabinose caused an unexplained delayed hypoglycemia, while d-fructose, d-mannose, d-xylose, l-arabinose, 3-methylglucose, d-glucosamine, galacturonic acid and saline had no effect. The tentative hypothesis that insulin secretion is stimulated by sugars which are both utilizable and insulin-sensitive is offered. No relationship between chemical structure and ability to cause insulin release was found.
539developed about the same aortic sensitivity as males. In comparison to females, castration did not have much effect on males, since little difference was noted when the aortae of operated animals were compared to normal ones. Likewise, the salt diet did not increase aortic responsiveness to epinephrine in castrated males beyond that found in normal males. These findings indicate that the presence of female sex hormones is required to maintain a low reactivity to epinephrine in the aorta. Removal of the male hormone, on the other hand, did not change the reactivity of the aorta, nor sensitize the animal to the salt diet. The mechanism whereby the salt diet increases the reactivity of vessel strips to epinephrine may be explainable by the theory of Raab ( 5 ) that increased intracellular sodium in smooth muscle of blood vessels potentiates the constrictor effects of epinephrine, possibly by raising the membrane electrical potentials of muscle cells upon which catecholamines act.Summary. Strips were prepared from aortae of rats and their reactivity to epinephrine tested by means of a lever system that recorded shortening of the smooth muscle. A 2% salt diet increased the sensitivity of the vessel to I-epinephrine in both sexes. Male aortae in all instances had greater sensitivity to epinephrine than those of females under the same conditions. Castration markedly increased the sensitivity to epinephrine in females, especially when the castrates were placed on the salt diet, In contrast, male aortae were not particularly changed by castration.
Glucagon is believed to cause hyperglycemia by promoting glycogenolysis in the liver. This is based on the following evidence which has been reviewed in detail recently (1) and which is largely indirect: 1) the hyperglycemic response to glucagon is decreased or absent in fasting, untreated diabetes, severe liver disease (2) and after evisceration ( 3 ) when the amount of liver glycogen is presumably low or absent; 2 ) glucagon is more effective when injected into the portal vein than by any other route of administration and is ineffective after occlusion of the liver circulation(2) ; 3) glucagon causes a sharp increase in splanchnic glucose production. as measured by venous catheterization in man ( 4 ) : 4) destruction of the pancreatic alpha cells, presumably accompanied by the liberation of preformed glucagon, causes an immediate hyperglycemia with a decrease in liver glycogen( 5 ) ; 5) glucagon promotes liver glycogenolysis in vitru by activating the phosphorylase system ( 6 ) . Although these findings would lead one to expect a decrease of liver glycogen in intact animals treated with glucagon, this effect has not been clearly demonstrated. Burger and Kramer(2) first reported a decrease in liver glycogen in dogs treated with glucagon. However, these pioneering results were obtained with crude preparations of glucagon heavily contaminated with insulin. Furthermore liver glycogen was determined in samples obtained by means of repeated biopsies, a traumatizing technic which may cause glycogenolysis in itself. Similarly, using an impure preparation of glucagon, Heard et a L ( 7 ) obtained a decrease in liver glycogen in normal rats, while Milman et al.(8) obtained similar results in vit. E-deficient rats. In contrast with these findings, the
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