No abstract

Significant amounts of glucagon immunoreactivity (GI) and glucagon-like immunoreactivity (GLI) were found in two portions of the canine brain-the hypothalamus and brain stem. Ratios of GLI to GI were low in the hypothalamus, and variable but low in the brain stem. Dilution curves of the extracts from both regions showed similar patterns to that of glucagon in radioimmunoassay using specific (30K) and cross-reacting (YG9) antisera. The hypothalamic extract contained a larger amount of 3,500 MW fraction comparable to glucagon and a lesser amount of 9,000 MW fraction resembling proglucagon. While displacement of 125I-glucagon from the rat liver cell membrane by the main fraction of the hypothalamus was compatible with that of glucagon, activation of adenylate cyclase by the hypothalamus extract was higher than glucagon and that by the extract of the brain stem was lower than glucagon. Although purification was not sufficient and specific binding of circulating glucagon to the brain has not been overlooked, the hypothalamic extract at least contains material immunologically and probably biologically resembling glucagon.

No abstract

Mechanisms of hyperglycemic action of neurotensin were investigated in anesthetized dogs. The intravenous administration of neurotensin 1.0 ,u g/kg for 5 min induced an immediate decrease in arterial blood pressure and increases in levels of blood glucose, glucagon and insulin. Although blood levels of glucagon and insulin were greatly reduced and not elevated by neurotensin in the presence of somatostatin, the response of blood glucose to neurotensin was similar to that in the absence of somatostatin. The rise in blood glucose produced by intraportal injection of neurotensin was not greater than that produced by injection of the same dose of neurotensin into the femoral vein. The increments of glucagon and insulin secretion caused by the intraportal injection were also the same as those produced by the peripheral injection. Participation of antihypotensive mechanisms in the neurotensin-induced hyperglycemia was investigated by use of aadrenoceptor blockade and baroceptor denervation. Only the combination of somatostatin and a-adrenoceptor blockade or the denervation of baroceptors could suppress the hyperglycemic response to neurotensin. Stimulation of the secretion of anterior pituitary hormones by neurotensin infusion could not be recognized in the present experiments. These results suggested the following : 1) both glucagon and catecholamines may contribute to neurotensin-induced hyperglycemia, 2) neurotensin does not directly act on the liver, 3) catecholamine response could be mediated by baroceptor stimulation through hypotension, and 4) the hyperglycemic effect of anterior pituitary hormones does not participate in neurotensininduced hyperglycemia.