Intranasal glucagon is effective and noninferior to injectable intramuscular glucagon for the correction of insulin-induced hypoglycemia in adults with type 1 diabetes, according to a randomized, cross-over study. The findings were published today in the online edition of Cell Metabolism. The increases in epinephrine and norepinephrine were comparable in diabetics and normals; thus, the blunted response in plasma IRG to the stimulus of low blood sugar in diabetics cannot be explained by a generalized defect in catecholamine secretion. Insulin and glucagon were delivered using two subcutaneous infusion pumps installed on the abdominal wall. In conclusion, the association of Clonidine to a protein meal caused impaired glucose tolerance presumably due to a direct glycogenolytic effect, occurring in the liver on account of an α-2 receptor stimulation, insulin and glucagon not being involved in this phenomenon. LY2189265 retained full receptor activity in vitro and elicited insulinotropic activity in islets similar to native peptide. From these results we conclude that although in diabetes excessive glucagon levels are observed with chronic arginine stimulation, the acute phase of glucagon secretion in response to arginine is normal.
Although the study does not show evidence for linkage in this chromosomal region in our Italian cohort, we cannot a priori exclude the possibility of an allelic or genotypic association. Full text Full text is available as a scanned copy of the original print version. Finally, in the fifth section, we summarize the concepts underlying the autonomic hypothesis, the evidence for it, and the implications of the autonomic hypothesis for the treatment of type 1 diabetes.