[Pathogenesis of diabetes in adulthood. I. Insulin secretion at different evolutionary phases of diabetes]

Intravenous loading with glucose and glucose+tolbutamid was conduced in five groups of subjects, selected in a way that the intensity of insulin secretion gradually decreases from one group to the other (control group, relatives of patients with diabetes, diabetics sensitive to SUP and diabetics resistant to SUP). With insulin deficiency (in the last three groups) the early insulin secretion (absence of summit in IRI curve at the tenth minute), was established to grow weak, whereas in latent diabetes and in SUP sensitive diabetics it was preserved and insulinemia was protracted during the second half of the test. Early insulin secretion, in the control group and in the relatives of the diabetics, with loading with glucose-tolbutamid was twice as high as compared with that, obtained with loading solely with glucose. Diabetes at a mature age is concluded to be with a changed sensitivity of B-cells, at the beginning, versus glucose as a stimulator with signaling character, but the ability for synthesis and secretion of insulin, in general, is preserved. With the evolution of diabetes defect, the falling-off of insulin-synthesis ability is included in the pathogenetic mechanisms. A state of complete insulin deficiency develops--hence non-sensitivity to SUP.