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[Effect of glucagon and insulin on the histochemical and functional alterations in the Langerhans islands after hepatectomy in dogs].

Changes of Langerhans islands after 40% hepatectomy, and effects of GI therapy on the islets were investigated in dogs. In control group, one week and four weeks after the hepatectomy, ivGTT was examined followed by a blood sampling from the portal vein to measure the changes of glucose, insulin and glucagon, and areal changes of the islets were measured. In GI group, the same experiment was done with added GI therapy after operation. The following results were obtained. 1) In control group, portal plasma insulin level and insulin response were decreased one week after surgery, and sizes of islets were enlarged four weeks after surgery. 2) In GI group, there were no decrease in portal plasma insulin level and insulin response one week after surgery, and no enlargement of the sizes of the islets four weeks after surgery. 3) Changes in glucagon level and glucagon response were same as those of insulin, glucose level and these response. There was no difference between the two groups. 4) According to these observation, glucagon and insulin are exhausted one week after hepatectomy in dogs. It seems to be necessary to provide the dog with glucagon and insulin after hepatectomy.

Animals↗

[Morphologic and functional changers in B-cells and vessels of the islands of Langerhans in patients with insulin-dependent diabetes mellitus].

Pancreatic biopsies from 49 patients with IDDM were studied. Ultrastructurally, a heterogeneity of B-cell morphological changes and microangiopathy of the Langerhans islands were observed. Langerhans islands containing B-cells with destructive changes were found in 27 biopsies, sclerosis and hyalinosis of vascular wall in 6 biopsies. Langerhans islands sclerosis was found in 13 biopsies and in 9 biopsies, in normal structure of the acinar compartment of the pancreas, Langerhans islands were not found. The authors findings and literature data allowed the conclusion on the stage pattern of IDDM development. The basis is an immune, autoimmune mechanism of B-cell and endotheliocyte of the Langerhans islands damage, and therefore, a decrease of the (pro)insulin synthesis and its transport into the circulation. This process is genetically predetermined, this being confirmed by the lack of the dependence of B-cell and vessels damage in the Langerhans islands upon the age and small fluctuations in the manifestations and duration of the disease.

Adult↗

[Protein composition and synthesis in islands of Langerhans isolated from normal rats and rats with alloxan diabetes].

Protein fractions with dissimilar electrophoretic mobility were identified in Langerhans, islands. In solitory islands, isolated from pancreas of rats with alloxan diabetes as compared with normal rats the protein composition varied distinctly: fractions of "constant" proteins and, specifically, the insulin fraction disappeared completely, total amount of identified fractions was decreased with relative alteration in their mobility. The total protein-synthesizing activity of Langerhans' islands from diabetic animals was 3-4-fold decreased as compared with that of control animals. An effect of "glucose repression" of protein synthesis was observed in isolated Langerhans' islands.

Animals↗