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  • Title: [The pathogenesis of diabetes produced by subtotal pancreatectomy, with special reference to the cell kinetics of the islet cells].
    Author: Yomemura Y, Takashima T, Matsuki N, Hagino S, Sawa T, Takashima S, Miwa K, Miyazaki I.
    Journal: Nihon Geka Gakkai Zasshi; 1984 Apr; 85(4):356-62. PubMed ID: 6379411.
    Abstract:
    The pathogenesis of the diabetes produced by the subtotal pancreatectomy was investigated from the pancreatic endocrine function and the cell kinetics of the islet cells. The authors prepared the following two groups in the rats. The first group was 90% pancreatectomized rats and the second group was the 60% pancreatectomized rats. Most of the 90% pancreatectomized rats developed diabetes twelve weeks after operation. In these diabetic rats the insulin secretion was undetectable during glucose infusion. To the contrary, the relative increase of the glucagon secretion was found during arginine infusion in spite of the hyperglycemia. However, non of the 60% pancreatectomized rats developed diabetes during post-operative course up to 6 months. To investigate the cell kinetics of the islet cells, the 3H-thymidine autoradiography was prepared at several intervals after operation. The results of the thymidine labelling index showed two phase of regeneration. The first phase was observed on three to seven days after pancreatectomy and the second phase was on fourteen to twenty-eight days. After the second phase of regeneration, the degeneration of the B-cells was observed in the 90% pancreatectomized rats. On the ninetieth days after operation the atrophy of the islets and the disturbance of the arrangement of A, B and D cells were observed by the immuno-histochemical studies. Meanwhile, the 60% pancreatectomized rats did not show degeneration of the islets. These results show that the onset of diabetes after subtotal pancreatectomy was produced by degeneration of the B cells surpassing their regenerative capacity.
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