腎不全時の糖代謝異常に関する研究 : 中分子量物質のインスリン分泌抑制作用及びその機構

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There have been numerous reports concerning the insulin response to glucose in uremia. But, a clear-cut explanation of these observations has not been presented. Meanwhile, recent investigations have suggested that middle molecular substances (MMS) are important uremic toxins. In the present study, therefore the direct effect of MMS on insulin release from rat islets in vitro and the mechanism of there action studied. Pancreatic islets were isolated from male Wistar rats by the conventional collagenase method. In the secretion studies, the islets were incubated with MMS and/or various agents for 60 min. in medium of 0.5 ml of Krebs-Henseleit bicarbonate buffer (KHBB) contains 5mg/ml bovine serum albumin and 8.3mM glucose under the gas phase of 95%0_2-5%C0_2. Insulin released in the medium was radio immunoassayed by double antibody method. Islets after incubation were frozen at-80℃ immediately and frozen-dried at -40℃, 0.001mmHg. ATP concetration of the islets were assayed by the enzymatic cycling method. In the other studies, the effect of MMS on the electron-transport system was examined using rat liver mitochondria. 1. MMS suppressed insulin release from rat pancratic islets as well as ATP concetration. 2. The suppressed insulin release by MMS was not restored by db-cAMP, theophylline, adenosine and high concentration of Ca++. 3. MMS inhibited the electron-transport chain of rat liver mitochondria. 4. These observations suggest that MMS suppress insulin release, possibly in association with inhibitor of the electron-transport chain. Further studies on the precise mechanism of the suppression of insulin release by MMS are needed.
神戸大学の論文

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小林哲夫
神戸大学医学部内科学第二講座

腎不全時の糖代謝異常に関する研究 : 中分子量物質のインスリン分泌抑制作用及びその機構

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