白细胞介素-1β抑制克隆的HIT-T15β细胞中的葡萄糖激酶活性。
Interleukin-1 beta inhibits glucokinase activity in clonal HIT-T15 beta-cells.
作者信息
Beggs M, Beresford G, Clarke J, Mertz R, Espinal J, Hammonds P
机构信息
Diabetes Section, Glaxo Research Laboratories, Research Triangle Park, NC.
出版信息
FEBS Lett. 1990 Jul 16;267(2):217-20. doi: 10.1016/0014-5793(90)80928-c.
Interleukin-1 beta (IL-1 beta) has been implicated in the pathogenesis of insulin-dependent diabetes mellitus. In the present study we have investigated the effects of IL-1 beta on glucose metabolism in clonal HIT-T15 beta cells. In the short-term (1 h), 25 U/ml IL-1 beta significantly increased the rates of insulin release and glucose utilisation, but not glucose oxidation. In contrast, after 48 h, IL-1 beta inhibited insulin release and glucose utilisation and oxidation. By assaying enzymes (hexokinase, glucokinase, pyruvate dehydrogenase, glucose 6-phosphatase) and nucleotides (ATP, ADP) associated with the regulation of glycolysis and glucose oxidation, we conclude that the inhibitory effects of IL-1 beta may be due to impaired glucokinase activity.
白细胞介素-1β（IL-1β）与胰岛素依赖型糖尿病的发病机制有关。在本研究中，我们研究了IL-1β对克隆的HIT-T15β细胞葡萄糖代谢的影响。在短期内（1小时），25 U/ml的IL-1β显著提高了胰岛素释放率和葡萄糖利用率，但未提高葡萄糖氧化率。相比之下，48小时后，IL-1β抑制了胰岛素释放、葡萄糖利用和氧化。通过检测与糖酵解和葡萄糖氧化调节相关的酶（己糖激酶、葡萄糖激酶、丙酮酸脱氢酶、葡萄糖6-磷酸酶）和核苷酸（ATP、ADP），我们得出结论，IL-1β的抑制作用可能是由于葡萄糖激酶活性受损所致。
Zotero 插件