INTERLEUKIN-1-BETA INHIBITS GLUCOKINASE ACTIVITY IN CLONAL HIT-T15 BETA-CELLS
INTERLEUKIN-1-BETA INHIBITS GLUCOKINASE ACTIVITY IN CLONAL HIT-T15 BETA-CELLS
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DOI：
10.1016/0014-5793(90)80928-c
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发表时间：
1990-07-16
期刊：
影响因子：
3.5
通讯作者：
HAMMONDS, P
中科院分区：
文献类型：
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作者：
BEGGS, M;BERESFORD, G;HAMMONDS, P
白细胞介素1受体(IL-1β，IL-1β)参与胰岛素依赖型糖尿病的发病机制。在本研究中，我们研究了IL-1β对克隆性HIT-T15β细胞葡萄糖代谢的影响。在短期内(1h)，25 IL-1β可显著增加胰岛素释放速率和葡萄糖利用率，但对葡萄糖氧化无明显影响。相反，48小时后，IL-1β抑制胰岛素的释放和葡萄糖的利用和氧化。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(三磷酸腺苷、三磷酸腺苷)，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降低所致。
Interleukin‐1β (IL‐1β) has been implicated in the pathogenesis of insulin‐dependent diabetes mellitus. In the present study we have investigated the effects of IL‐1β on glucose metabolism in clonal HIT‐T15 β cells. In the short‐term (1 h), 25 IL‐1β significantly increased the rates of insulin release and glucose utilisation, but not glucose oxidation. In contrast, after 48 h, IL‐1β 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‐1β may be due to impaired glucokinase activity.