Hesketh J E, McKenzie N, Campbell G P
Biochemistry Division, Rowett Research Institute, Aberdeen, Scotland.
FEBS Lett. 1988 Dec 5;241(1-2):115-8. doi: 10.1016/0014-5793(88)81042-1.
Insulin stimulated protein synthesis in quiescent 3T3 fibroblasts. This effect of the hormone was greater in the presence of the diacylglycerol kinase inhibitor R59022 (10(-5) M) over a range of insulin concentrations from 1 microU to 1 mU/ml; R59022 increased the sensitivity of cells to insulin. The amount of radioactive diacylglycerol recovered from cells prelabelled with [3H]glycerol was increased transiently in response to insulin; the response was larger and prolonged in cells given the kinase inhibitor. The results (i) support the hypothesis that diacylglycerol production is part of the signal pathway by which insulin stimulates protein synthesis and (ii) suggest that inhibition of diacylglycerol breakdown leads to increased sensitivity to the hormone.
胰岛素刺激静止的3T3成纤维细胞中的蛋白质合成。在1微单位至1毫单位/毫升的一系列胰岛素浓度范围内,二酰基甘油激酶抑制剂R59022(10⁻⁵ M)存在时,该激素的这种作用更强;R59022增加了细胞对胰岛素的敏感性。用[³H]甘油预标记的细胞中回收的放射性二酰基甘油的量,对胰岛素有短暂增加的反应;给予激酶抑制剂的细胞中,该反应更大且持续时间更长。这些结果(i)支持二酰基甘油生成是胰岛素刺激蛋白质合成的信号通路一部分的假说,并且(ii)表明抑制二酰基甘油分解会导致对该激素的敏感性增加。