Szkudelski T, Szkudelska K
Department of Animal Physiology and Biochemistry, University of Agriculture, Poznan, Poland.
Physiol Res. 2000;49(2):213-7.
In order to elucidate the direct effect of glucose on lipolysis in isolated rat adipocytes, cells were incubated in a buffer with different concentrations of this sugar: 2, 8 or 16 mmol/l. The increase in glucose concentration from 2 mmol/l to 8 or 16 mmol/l enhanced basal lipolysis by 30% and 47%, respectively. Epinephrine-induced lipolysis (1 micromol/l) was also increased by 31% and 32%, when glucose concentration was increased from 2 mmol/l to 8 or 16 mmol/l, respectively. The rise in lipolysis caused by glucose was restricted by H-89 (an inhibitor of protein kinase A, 30 micromol/l), but insulin (1 nmol/l) had no inhibitory action. The augmentation of lipolysis by glucose did not require its metabolism (as demonstrated using 2-deoxyglucose) and was due to the action of this sugar on the final steps of the lipolytic cascade, particularly on protein kinase A. However, short-term exposure of adipocytes to higher glucose concentrations did not restrict the inhibitory action of insulin on lipolysis induced by epinephrine.
为了阐明葡萄糖对分离的大鼠脂肪细胞脂解作用的直接影响,将细胞置于含有不同浓度该糖(2、8或16 mmol/L)的缓冲液中孵育。葡萄糖浓度从2 mmol/L增加到8或16 mmol/L时,基础脂解作用分别增强了30%和47%。当葡萄糖浓度从2 mmol/L分别增加到8或16 mmol/L时,肾上腺素诱导的脂解作用(1 μmol/L)也分别增加了31%和32%。葡萄糖引起的脂解作用增强受到H-89(蛋白激酶A抑制剂,30 μmol/L)的限制,但胰岛素(1 nmol/L)没有抑制作用。葡萄糖对脂解作用的增强并不需要其代谢(如使用2-脱氧葡萄糖所证明),而是由于该糖作用于脂解级联反应的最后步骤,特别是作用于蛋白激酶A。然而,脂肪细胞短期暴露于较高葡萄糖浓度并不会限制胰岛素对肾上腺素诱导的脂解作用的抑制作用。