Ivanov V V, Shakhristova E V, Stepovaya E A, Nosareva O L, Fedorova T S, Ryazantseva N V, Novitsky V V
Siberian State Medical University, Tomsk, 634050, Russia.
Biochemistry (Mosc). 2015 Jan;80(1):87-96. doi: 10.1134/S0006297915010101.
Spontaneous lipolysis was found to be increased in adipocytes of rats with alloxan-induced diabetes. In addition, isoproterenol-stimulated hydrolysis of triacylglycerols was inhibited against the background of oxidative stress and decreased redox-status of cells. A decrease in the ability of insulin to inhibit isoproterenol-stimulated lipolysis in adipocytes that were isolated from adipose tissue of rats with experimental diabetes was found, which shows a disorder in regulation of lipolysis in adipocytes by the hormone in alloxan-induced diabetes. Based on these findings, we concluded that there is an influence of reactive oxygen species, superoxide anion radical in particular, and redox potential of the glutathione system on molecular mechanisms of change in lipolysis intensity in rat adipocytes in alloxan-induced oxidative stress. Activation of spontaneous lipolysis under conditions of oxidative stress might be a reason for the high concentration of free fatty acids in blood plasma in experimental diabetes, and this may play a significant role in development of insulin resistance and appearance of complications of diabetes.
研究发现，在四氧嘧啶诱导的糖尿病大鼠的脂肪细胞中，自发脂解作用增强。此外，在氧化应激和细胞氧化还原状态降低的背景下，异丙肾上腺素刺激的三酰甘油水解受到抑制。实验性糖尿病大鼠脂肪组织分离出的脂肪细胞中，胰岛素抑制异丙肾上腺素刺激的脂解作用的能力下降，这表明在四氧嘧啶诱导的糖尿病中，激素对脂肪细胞脂解的调节出现紊乱。基于这些发现，我们得出结论：活性氧物种，特别是超氧阴离子自由基，以及谷胱甘肽系统的氧化还原电位对四氧嘧啶诱导的氧化应激下大鼠脂肪细胞脂解强度变化的分子机制有影响。氧化应激条件下自发脂解的激活可能是实验性糖尿病血浆中游离脂肪酸浓度升高的原因，这可能在胰岛素抵抗的发展和糖尿病并发症的出现中起重要作用。
