Obrosova I G, Efimov A S, Velikiĭ N N, Zimatkina T I, Moiseenok A G
Biull Eksp Biol Med. 1988 May;105(5):549-52.
Enzymatic systems of hepatic hyperlipogenesis supply by substrate (acetyl-CoA) and cofactors (NADPH and ATP) were studied in experiments on diabetic C57Bl/Ks J mice (db/db) that served as a model of non-insulin dependent diabetes. The rise in acetyl-CoA synthetase activity catalyzing the primary step of lipogenesis from acetate has been found, while pyruvate dehydrogenase complex activity did not differ from the control and ATP-citrate lyase activity was lowered. Hyperlipogenesis in non-insulin dependent diabetes was induced by the activation of cellular energy supply revealed in enhanced 2-oxoglutarate dehydrogenase activity and elevated ATP level, as well as changes in the activity ratio of NADPH supply and utilization and the rise in fructose-1,6-diphosphate, allosteric effector of fatty acid synthetase, which resulted in the increase of the enzyme activity and created wider potentials of NADPH utilization as a reducing equivalent in lipogenesis.
在以非胰岛素依赖型糖尿病模型的糖尿病C57Bl/Ks J小鼠（db/db）实验中，研究了肝脏脂肪生成增加时由底物（乙酰辅酶A）和辅因子（NADPH和ATP）提供的酶系统。已发现催化从乙酸盐进行脂肪生成第一步的乙酰辅酶A合成酶活性升高，而丙酮酸脱氢酶复合物活性与对照无差异，且ATP-柠檬酸裂解酶活性降低。非胰岛素依赖型糖尿病中的脂肪生成增加是由细胞能量供应的激活诱导的，这表现为2-氧代戊二酸脱氢酶活性增强和ATP水平升高，以及NADPH供应与利用的活性比率变化和脂肪酸合成酶的变构效应剂果糖-1,6-二磷酸增加，这导致酶活性增加，并为脂肪生成中作为还原当量的NADPH利用创造了更广泛的潜力。
