Freed L E, Endemann G, Tomera J F, Gavino V C, Brunengraber H
Department of Nutrition and Food Science, Massachusetts Institute of Technology, Cambridge.
Diabetes. 1988 Jan;37(1):50-5. doi: 10.2337/diab.37.1.50.
Production of ketone bodies and their contribution to lipogenesis were measured in isolated livers from normal and streptozocin-induced diabetic (STZ-D) rats perfused with tracer amounts of 3H2O and (R)-3-hydroxy[3-14C]butyrate. Diabetes decreased by 80-95% the total rates of fatty acid and 3-beta-hydroxysterol synthesis in perfused livers and livers of live rats. The activity of cytosolic acetoacetyl-CoA synthetase was slightly (17%) decreased in livers from STZ-D rats. The incorporation of ketone bodies into fatty acids and sterols was markedly inhibited in perfused livers from STZ-D rats despite the stimulation of ketogenesis by diabetes and the presence of oleate. Treatment of the rats with insulin before liver perfusion led to a normalization of the rates of ketogenesis and fatty acid synthesis. The rates of sterol synthesis were only partially normalized by insulin treatment. We conclude that in STZ-D, ketosis does not stimulate hepatic lipogenesis via cytosolic activation of acetoacetate.
在灌注微量3H2O和（R）-3-羟基[3-14C]丁酸的正常大鼠和链脲佐菌素诱导的糖尿病（STZ-D）大鼠的离体肝脏中，测定了酮体的生成及其对脂肪生成的贡献。糖尿病使灌注肝脏和活体大鼠肝脏中脂肪酸和3-β-羟基甾醇的总合成率降低了80-95%。STZ-D大鼠肝脏中胞质乙酰乙酰辅酶A合成酶的活性略有降低（17%）。尽管糖尿病刺激了酮体生成且存在油酸，但STZ-D大鼠灌注肝脏中酮体掺入脂肪酸和甾醇的过程受到明显抑制。肝脏灌注前用胰岛素治疗大鼠可使酮体生成率和脂肪酸合成率恢复正常。胰岛素治疗仅使甾醇合成率部分恢复正常。我们得出结论，在STZ-D大鼠中，酮血症不会通过乙酰乙酸的胞质活化来刺激肝脏脂肪生成。
