Rath E A, Hems D A, Beloff-Chain A
Diabetologia. 1980 Jun;18(6):507-11. doi: 10.1007/BF00261708.
Fatty acid synthesis was measured in vitro in pieces of adipose tissue from lean and obese-hyperglycaemic (ob/ob) mice, using 14C-glucose or 14C-lactate and 3H2O to obtain absolute rates of total fatty acid synthesis. In the presence of lipoprotein-triglyceride (2.5 mumol/l) metabolic interaction occurred which decreased glucose incorporation into fatty acids by 30% in lean mouse tissue, but not in obese mouse tissue. In the absence of added insulin, the contribution of glucose to total fatty acid synthesis was 69% in obese mouse tissue, significantly lower than the value of 87% obtained in lean mouse tissue. Insulin increased the contribution of glucose to total synthesis in both lean and obese mouse tissues, although the value in obese mouse tissue (83%) remained lower than the value in lean mouse tissue (100%). Lactate was not a major precursor for fatty acid synthesis. When both lactate (2 mmol/l) and glucose (15 mmol/l) were present, the contribution of lactate to total fatty acid synthesis was not increased in obese mouse tissue, suggesting that even in the presence of insulin, about 30% of the carbon was provided by intracellular precursors.
利用14C-葡萄糖或14C-乳酸以及3H2O来测定瘦小鼠和肥胖高血糖(ob/ob)小鼠脂肪组织切片中脂肪酸的体外合成,以获得总脂肪酸合成的绝对速率。在脂蛋白甘油三酯(2.5 μmol/l)存在的情况下,发生了代谢相互作用,这使得瘦小鼠组织中葡萄糖掺入脂肪酸的量减少了30%,但在肥胖小鼠组织中没有减少。在不添加胰岛素的情况下,肥胖小鼠组织中葡萄糖对总脂肪酸合成的贡献为69%,显著低于瘦小鼠组织中获得的87%的值。胰岛素增加了瘦小鼠和肥胖小鼠组织中葡萄糖对总合成的贡献,尽管肥胖小鼠组织中的值(83%)仍低于瘦小鼠组织中的值(100%)。乳酸不是脂肪酸合成的主要前体。当同时存在乳酸(2 mmol/l)和葡萄糖(15 mmol/l)时,肥胖小鼠组织中乳酸对总脂肪酸合成的贡献并未增加,这表明即使在胰岛素存在的情况下,约30%的碳是由细胞内前体提供的。