Loten E G, Le Marchand Y, Assimacopoulos-Jeannet F, Denton R M, Jeanrenaud B
Am J Physiol. 1976 Mar;230(3):602-7. doi: 10.1152/ajplegacy.1976.230.3.602.
After a 1-h preincubation to remove endogenous insulin, adipose tissue of obese mice (C57BL/L4 ob/ob) had a lower rate of glucose metabolism than tissue which was not preincubated. In contrast, preincubation did not change the metabolism of adipose tissue from lean mice (C57B1/6J +/+). The preincubation effect was abolished in obese mice which had had their serum insulin levels lowered toward normal by streptozotocin treatment. Injection of anti-insulin serum to obese mice caused adipose tissue removed 15 min after the injection to display a rate of glucose metabolsim lower than that of tissue removed before the injection. No such effect was seen in lean mice. These data are consistent with the hypothesis that hyperinsulinemia in the obese mice causes a chronic state of insulin stimulation of their adipose tissue, possibly contributing to their high rates of lipogenesis and their obesity. Several lipogenic enzymes were measured in adipose tissue of both lean and obese mice, and no single enzymatic abnormality was detected which might explain the hyperlipogenesis. Pyruvate dehydrogenase and acetyl-CoA carboxylase were both insulin-sensitive enzymes in lean and obese mice.
在进行1小时的预孵育以去除内源性胰岛素后,肥胖小鼠(C57BL/L4 ob/ob)的脂肪组织葡萄糖代谢率低于未进行预孵育的组织。相比之下,预孵育并未改变瘦小鼠(C57B1/6J +/+)脂肪组织的代谢。在通过链脲佐菌素治疗使血清胰岛素水平降至正常的肥胖小鼠中,预孵育效应消失。给肥胖小鼠注射抗胰岛素血清导致注射后15分钟取出的脂肪组织显示出的葡萄糖代谢率低于注射前取出的组织。在瘦小鼠中未观察到这种效应。这些数据与以下假设一致:肥胖小鼠中的高胰岛素血症导致其脂肪组织处于胰岛素刺激的慢性状态,这可能是导致它们脂肪生成率高和肥胖的原因。在瘦小鼠和肥胖小鼠的脂肪组织中测量了几种脂肪生成酶,未检测到任何可能解释脂肪生成过多的单一酶异常。丙酮酸脱氢酶和乙酰辅酶A羧化酶在瘦小鼠和肥胖小鼠中都是胰岛素敏感酶。