Wieser P B, Fain J N
Endocrinology. 1975 May;96(5):1221-5. doi: 10.1210/endo-96-5-1221.
Insulin-stimulated glucose oxidation was enhanced by the addition of N6 (phenylisopropyl)adenosine (PIA), prostaglandin E1 (PGE1) or nicotinic acid during a 1-h incubation of small amounts 5-8 mg/ml) of rat fat cells. Basal lipolysis was appreciable if low numbers of fat cells were incubated per ml. Insulin inhibited basal lipolysis at 20 to 50 mugU/ml and abolished lipolysis of 100 mugU/ml was present over a l-h period. However PIA, PGE1 or nicotinic acid potentiated glucose oxidation due to the 100 mugU/ml dose of insulin indicating that these agents are not increasing glucose oxidation solely as a result of an inhibition of lipolysis. PIA, PGE1 and nicotinic acid acted synergistically with insulin in stimulating glucose oxidation and inhibiting lipolysis in the presence of norepinephrine. Insulin was unable to decrease basal cyclic AMP accumulation or the increase in cyclic AMP seen with norepinephrine and theophylline after various time periods (2 to 60 min) but PIA, PGE1 and nicotinic acid were able to inhibit cyclic AMP accumulation at all times tested.
在对少量（5 - 8毫克/毫升）大鼠脂肪细胞进行1小时孵育期间，添加N6 - （苯异丙基）腺苷（PIA）、前列腺素E1（PGE1）或烟酸可增强胰岛素刺激的葡萄糖氧化。如果每毫升孵育的脂肪细胞数量较少，基础脂解作用较为明显。胰岛素在20至50微克单位/毫升时抑制基础脂解作用，并在100微克单位/毫升时在1小时内消除脂解作用。然而，PIA、PGE1或烟酸增强了由100微克单位/毫升剂量胰岛素引起的葡萄糖氧化，这表明这些药物并非仅仅由于抑制脂解作用而增加葡萄糖氧化。在去甲肾上腺素存在的情况下，PIA、PGE1和烟酸与胰岛素协同作用，刺激葡萄糖氧化并抑制脂解作用。在不同时间段（2至60分钟）后，胰岛素无法降低基础环磷酸腺苷（cAMP）积累或去甲肾上腺素和茶碱引起的cAMP增加，但PIA、PGE1和烟酸在所有测试时间均能抑制cAMP积累。
