Das S, Chatterjee T K, Ghosh J J
Biochem Pharmacol. 1984 Apr 1;33(7):951-4. doi: 10.1016/0006-2952(84)90499-4.
Morphine treatment in normal intact rats caused a dose-dependent increase in hepatic tyrosine aminotransferase (TAT) activity, as demonstrable up to 2 hr of exposure to the opioid alkaloid. However, such increase in TAT activity was invariably preceded by a prior decline in the enzyme level, as observed after 15 min of morphine treatment. Such an initial decline in activity was not demonstrable in diabetic animals. Further studies indicate that morphine inhibited the insulin-induced increase in TAT activity, a phenomenon which could be reversed by the opioid antagonist naloxone. The results suggest an opioid control mechanism in the regulation of the insulin-inducible form of TAT and indicate the possibilities of a trophic role of endogenous opiates in gluconeogenesis.
在正常完整大鼠中，吗啡治疗导致肝脏酪氨酸转氨酶（TAT）活性呈剂量依赖性增加，这种增加在接触阿片生物碱长达2小时时都可显现。然而，正如吗啡治疗15分钟后所观察到的那样，TAT活性的这种增加总是先伴随着酶水平的下降。在糖尿病动物中未观察到这种活性的初始下降。进一步的研究表明，吗啡抑制胰岛素诱导的TAT活性增加，而阿片拮抗剂纳洛酮可逆转这一现象。结果提示在胰岛素诱导型TAT的调节中存在阿片控制机制，并表明内源性阿片在糖异生中具有营养作用的可能性。
