Carnovale C E, Catania V A, Monti J A, Carrillo M C
Instituto de Fisiologia Experimental, Facultad de Ciencias Bioquímicas y Farmacéuticas, Universidad Nacional de Rosario, Argentina.
Can J Physiol Pharmacol. 1992 May;70(5):727-31. doi: 10.1139/y92-096.
Microsomal glutathione S-transferase, UDP-glucuronyl transferase, and aniline hydroxylase activities were determined in liver, renal cortex, and small intestine of control, streptozotocin-diabetic, alloxan-diabetic, and untreated insulin-injected male Wistar rats. Renal microsomal glutathione S-transferase activity showed a direct linear relationship with insulin blood levels, in agreement with our previous report on cytosolic glutathione S-transferase. This result suggests a possible regulatory mechanism of insulin that needs to be further examined. The hepatic microsomal UDP-glucuronyl transferase was only decreased in streptozotocin-diabetic rats and was not restored by insulin treatment. Intestinal UDP-glucuronyl transferase exhibited an opposite response in streptozotocin-treated animals that was not normalized by the administration of insulin. Hepatic aniline hydroxylase showed the same behaviour as intestinal UDP-glucuronyl transferase. These results suggest that streptozotocin and (or) its metabolites have a direct effect on hepatic and intestinal UDP-glucuronyl transferase activity and on hepatic aniline hydroxylase activity. On the other hand, insulin regulation of enzyme activity varies from one organ to another.
在对照、链脲佐菌素诱导糖尿病、四氧嘧啶诱导糖尿病以及未处理的注射胰岛素的雄性Wistar大鼠的肝脏、肾皮质和小肠中，测定了微粒体谷胱甘肽S-转移酶、UDP-葡糖醛酸基转移酶和苯胺羟化酶的活性。肾微粒体谷胱甘肽S-转移酶活性与胰岛素血药浓度呈直接线性关系，这与我们之前关于胞质谷胱甘肽S-转移酶的报告一致。该结果提示了一种可能的胰岛素调节机制，有待进一步研究。肝微粒体UDP-葡糖醛酸基转移酶仅在链脲佐菌素诱导糖尿病大鼠中降低，且胰岛素治疗不能使其恢复。在链脲佐菌素处理的动物中，肠道UDP-葡糖醛酸基转移酶表现出相反的反应，胰岛素给药不能使其恢复正常。肝苯胺羟化酶表现出与肠道UDP-葡糖醛酸基转移酶相同的行为。这些结果表明，链脲佐菌素和（或）其代谢产物对肝和肠UDP-葡糖醛酸基转移酶活性以及肝苯胺羟化酶活性有直接影响。另一方面，胰岛素对酶活性的调节因器官而异。
