ARGININE AND INSULIN RESPONSE IN ADIPOCYTES

本研究旨在探讨L-精氨酸（L-Arg）在肝纤维化中的作用 在培养的分化的3 T3-L1脂肪细胞中的葡萄糖代谢中。 单独使用L-Arg对2-脱氧葡萄糖摄取或基础糖原没有影响 合成，但这种氨基酸增加了153 ± 10%（p<0.01）， 在胰岛素处理的细胞中，葡萄糖掺入糖原。 L-精氨酸的主要代谢产物L-谷氨酸（L-Glu）也能增强 胰岛素刺激的糖原合成。 对胰岛素的反应不是 L-赖氨酸（L-Lys）可使其改变，而L-精氨酸（L-Arg）的作用则显著 用L-Lys减毒。 细胞与L-Arg的孵育显著增强 酶介导的尿素合成，而L-Lys消除这种反应。 L-精氨酸对胰岛素刺激糖原合成的促进作用 似乎并没有被占的产生多胺或 一氧化氮的产生，两者都可能来自酶促 L-Arg的转化。 在胰岛素存在的情况下， L-精氨酸、L-谷氨酸和L-赖氨酸也能显著增加细胞凋亡。 这些 数据表明，L-Arg的代谢降解与柠檬酸无关， 酸循环活性在L-Arg增强的机制中是重要的。 胰岛素刺激的糖原合成。

The present study was undertaken to define the role of L-arginine (L-Arg) in glucose metabolism in differentiated 3T3-L1 adipocytes in culture. L-Arg alone had no effect on 2-deoxyglucose uptake or basal glycogen synthesis, but this amino acid increased by 153+10% (p<0.01) the incorporation of glucose into glycogen in insulin-treated cells. L-Glutamate (L-Glu), a major metabolite of L-Arg, also enhanced insulin-stimulated glycogen synthesis. The response to insulin was not altered by L-lysine (L-Lys), but the effect of L-Arg was markedly attenuated by L-Lys. Cell incubation with L-Arg markedly enhanced arginase-mediated urea synthesis while L-Lys abolished this response. The stimulatory effect of L-Arg on insulin-stimulated glycogen synthesis did not appear to be accounted for by the generation of polyamines or the production of nitric oxide, both potentially derived from the enzymatic conversion of L-Arg. In the presence of insulin, cellular ATP levels were significantly increased by L-Arg, L-Glu and L-Lys as well. These data suggest that metabolic degradation of L-Arg not related to citric acid cycle activity is important in the mechanism by which L-Arg enhances insulin-stimulated glycogen synthesis.