ARGININE AND INSULIN RESPONSE IN ADIPOCYTES

本研究旨在明确L-精氨酸(L-精氨酸)的作用。 在分化的3T3-L1脂肪细胞培养中的糖代谢。 L-精氨酸单独对2-脱氧葡萄糖摄取或基础糖原无影响 但这种氨基酸增加了153±10%(p&lt；0.01)。 在胰岛素处理的细胞中，将葡萄糖掺入糖原。 L-精氨酸的主要代谢产物--L-谷氨酸(L-谷氨酸)也有所增强 胰岛素刺激的糖原合成。对胰岛素的反应不是 被L-赖氨酸(L-赖氨酸)改变，但L-精氨酸的作用显著 由L-赖斯衰减。L-精氨酸显著促进细胞孵育 精氨酸酶介导的尿素合成，而L-赖斯取消了这一反应。 L精氨酸对胰岛素刺激的糖原合成的促进作用 似乎不是由于多胺的产生或 一氧化氮的产生，两者都可能来自酶促反应 L-阿格的转换。在胰岛素存在的情况下，细胞内的ATP水平 L-精氨酸、L-Glu和L-赖斯也显著增加。这些 数据提示L-精氨酸的代谢降解与柠檬酸无关 酸循环活性在L-精氨酸增强的机制中起重要作用 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.