PHOSPHATIDIC-ACID AND PHOSPHATIDYLINOSITOL LABELING IN ADIPOSE-TISSUE - RELATIONSHIP TO THE METABOLIC EFFECTS OF INSULIN AND INSULIN-LIKE AGENTS
PHOSPHATIDIC-ACID AND PHOSPHATIDYLINOSITOL LABELING IN ADIPOSE-TISSUE - RELATIONSHIP TO THE METABOLIC EFFECTS OF INSULIN AND INSULIN-LIKE AGENTS
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DOI：
10.1042/bj2120489
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发表时间：
1983-01-01
影响因子：
4.1
通讯作者：
SCHIMMEL, RJ
中科院分区：
文献类型：
--
作者：
HONEYMAN, TW;STROHSNITTER, W;SCHIMMEL, RJ
在大鼠脂肪组织和分离的脂肪细胞中，暴露于磷脂酶C可使[~(32)P]PI掺入磷脂酸盐、磷脂酸-磷脂酸酯和磷脂酰肌醇。在胰岛素和催产素的反应中也观察到了类似的效果。茶碱、3-异丁基-1-甲基黄嘌呤和腺苷脱氨酶使[~(32)P]PI参入减少，腺苷和N_6-苯基异丙基腺苷则逆转这些作用。与胰岛素一样，脂肪组织暴露在磷脂酶C下会刺激葡萄糖、丙酮酸和亮氨酸的氧化，并激活丙酮酸脱氢酶。催产素和腺苷也模拟了胰岛素对亮氨酸氧化和丙酮酸脱氢酶的影响。只有胰岛素刺激糖原合酶活性，提示合酶的调节可能是通过不同于调节磷脂代谢、糖运输和线粒体酶活性变化的细胞内事件来实现的。显然，暴露在磷脂酶C下会形成二酰基甘油，它被磷酸化生成磷脂酸盐。CMP-磷脂酸盐和磷脂酰肌醇的标记增加是磷脂酸盐转化为这些脂类的结果。磷脂酶C对磷脂酸盐合成的影响与脂肪组织代谢变化之间的相关性表明，磷脂酶C的增加可能直接或间接地导致膜转运和酶活性的变化。胰岛素、腺苷和催产素产生的磷脂标记模式表明，这些刺激也可能增加磷脂酸盐的合成，如果是这样的话，磷脂代谢的变化可能解释了这些刺激的一些代谢作用。
Exposure to phospholipase C increased the incorporation of [32P]Pi into phosphatidate, CMP-phosphatidate and phosphatidylinositol in rat adipose tissue and isolated adipocytes. A similar effect was observed in response to insulin and oxytocin. Theophylline, 3-isobutyl-1-methylxanthine and adenosine deaminase decreased [32P]Pi incorporation, and adenosine and N6-phenylisopropyladenosine reversed these effects. As with insulin, exposure of adipose tissue to phospholipase C stimulated oxidation of glucose, pyruvate and leucine, and activated pyruvate dehydrogenase. Oxytocin and adenosine also mimicked the effects of insulin on leucine oxidation and pyruvate dehydrogenase. Only insulin stimulated glycogen synthase activity, indicating that the regulation of synthase may be achieved by intracellular events distinct from those regulating changes in phospholipid metabolism, sugar transport and mitochondrial enzyme activities. Apparently, exposure to phospholipase C forms diacylglycerol, which is phosphorylated to yield phosphatidate. The increased labeling of CMP-phosphatidate and phosphatidylinositol results from the conversion of phosphatidate into these lipids. The correlation between the effects of phospholipase C on phosphatidate synthesis and changes in adipose-tissue metabolism suggests the possibility that increased phosphatidate may directly or indirectly produce changes in membrane transport and enzyme activities. The pattern of phospholipid labeling produced by insulin, adenosine and oxytocin suggests that these stimuli may also increase phosphatidate synthesis, and, if so, changes in phospholipid metabolism could account for some of the metabolic actions of these stimuli.