Yamauchi K, Hashizume K, Miyamoto T, Otsuka H, Ichikawa K, Nishii Y, Yamada T
Department of Gerontology, Endocrinology, and Metabolism, Shinshu University School of Medicine, Matsumoto, Japan.
Endocrinology. 1988 Dec;123(6):2800-4. doi: 10.1210/endo-123-6-2800.
Previously we demonstrated that glucagon inhibits high affinity insulin binding without influence on low affinity binding in rat adipocytes in vitro. In this study we investigated the effects of glucagon on insulin actions in adipocytes in vitro. Glucagon modified neither glucose oxidation nor lipogenesis stimulated by insulin. The antilipolytic action of insulin was decreased by preincubation of the cells with glucagon. Glucose transport enhanced by insulin was diminished by preincubation of the cells with glucagon. The decrease in antilipolysis was a lowering of the maximal response to insulin, whereas the decrease in glucose transport was a lowering of the sensitivity to insulin. These results suggested that glucagon does not necessarily inhibit all of the insulin actions, and that the mechanism of insulin stimulation of glucose transport, which is supposed to be mediated by glucagon-sensitive insulin receptor, is different from those of insulin-induced antilipolysis, glucose oxidation, and lipogenesis.
此前我们证明，在体外培养的大鼠脂肪细胞中，胰高血糖素可抑制高亲和力胰岛素结合，而不影响低亲和力结合。在本研究中，我们调查了胰高血糖素对体外培养的脂肪细胞中胰岛素作用的影响。胰高血糖素既不改变胰岛素刺激的葡萄糖氧化，也不改变脂肪生成。用胰高血糖素预孵育细胞可降低胰岛素的抗脂解作用。用胰高血糖素预孵育细胞可减少胰岛素增强的葡萄糖转运。抗脂解作用的降低是胰岛素最大反应的降低，而葡萄糖转运的降低是对胰岛素敏感性的降低。这些结果表明，胰高血糖素不一定抑制所有胰岛素作用，并且胰岛素刺激葡萄糖转运的机制（该机制被认为由对胰高血糖素敏感的胰岛素受体介导）与胰岛素诱导的抗脂解、葡萄糖氧化和脂肪生成的机制不同。
