Saggerson D, Orford M, Chatzipanteli K, Shepherd J
Department of Biochemistry and Molecular Biology, University College London, U.K.
Cell Signal. 1991;3(6):613-24. doi: 10.1016/0898-6568(91)90038-v.
(1) Streptozotocin-diabetes decreased the responsiveness of noradrenaline- or forskolin-stimulated lipolysis to inhibition by phenylisopropyladenosine (PIA), prostaglandin E1 (PGE1) and nicotinate in rat adipocytes. (2) Diabetes had no effect on high affinity binding of [3H]PIA to adipocyte plasma membranes. (3) Plasma membranes from diabetic animals had increased abundance of alpha-subunits of Gi1 and Gi2. The effect of pertussis toxin in overcoming inhibition of lipolysis by PIA was delayed in adipocytes from diabetic rats. (4) Diabetes decreased the GTP-dependent right-wards shift in the dose-curve for displacement of the antagonist [3H]DPCPX by PIA in adipocyte plasma membranes. (5) It is concluded that, despite increased abundance of Gi in diabetic adipocytes, less of this is functional. This may contribute to reduced sensitivity to PIA, PGE1 and nicotinate and explains some of the loss of control of lipolysis in insulin-dependent diabetes.
(1) 链脲佐菌素诱导的糖尿病降低了去甲肾上腺素或福斯高林刺激的脂肪分解对苯异丙基腺苷（PIA）、前列腺素E1（PGE1）和烟酸抑制作用的反应性，该反应发生在大鼠脂肪细胞中。(2) 糖尿病对[3H]PIA与脂肪细胞质膜的高亲和力结合没有影响。(3) 糖尿病动物的质膜中Gi1和Gi2的α亚基丰度增加。百日咳毒素克服PIA对脂肪分解抑制作用的效果在糖尿病大鼠的脂肪细胞中延迟出现。(4) 糖尿病降低了脂肪细胞质膜中PIA对拮抗剂[3H]DPCPX置换的剂量曲线中GTP依赖性的右移。(5) 得出的结论是，尽管糖尿病脂肪细胞中Gi的丰度增加，但其功能性的部分较少。这可能导致对PIA、PGE1和烟酸的敏感性降低，并解释了胰岛素依赖型糖尿病中脂肪分解控制丧失的部分原因。
