Deaciuc I V, Spitzer J A
Department of Physiology, Louisiana State University Medical Center, New Orleans 70112-1393.
Proc Soc Exp Biol Med. 1991 Jun;197(2):193-6. doi: 10.3181/00379727-197-43245.
Previous experimental data documenting an insulin like-effect of 12-O-tetradecanoyl phorbol 13-acetate (TPA), a specific activator of protein kinase C, on glucose transport in adipocytes prompted us to test the hypothesis that TPA might display another insulin-like effect, i.e., antagonize catecholamine-induce lipolysis. TPA (100 nM) led to a decrease of both free fatty acid (41%) and glycerol (58%) release due to 1 microM norepinephrine stimulation in isolated rat adipocytes. TPA also diminished the antilipolytic effect of insulin (5 ng.ml-1) in the presence of 1 microM norepinephrine. Thus, the residual lipolysis with insulin was 25% for free fatty acids and 24% for glycerol release. In the presence of TPA, these values increased to 50% and 45%, respectively. TPA (100 nM) addition to isolated adipocytes induced protein kinase C translocation from the cytosol to the membrane fraction. In control cells, 94.7 +/- 2.9% of the enzyme was found in the cytosol, with the rest found in the membrane. At 10 min after TPA (100 nM) addition, the corresponding value was 43.6 +/- 17.4%, with the rest in the membrane (n = 6, P less than 0.05). These findings indicate that protein kinase C might be involved not only in the insulin action on glucose transport, but also in the mechanism of insulin's antilipolytic action.
先前的实验数据表明，蛋白激酶C的特异性激活剂12 - O - 十四烷酰佛波醇13 - 乙酸酯（TPA）对脂肪细胞中的葡萄糖转运具有胰岛素样作用，这促使我们检验TPA可能具有另一种胰岛素样作用的假说，即拮抗儿茶酚胺诱导的脂解作用。在分离的大鼠脂肪细胞中，TPA（100 nM）可使1 microM去甲肾上腺素刺激引起的游离脂肪酸释放（41%）和甘油释放（58%）均减少。在存在1 microM去甲肾上腺素的情况下，TPA还减弱了胰岛素（5 ng.ml-1）的抗脂解作用。因此，胰岛素存在时的残余脂解作用，游离脂肪酸释放为25%，甘油释放为24%。在存在TPA的情况下，这些值分别增至50%和45%。向分离的脂肪细胞中添加TPA（100 nM）可诱导蛋白激酶C从胞质溶胶转位至膜部分。在对照细胞中，94.7±2.9%的该酶存在于胞质溶胶中，其余存在于膜中。添加TPA（100 nM）后10分钟，相应的值为43.6±17.4%，其余存在于膜中（n = 6，P < 0.05）。这些发现表明，蛋白激酶C可能不仅参与胰岛素对葡萄糖转运的作用，还参与胰岛素抗脂解作用的机制。
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