胰岛素调节大鼠脂肪细胞中蛋白激酶C同工型的信使核糖核酸。

Insulin regulated PKC isoform mRNA in rat adipocytes.

作者信息

Ishizuka T, Kajita K, Yamada K, Miura A, Kanoh Y, Ishizawa M, Wada H, Itaya S, Yamamoto M, Yasuda K, Nagata K, Okano Y

机构信息

Third Department of Internal Medicine, Gifu University School of Medicine, Japan.

出版信息

Diabetes Res Clin Pract. 1996 Aug;33(3):159-67. doi: 10.1016/0168-8227(96)01324-1.

DOI:10.1016/0168-8227(96)01324-1

PMID:8922537

Abstract

Insulin and 12-O-tetradecanoyl phorbol-13-acetate (TPA) induce both glucose uptake and translocation of protein kinase C (PKC) from cytosol to membrane in insulin-sensitive tissues as previously reported by several investigators. We examined insulin-mediated PKC beta I, beta II, and epsilon translocation from cytosol to cytoskeleton, and expression of PKC alpha, beta I, beta II, gamma, and epsilon isoforms using the reverse transcription polymerase chain reaction (RT-PCR) method during treatment with insulin for 240 min in rat adipocytes. Insulin-induced increases in PKC beta I, beta II, and epsilon were greater in the cytoskeleton fraction than those in the membrane fraction. Insulin induced time-dependent increases in PKC alpha, gamma, epsilon and zeta mRNA levels for up to 240 min (555%, 117%, 236% and 138% increase, respectively). TPA also induced time-dependent increases in PKC alpha and gamma (34% and 500% increase, respectively) but not in PKC zeta. However, PKC beta I mRNA was decreased for up to 60 min and then maintained at under the basal level during stimulation with insulin and TPA. On the other hand, PKC beta II mRNA was markedly increased for up to 240 min. These results suggest that insulin-regulated PKC alpha, gamma and epsilon mRNA levels and PKC beta mRNA alternative splicing may occur in rat adipocytes.

摘要

如先前几位研究者所报道，胰岛素和12 - O - 十四烷酰佛波醇 - 13 - 乙酸酯（TPA）可诱导胰岛素敏感组织中的葡萄糖摄取以及蛋白激酶C（PKC）从胞质溶胶向细胞膜的转位。我们使用逆转录聚合酶链反应（RT - PCR）方法，检测了大鼠脂肪细胞在胰岛素处理240分钟期间，胰岛素介导的PKCβI、βII和ε从胞质溶胶向细胞骨架的转位，以及PKCα、βI、βII、γ和ε亚型的表达。胰岛素诱导的PKCβI、βII和ε在细胞骨架部分的增加幅度大于在细胞膜部分。胰岛素诱导PKCα、γ、ε和ζ的mRNA水平随时间增加，直至240分钟（分别增加555%、117%、236%和138%）。TPA也诱导PKCα和γ随时间增加（分别增加34%和500%），但不诱导PKCζ。然而，PKCβI的mRNA在长达60分钟时下降，然后在胰岛素和TPA刺激期间维持在基础水平以下。另一方面，PKCβII的mRNA在长达240分钟时显著增加。这些结果表明，在大鼠脂肪细胞中可能发生胰岛素调节的PKCα、γ和ε的mRNA水平以及PKCβ的mRNA可变剪接。