| Autor: |
Ishizuka, Tatsuo, Miura, Atsushi, Kajita, Kazuo, Ishizawa, Masayoshi, Kimura, Mika, Huang, Yannan, Kawai, Yasunori, Morita, Hiroyuki, Uno, Yoshihiro, Yasuda, Keigo |
| Předmět: |
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| Zdroj: |
IUBMB Life; May2001, Vol. 51 Issue 5, p299-304, 6p, 2 Diagrams, 1 Graph |
| Abstrakt: |
Insulin stimulates glucose uptake in association with phosphatidylinositol (PI) 3-kinase activation mechanisms in rat adipocytes. Insulin stimulated glucose uptake to 6.5-fold, and 12-o-tetradecanoyl phorbol 13-acetate (TPA) also stimulated glucose uptake to 4.5-fold in rat adipocytes. We examined these differences in glucose uptake, PKCζ activation, and PI 3-kinase activation after stimulation with insulin and TPA. TPA stimulated PI 3-kinase activity and increased the p85 subunit of PI 3-kinase immunoreactivity in anti-phosphotyrosine antibody-immunoprecipitated protein. Insulin and TPA provoked increases in membrane PKC ζ immunoreactivity.The PI 3-kinase inhibitor,wortmannin, suppressed insulin-induced increases in glucose uptake, PI 3-kinase activity, and PKCζ activation. Wortmannin also suppressed TPA-induced PI 3-kinase activity and PKCζ activation but suppressed TPA-induced glucose uptake to only a small extent. The PKC inhibitor, Go6976, which only inhibits conventional PKCα and _, suppressed TPA-induced glucose uptake, but suppressed insulin-induced glucose uptake to only a small extent. On the other hand, the PKC inhibitor, RO32-0432, which inhibits conventional, novel, and atypical PKCs, markedly suppressed both insulin- and TPA-induced glucose uptake. These results suggest that insulin-induced glucose uptake is mainly mediated by PI 3-kinase-PKCζ signaling, whereas phorbol ester-induced glucose uptake is mainly mediated by conventional PKC despite PI 3-kinase and PKCζ activations. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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