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Enhancing Effect of Extracts of Phellodendri Cortex on Glucose Uptake in Normal and Insulin-resistant 3T3-L1 Adipocytes  

Kim, So-Hui (Department of Biotechnology, Graduate School, Handong Global University)
Shin, Eun-Jung (Department of Biotechnology, Graduate School, Handong Global University)
Hyun, Chang-Kee (Department of Biotechnology, Graduate School, Handong Global University,School of Life and Food Sciences, Handong Global University)
Publication Information
Korean Journal of Pharmacognosy / v.36, no.4, 2005 , pp. 291-298 More about this Journal
Abstract
Anti-hyperglycemic effects of 17 medicinal plants that have been used for ameliorating diabetes in oriental medicine were evaluated using glucose transport assay in 3T3-L1 adipocytes. Higher activities were obtained by treating water or alcohol extract of Phellodendri Cortex (PC), which showed enhancing effects both on basal and insulin-stimulated glucose uptake. The latter effect of PC was completely inhibited by wortmannin, a specific inhibitor for phosphatidyl inositol 3-kinase (PI 3-kinase), but not affected by SB203580, A specific inhibitor for p38 mitogen-activatedprotein kinase(MAPK). Genistein, an inhibitor for tyrosine kinases, abolished the PC effects completely. Treatment of vanadate, an inhibitor for tyrosine phosphatases, together with PC showed no significant synergic enhancement in glucose uptake. The results of inhibitors associated with insulin signaling pathway indicated that extracts of PC enhance glucose uptake by PI-3 kinase activation which is an upstream event for GLUT4 translocation. Antidiabetic effects of PC extract might be also due to enhanced tyrosine phosphorylation and reduced tyrosine dephosphorylation. In addition, PC accelerated insulin-stimulated glucose uptake in insulin-resistant cells, recovering the uptake level close to that of normal cells. These findings may offer a new way to utilize extracts of PC as novel anti-hyperglycemic agents.
Keywords
Phellodendri Cortex; anti-hyperglycemic effect; glucose uptake; insulin resistance; 3T3-L1 adipocytes;
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