Structure-Dependent Inhibitory Effects of Green Tea Catechins on Insulin Secretion from Pancreatic β-Cells

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  • Kaneko Yukiko K.
    Department of Pharmacology, Graduate School of Pharmaceutical Sciences, University of Shizuoka
  • Takii Miki
    Department of Pharmacology, Graduate School of Pharmaceutical Sciences, University of Shizuoka
  • Kojima Yumiko
    Department of Pharmacology, Graduate School of Pharmaceutical Sciences, University of Shizuoka
  • Yokosawa Hiroko
    Department of Pharmacology, Graduate School of Pharmaceutical Sciences, University of Shizuoka
  • Ishikawa Tomohisa
    Department of Pharmacology, Graduate School of Pharmaceutical Sciences, University of Shizuoka

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The effects of green tea catechins on glucose-stimulated insulin secretion (GSIS) were investigated in the β-cell line INS-1D. Epigallocatechin gallate (EGCG) at 10 µM or gallocatechin gallate (GCG) at 30 µM caused significant inhibitory effects on GSIS, and each of these at 100 µM almost abolished it. In contrast, epicatechin (EC) or catechin (CA) had no effect on GSIS at concentrations up to 100 µM. We thus investigated the structure–activity relationship by using epigallocatechin (EGC) and gallocatechin (GC) containing a trihydroxyl group in the B-ring, and epicatechin gallate (ECG) and catechin gallate (CG) containing the gallate moiety. EGC, GC, and ECG caused an inhibition of GSIS, although significant effects were obtained only at 100 µM. At this concentration, EGC almost abolished GSIS, whereas GC and ECG partially inhibited it. In contrast, CG did not affect GSIS at concentrations up to 100 µM. EGCG also abolished the insulin secretion induced by tolbutamide, an ATP-sensitive K+ channel blocker, and partially inhibited that induced by 30 mM K+. Moreover, EGCG, but not EC, inhibited the oscillation of intracellular Ca2+ concentration induced by 11.1 mM glucose. These results suggest that some catechins at supraphysiological concentrations have inhibitory effects on GSIS, the potency of which depends on their structure; the order of potency was EGCG>GCG>EGC>GC≈ECG. The inhibitory effects seem to be mediated by the inhibition of voltage-dependent Ca2+ channels, which is caused, at least in part, by membrane hyperpolarization resulting from the activation of K+ channels.

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