Planta Med 2010; 76(15): 1694-1698
DOI: 10.1055/s-0030-1249877
Pharmacology
Letters
© Georg Thieme Verlag KG Stuttgart · New York

Green Tea Epigallocatechin Gallate Inhibits Insulin Stimulation of Adipocyte Glucose Uptake via the 67-Kilodalton Laminin Receptor and AMP-Activated Protein Kinase Pathways

Chi-Fen Hsieh1 [*] , Yi-Wei Tsuei2 [*] , Chi-Wei Liu1 , Chung-Cheng Kao2 , Li-Jane Shih3 , Low-Tone Ho4 , Liang-Yi Wu5 , Chi-Peng Wu1 , Pei-Hua Tsai1 , Hsin-Huei Chang1 , Hui-Chen Ku1 , Yung-Hsi Kao1
  • 1Department of Life Sciences, National Central University, Jhongli, Taiwan
  • 2Department of Emergency, Armed Forces Taoyuan General Hospital, Taoyuan, Taiwan
  • 3Department of Joint Laboratory, Armed Forces Taoyuan General Hospital, Taoyuan, Taiwan
  • 4Department of Internal Medicine, Veterans General Hospital, Taipei, Taiwan
  • 5Department of Bioscience Technology, Chung-Yuan Christian University, Jhongli, Taiwan
Further Information

Publication History

received January 16, 2010 revised March 25, 2010

accepted March 29, 2010

Publication Date:
07 May 2010 (online)

Abstract

Insulin and (−)-epigallocatechin gallate (EGCG) are reported to regulate obesity and fat accumulation, respectively. This study investigated the pathways involved in EGCG modulation of insulin-stimulated glucose uptake in 3T3-L1 and C3H10T1/2 adipocytes. EGCG inhibited insulin stimulation of adipocyte glucose uptake in a dose- and time-dependent manner. The concentration of EGCG that decreased insulin-stimulated glucose uptake by 50–60 % was approximately 5–10 µM for a period of 2 h. At 10 µM, EGCG and gallic acid were more effective than (−)-epicatechin, (−)-epigallocatechin, and (−)-epicatechin 3-gallate. We identified the EGCG receptor [also known as the 67-kDa laminin receptor (67LR)] in fat cells and extended the findings for this study to clarify whether EGCG-induced changes in insulin-stimulated glucose uptake in adipocytes could be mediated through the 67LR. Pretreatment of adipocytes with a 67LR antibody, but not normal rabbit immunoglobulin, prevented the effects of EGCG on insulin-increased glucose uptake. This suggests that the 67LR mediates the effect of EGCG on insulin-stimulated glucose uptake in adipocytes. Moreover, pretreatment with an AMP-activated protein kinase (AMPK) inhibitor, such as compound C, but not with a glutathione (GSH) activator, such as N-acetyl-L-cysteine (NAC), blocked the antiinsulin effect of EGCG on adipocyte glucose uptake. These data suggest that EGCG exerts its anti-insulin action on adipocyte glucose uptake via the AMPK, but not the GSH, pathway. The results of this study possibly support that EGCG mediates fat content.

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1 These authors contributed equally to this work.

Dr. Yung-Hsi Kao

Department of Life Science
National Central University

No. 300, Jhongda Road

Jhongli City, Taoyuan County 32001

Taiwan

Phone: + 88 6 34 26 08 39

Fax: + 88 6 34 22 84 82

Email: ykao@cc.ncu.edu.tw

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