[#2011-10] Poria Li, Tzu-Hsuan et al. Anti-Hyperglycemic properties of Crude Extract and Triterpenes from Poria cocos

Anti-Hyperglycemic Properties of Crude Extract and Triterpenes from Poria cocos

Tzu-Hsuan Li,1,2 Chia-Chung Hou,1 Cicero Lee-Tian Chang,3 and Wen-Chin Yang1,2,4,5

1Agricultural Biotechnology Research Center, Academia Sinica Taipei 115, Taiwan

2Department and Institute of Pharmacology, National Yang-Ming University Taipei 112, Taiwan

3Department of Veterinary Medicine, National Chung Hsing University Taichung, Taiwan

4Institute of Zoology, National Taiwan University Taipei 10617, Taiwan

5Department of Life Sciences, National Chung Hsing University Taichung, Taiwan

 

Poria cocos, Bai Fu Ling in Chinese, is used in traditional Chinese medicine to treat diabetes. However, its claimed benefits and mechanism are not fully understood. This study aimed to investigate the effect and action of P. cocos on type 2 diabetes. We first performed phytochemical analysis on the crude extract and factions of P. cocos. P. cocos crude extract at 50 mg/kg body weight or more significantly decreased blood glucose levels in db/db mice. Based on a bioactivity-directed fractionation and isolation (BDFI) strategy, chloroform fraction and subfractions 4 and 6 of the P. cocos crude extract possessed a blood glucose-lowering effect. Dehydrotumulosic acid, dehydrotrametenolic acid, and pachymic acid were identified from the chloroform sub-fractions 4, 3, and 2, respectively. Dehydrotumulosic acid had anti-hyperglycemic effect to a greater extent than dehydrotrametenolic acid and pachymic acid. Mechanistic study on streptozocin- (STZ-) treated mice showed that the crude extract, dehydrotumulosic acid, dehydrotrametenolic acid, and pachymic acid of P. cocos exhibited different levels of insulin sensitizer activity. However, the P. cocos crude extract and triterpenes appeared not to activate PPAR-γ pathway. Overall, the data suggest that the P. cocos extract and its triterpenes reduce postprandial blood glucose levels in db/db mice via enhanced insulin sensitivity irrespective of PPAR-γ.