Proanthocyanidins from Chinese bayberry (Myrica rubra Sieb. et Zucc.) leaves regulate lipid metabolism and glucose consumption by activating AMPK pathway in HepG2 cells

• Published in: Journal of functional foods Vol. 29; pp. 217 - 225
• Main Authors: Zhang, Yu, Chen, Shiguo, Wei, Chaoyang, Chen, Jianchu, Ye, Xingqian
• Format: Journal Article
• Language: English
• Published: Elsevier Ltd 01.02.2017; Elsevier
• Subjects: AMPK; Chinese bayberry leaves; Glucose metabolism; Lipid metabolism; Proanthocyanidins; Chinese bayberry leaves; Glucose metabolism; AMPK; Lipid metabolism; Proanthocyanidins
• ISSN: 1756-4646; 2214-9414
• DOI: 10.1016/j.jff.2016.12.030

•BLPs reduced the activity of pancreatic lipase.•SPBLPs and UDBLPs significantly activated AMPK in dose dependent manner.•SPBLPs and UDBLPs reduced triglycerides synthesis by phosphorylating ACC.•SPBLPs and UDBLPs reduced sterols biosynthesis by mainly inhibiting SREBP-1.•SPBLPs promoted glucose consumption in HepG2 cells. The increasing rate of hyperlipidemia has drawn great attention and natural products may play a potential role in prevention of these disorders. Chinese bayberry leaves proanthocyanidin (BLPs) with epigallocatechin-3-O-gallate (EGCG) as its terminal and major extension units is unusual in the plant kingdom. Crude, purified and ultrasound depolymerized BLPs (CBLPs, SPBLPs and UDBLPs) were prepared with the aim to investigate their hypolipidemic mechanisms. BLPs inhibited the lipase activity in vitro and reduced the accumulation of total triacylglycerols (TAG) and cholesterol induced by oleic acid in HepG2 cells. SPBLPs and UDBLPS significantly increased the phosphorylation of AMP-activated protein kinase (AMPK) and thus reduced TAG and sterols biosynthesis by inhibiting its downstream proteins, such as acetyl-CoA carboxylase, 3-hydroxy-3-methylglutaryl-CoA reductase and sterol regulatory element-binding protein. BLPs also promoted glucose consumption in oleic acid induced HepG2 cells. Overall, this study suggests the hypolipidemic property and promotion of glucose consumption of BLPs via AMPK pathway.