title: The AMPK pathway mediates an anti-adipogenic effect of fruits of Hovenia dulcis Thunb.
abstract: Hovenia dulcis Thunb. is well known as a treatment for liver disease. Several studies have demonstrated that extracts of Hovenia dulcis Thunb. or its purified compounds can serve as detoxifying agents for alcohol poisoning. However, its anti-obesity effect has not been reported thus far. In this study, the anti-obesity effect of water extracts from the fruits or stems of Hovenia dulcis Thunb. was examined in 3T3-L1 preadipocytes. The cellular lipid contents in 3T3-L1 adipocytes were assessed by Oil Red O staining. Fruits of Hovenia dulcis Thunb. (FHD) significantly inhibit lipid accumulation during adipogenesis in a dose-dependent manner, but not stems of Hovenia dulcis Thunb. FHD (100 μg ml(-1)) significantly down-regulates the expression of the peroxisome proliferator-activated receptor-γ, CCAAT/enhancer-binding protein-α, adipocyte fatty acid-binding protein 2, adiponectin, and resistin, and the inhibition rates were 29.33%, 54.36%, 34.5%, 55.69%, and 60.39%, respectively. In addition, FHD (100 μg ml(-1)) also up-regulates the phosphorylation of AMP-activated protein kinase (AMPK)-α, liver kinase B1 as a major AMPK kinase, and the downstream substrate acetyl-CoA carboxylase, and the inhibition rates were 43.52%, 38.25%, and 20.39%, respectively. These results indicate that FHD has a significant anti-obesity effect through the modulation of the AMPK pathway, suggesting that FHD has a potential benefit in preventing obesity.
authors.affiliation: College of Korean Medicine, Institute of Korean Medicine, Kyung Hee University, 26, Kyungheedae-ro, Dongdaemun-gu, Seoul, Republic of Korea. jyum@khu.ac.kr.
authors.forename: Hye-Lin
authors.initials: HL
authors.lastname: Kim
authors.forename: Jung-Eun
authors.initials: JE
authors.lastname: Sim
authors.forename: Hyun-Myung
authors.initials: HM
authors.lastname: Choi
authors.forename: In-Young
authors.initials: IY
authors.lastname: Choi
authors.forename: Mi-Young
authors.initials: MY
authors.lastname: Jeong
authors.forename: Jinbong
authors.initials: J
authors.lastname: Park
authors.forename: Yunu
authors.initials: Y
authors.lastname: Jung
authors.forename: Dong-Hyun
authors.initials: DH
authors.lastname: Youn
authors.forename: Jung-Hee
authors.initials: JH
authors.lastname: Cho
authors.forename: Ji-Hyun
authors.initials: JH
authors.lastname: Kim
authors.forename: Min-Woo
authors.initials: MW
authors.lastname: Hwang
authors.forename: Jong-Sik
authors.initials: JS
authors.lastname: Jin
authors.forename: Seung-Heon
authors.initials: SH
authors.lastname: Hong
authors.forename: Hyun-Woo
authors.initials: HW
authors.lastname: Cho
authors.forename: Jae-Young
authors.initials: JY
authors.lastname: Um
mesh_terms: D041721:3T3-L1 Cells; D055372:AMP-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism*; D000103:Acetyl-CoA Carboxylase / Q000235:genetics / Q000378:metabolism; D017667:Adipocytes / Q000187:drug effects; D050156:Adipogenesis / Q000187:drug effects*; D052242:Adiponectin / Q000378:metabolism; D000818:Animals; D022762:CCAAT-Enhancer-Binding Proteins / Q000235:genetics / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D015536:Down-Regulation; D050556:Fatty Acid-Binding Proteins / Q000235:genetics / Q000378:metabolism; D005638:Fruit / Q000737:chemistry*; D051379:Mice; D009765:Obesity / Q000517:prevention & control; D047495:PPAR gamma / Q000235:genetics / Q000378:metabolism; D010766:Phosphorylation; D010936:Plant Extracts / Q000494:pharmacology*; D052243:Resistin / Q000378:metabolism; D027823:Rhamnaceae / Q000737:chemistry*; D015398:Signal Transduction / Q000187:drug effects*; D015854:Up-Regulation
chemical_list: D052242:Adiponectin; D022762:CCAAT-Enhancer-Binding Proteins; C530718:CEBPA protein, mouse; D050556:Fatty Acid-Binding Proteins; D047495:PPAR gamma; D010936:Plant Extracts; D052243:Resistin; D055372:AMP-Activated Protein Kinases; D000103:Acetyl-CoA Carboxylase