title: Ginsenoside Rh1 ameliorates high fat diet-induced obesity in mice by inhibiting adipocyte differentiation.
abstract: Ginseng (the root of Panax ginseng C. A. MEYER), which contains protopanaxadiols and protopanaxatriols as its main constituents, has been used for many disorders, such as cancer, diabetes, inflammation, and hyperlipidemia. Of these ginsenosides, protopanaxadiol ginsenoside Rh2 alone is reported to inhibit adipogenesis in 3T3-L1 in vitro. Therefore, we investigated the effect of protopanaxatriol ginsenoside Rh1 on adipogenesis in 3T3-L1 cells and high fat diet-induced obesity (DIO) mice. Treatment with ginsenoside Rh1 inhibited adipogenesis, as evidenced by Oil red O staining and lipid droplet extraction assay. Reverse transcription-polymerase chain reaction (RT-PCR) analysis revealed that ginsenoside Rh1 decreased the expressions of peroxisome proliferator-activated receptor (PPAR)-γ, CCAAT/enhancer-binding protein (C/EBP)-α, fatty acid synthase, and adipocyte fatty acid-binding protein. Oral administration of ginsenoside Rh1 (20 mg/kg) suppressed body and epididymal fat weight gains and plasma triglyceride level in DIO mice. Ginsenoside Rh1 also inhibited the expressions of PPAR-γ, C/EBP-α, fatty acid synthase, adipocyte fatty acid-binding protein, as well as F4/80, CD68, tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β in DIO mice by real time PCR analysis. Based on these findings, ginsenoside Rh1 may ameliorate obesity, by inhibiting adipocyte differentiation and inflammation.
authors.affiliation: Department of Life and Nanopharmaceutical Sciences, Kyung Hee University, Seoul 130–701, Republic of Korea.
authors.forename: Wan
authors.initials: W
authors.lastname: Gu
authors.forename: Kyung-Ah
authors.initials: KA
authors.lastname: Kim
authors.forename: Dong-Hyun
authors.initials: DH
authors.lastname: Kim
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D000818:Animals; D019440:Anti-Obesity Agents / Q000494:pharmacology / Q000627:therapeutic use*; D022763:CCAAT-Enhancer-Binding Protein-alpha / Q000235:genetics; D002454:Cell Differentiation / Q000187:drug effects; D002784:Cholesterol / Q000097:blood; D016207:Cytokines / Q000378:metabolism; D059305:Diet, High-Fat; D004822:Epididymis / Q000187:drug effects / Q000378:metabolism; D064429:Fatty Acid Synthases / Q000235:genetics; D050556:Fatty Acid-Binding Proteins / Q000235:genetics; D036145:Ginsenosides / Q000494:pharmacology / Q000627:therapeutic use*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000188:drug therapy* / Q000378:metabolism; D047495:PPAR gamma / Q000235:genetics; D014280:Triglycerides / Q000097:blood
chemical_list: D019440:Anti-Obesity Agents; D022763:CCAAT-Enhancer-Binding Protein-alpha; D016207:Cytokines; D050556:Fatty Acid-Binding Proteins; D036145:Ginsenosides; D047495:PPAR gamma; D014280:Triglycerides; C425564:ginsenoside Rh1; D002784:Cholesterol; D064429:Fatty Acid Synthases