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Capscoside G suppresses adipogenesis by regulating the expression of adipogenic transcription factors and the activation of AMP‐activated protein kinase (1045.12)
Author(s) -
Sung Jeehye,
Lim Yongrae,
Lee Junsoo
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1045.12
Subject(s) - adipogenesis , ampk , protein kinase a , adipocyte , chemistry , amp activated protein kinase , adipocyte protein 2 , glycerol kinase , intracellular , kinase , microbiology and biotechnology , biochemistry , fatty acid , biology , adipose tissue , enzyme
Obesity is a health hazard which is closely associated with various complications including insulin resistance and type 2 diabetes. Capsicoside G isolated from pepper seeds is widely known for antioxidant and anti‐inflammatory activities. However, the mechanism for its anti‐adipogenic effect has largely remained unknown. The objective of this study was to elucidate anti‐adipogenic mechanism of capsicoside G. Preadipocyte differentiation was induced in the presence or absence of capsicoside G for 4 days. After differentiation intracellular lipids were stained with Oil Red O and colorimetric intensity was measured. The expression of proteins associated with adipogenesis was measured using western blotting. The mRNA levels of fatty acid oxidation genes were also confirmed by real‐time PCR. Capsicoside G dose‐dependently inhibited intracellular lipid droplet accumulation in adipocyte without cytotoxicity. Treatments with capsicoside G inhibited the expression of the key adipocyte differentiation regulators and their target genes such as fatty acid binding protein (aP2). Moreover, capsicoside G significantly increased activation of 5’‐adenosine monophosphate‐activated protein kinase (AMPK), a major regulator of cellular energy balance, phosphorylation. This study also investigated the involvement of AMPK in the expression of a major transcription factor, PPARγ. Pretreatment with compound C, a cell permeable inhibitor of AMPK, abolished the inhibitory effects of capsicoside G on PPARγ expression. Moreover, capsicoside G suppressed the expression of glycerol synthesis enzyme GPAT‐1 and increased expression of fatty acid oxidative enzyme CPT‐1. These results suggest that capsicoside G exerts anti‐adipogenic effect on adipocyte differentiation through the activation of the AMPK signaling pathway. Capsicoside G may be a promising compound for the treatment of obesity.