Abstract Title:

Bixin regulates mRNA expression involved in adipogenesis and enhances insulin sensitivity in 3T3-L1 adipocytes through PPARgamma activation.

Abstract Source:

Biochem Biophys Res Commun. 2009 Dec 25 ;390(4):1372-6. Epub 2009 Nov 3. PMID: 19891958

Abstract Author(s):

Nobuyuki Takahashi, Tsuyoshi Goto, Aki Taimatsu, Kahori Egawa, Sota Katoh, Tatsuya Kusudo, Tomoya Sakamoto, Chie Ohyane, Joo-Young Lee, Young-Il Kim, Taku Uemura, Shizuka Hirai, Teruo Kawada

Article Affiliation:

Nobuyuki Takahashi


Insulin resistance is partly due to suppression of insulin-induced glucose uptake into adipocytes. The uptake is dependent on adipocyte differentiation, which is controlled at mRNA transcription level. The peroxisome proliferator-activated receptor (PPAR), a ligand-regulated nuclear receptor, is involved in the differentiation. Many food-derived compounds serve as ligands to activate or inactivate PPAR. In this study, we demonstrated that bixin and norbixin (annatto extracts) activate PPARgamma by luciferase reporter assay using GAL4-PPAR chimera proteins. To examine the effects of bixin on adipocytes, 3T3-L1 adipocytes were treated with bixin or norbixin. The treatment induced mRNA expression of PPARgamma target genes such as adipocyte-specific fatty acid-binding protein (aP2), lipoprotein lipase (LPL), and adiponectin in differentiated 3T3-L1 adipocytes and enhanced insulin-dependent glucose uptake. The observations indicate that bixin acts as an agonist of PPARgamma and enhances insulin sensitivity in 3T3-L1 adipocytes, suggesting that bixin is a valuable food-derived compound as a PPAR ligand to regulate lipid metabolism and to ameliorate metabolic syndrome.

Study Type : In Vitro Study

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