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J Agric Food Chem. 2016 Feb 3;64(4):821-30. doi: 10.1021/acs.jafc.5b05577. Epub 2016 Jan 25.

Bisdemethoxycurcumin Inhibits Adipogenesis in 3T3-L1 Preadipocytes and Suppresses Obesity in High-Fat Diet-Fed C57BL/6 Mice.

Author information

1
Institute of Food Science and Technology, National Taiwan University , Taipei 10617, Taiwan.
2
Department of Seafood Science, National Kaohsiung Marine University , Kaohsiung, Taiwan.
3
Sabinsa Corporation , 20 Lake Drive, East Windsor, New Jersey 08520, United States.
4
Department of Food Science, Rutgers University , New Brunswick, New Jersey 08901, United States.
5
Department of Obstetrics and Gynecology, Kaohsiung Veterans General Hospital , Kaohsiung, Taiwan.
6
Hubei Key Laboratory of Economic Forest Germplasm Improvement and Resources Comprehensive Utilization, College of Life Science, Huanggang Normal University , Hubei, China.
7
Department of Medical Research, China Medical University Hospital, China Medical University , Taichung 40402, Taiwan.
8
Department of Health and Nutrition Biotechnology, Asia University , Taichung, Taiwan.

Abstract

Obesity is caused by excessive accumulation of body fat and is closely related to complex metabolic diseases. Adipogenesis is a key process that is required in adipocyte hypertrophy in the development of obesity. Curcumin (Cur) has been reported to inhibit adipocyte differentiation, but the inhibitory effects of other curcuminoids present in turmeric, such as demethoxycurcumin (DMC) and bisdemethoxycurcumin (BDMC), on adipogenesis have not been investigated. Here, we investigated the effects of curcuminoids on adipogenesis and the molecular mechanisms of adipocyte differentiation. Among three curcuminoids, BDMC was the most effective suppressor of lipid accumulation in adipocytes. BDMC suppressed adipogenesis in the early stage primarily through attenuation of mitotic clonal expansion (MCE). In BDMC-treated preadipocytes, cell cycle arrest at the G0/G1 phase was found after initiation of adipogenesis and was accompanied by downregulation of cyclin A, cyclin B, p21, and mitogen-activated protein kinase (MAPK) signaling. The protein levels of the adipogenic transcription factors peroxisome proliferator-activated receptor (PPAR)γ and CCAAT/enhancer-binding proteins (C/EBP)α were also reduced by BDMC treatment. Furthermore, 0.5% dietary BDMC (w/w) significantly lowered body weight gain and adipose tissue mass in high-fat diet (HFD)-fed mice. The results of H&E staining showed that dietary BDMC reduced hypertrophy in adipocytes. These results demonstrate for the first time that BDMC suppressed adipogenesis in 3T3-L1 adipocytes and prevented HFD-induced obesity. Our results suggest that BDMC has the potential to prevent obesity.

KEYWORDS:

adipogenesis; bisdemethoxycurcumin (BDMC); high-fat diet; mitotic clonal expansion (MCE); obesity

PMID:
26777574
DOI:
10.1021/acs.jafc.5b05577
[Indexed for MEDLINE]

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