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首页> 外文期刊>Journal of Agricultural and Food Chemistry >Bisdemethoxycurcumin Inhibits Adipogenesis in 3T3-L1 Preadipocytes and Suppresses Obesity in High-Fat Diet-Fed C57BL/6 Mice
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Bisdemethoxycurcumin Inhibits Adipogenesis in 3T3-L1 Preadipocytes and Suppresses Obesity in High-Fat Diet-Fed C57BL/6 Mice

机译：双去甲氧基姜黄素抑制高脂饮食喂养的C57BL / 6小鼠3T3-L1前脂肪细胞的脂肪生成并抑制肥胖。

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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 dong expansion (MCE). In BDMC-treated preadipocytes, cell cycle arrest at the G(0)/G(1) phase was found after initiation of adipogenesis and was accompanied by downregulation of cyclin A, cydin B, p21, and mitogen-activated protein kinase (MAPK) signaling. The protein levels of the adipogenic transcription factors peroxisome proliferator-activated receptor (PPAR)gamma and CCAAT/enhancer-binding proteins (C/EBP)alpha 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 mite. 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.
机译：肥胖是由于体内脂肪过多积聚引起的，与复杂的代谢疾病密切相关。脂肪形成是肥胖发展中脂肪细胞肥大所需的关键过程。姜黄素（Cur）可以抑制脂肪细胞分化，但姜黄中存在的其他姜黄素类化合物（如脱甲氧基姜黄素（DMC）和双去甲氧基姜黄素（BDMC））对脂肪形成的抑制作用尚未进行研究。在这里，我们研究了姜黄素对脂肪形成的影响以及脂肪细胞分化的分子机制。在三种姜黄素中，BDMC是最有效的脂肪细胞脂质堆积抑制剂。 BDMC在早期主要通过减弱有丝分裂的dong扩张（MCE）来抑制脂肪形成。在BDMC处理的前脂肪细胞中，在成脂开始后发现细胞周期停滞在G（0）/ G（1）期，并伴随着细胞周期蛋白A，cydin B，p21和有丝分裂原激活的蛋白激酶（MAPK）的下调。信号。 BDMC处理还降低了成脂转录因子过氧化物酶体增殖物激活受体（PPAR）γ和CCAAT /增强子结合蛋白（C / EBP）α的蛋白水平。此外，0.5％的BDMC（w / w）可以显着降低高脂饮食（HFD）喂养的螨的体重增加和脂肪组织质量。 H＆E染色的结果表明，膳食BDMC可以减少脂肪细胞的肥大。这些结果首次证明BDMC抑制3T3-L1脂肪细胞中的脂肪生成并预防HFD诱导的肥胖。我们的研究结果表明，BDMC具有预防肥胖的潜力。

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