首页> 美国卫生研究院文献>Biomolecules Therapeutics >Capsanthin Inhibits both Adipogenesis in 3T3-L1 Preadipocytes and Weight Gain in High-Fat Diet-Induced Obese Mice
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Capsanthin Inhibits both Adipogenesis in 3T3-L1 Preadipocytes and Weight Gain in High-Fat Diet-Induced Obese Mice

机译:辣椒红素既抑制3T3-L1前脂肪细胞的脂肪生成又抑制高脂饮食诱导的肥胖小鼠的体重增加

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摘要

Adipogenesis in murine preadipocyte 3T3L-1 has been used as a model system to study anti-obese bioactive molecules. During adipogenesis in 3T3-L1 preadipocytes, we found that capsanthin inhibited adipogenesis (IC50; 2.5 μM) and also showed lipolytic activity in differentiated adipocytes from the preadipocytes (ED50; 872 nM). We identified that the pharmacological activity of capsanthin on adipogenesis in 3T3-L1 was mainly due to its adrenoceptor-β2-agonistic activity. In high-fat diet animal model study, capsanthin significantly enhanced spontaneous locomotive activities together with progressive weight-loss. The capsanthin-induced activation of kinetic behavior in mice was associated with the excessive production of ATP initiated by both the enhanced lipolytic activity together with accelerated oxidation of fatty acids due to the adrenoceptor β2-agonistic activity of capsanthin. Capsanthin also dose-dependently increased adiponectin and p-AMPK activity in high fat diet animals, suggesting that capsanthin has both anti-obesity and insulin sensitizing activities.
机译:鼠前脂肪细胞3T3L-1中的脂肪形成已用作研究抗肥胖生物活性分子的模型系统。在3T3-L1前脂肪细胞的脂肪形成过程中,我们发现辣椒红素抑制脂肪形成(IC50; 2.5μM),并且在与前脂肪细胞(ED50; 872 nM)分化的脂肪细胞中也显示出脂解活性。我们发现辣椒红素对3T3-L1中脂肪形成的药理活性主要是由于其肾上腺素受体β2激动活性。在高脂饮食动物模型研究中,辣椒红素显着增强了自发机车活动并逐渐减轻了体重。辣椒红素诱导的小鼠动力学行为的激活与ATP的过量产生有关,ATP的过量产生是由于辣椒红素的肾上腺素受体β2激动活性引起的增强的脂解活性以及脂肪酸的加速氧化所致。辣椒红素还可以剂量依赖性地增加高脂饮食动物的脂联素和p-AMPK活性,这表明辣椒红素具有抗肥胖和胰岛素增敏的作用。

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