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Effect of Black Soybean Koji Extract on Glucose Utilization and Adipocyte Differentiation in 3T3-L1 Cells

机译:黑豆曲提取物对3T3-L1细胞葡萄糖利用和脂肪细胞分化的影响

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Adipocyte differentiation and the extent of subsequent fat accumulation are closely related to the occurrence and progression of diseases such as insulin resistance and obesity. Black soybean koji (BSK) is produced by the fermentation of black soybean with Aspergilllus awamori. Previous study indicated that BSK extract has antioxidative and multifunctional bioactivities, however, the role of BSK in the regulation of energy metabolism is still unclear. We aimed to investigate the effect of glucose utilization on insulin-resistant 3T3-L1 preadipocytes and adipogenesis-related protein expression in differentiated adipocytes with BSK treatment. Cytoxicity assay revealed that BSK did not adversely affect cell viability at levels up to 200 μg/mL. The potential for glucose utilization was increased by increased glucose transporter 1 (GLUT1), GLUT4 and protein kinase B (AKT) protein expression in insulin-resistant 3T3-L1 cells in response to BSK treatment. Simultaneously, BSK inhibited lipid droplet accumulation in differentiated 3T3-L1 cells. The inhibitory effect of adipogenesis was associated with downregulated peroxisome proliferator-activated receptor γ (PPARγ) level and upregulated Acrp30 protein expression. Our results suggest that BSK extract could improve glucose uptake by modulating GLUT1 and GLUT4 expression in a 3T3-L1 insulin-resistance cell model. In addition, BSK suppressed differentiation and lipid accumulation in mature 3T3-L1 adipocytes, which may suggest its potential for food supplementation to prevent obesity and related metabolic abnormalities.
机译:脂肪细胞的分化和随后脂肪堆积的程度与诸如胰岛素抵抗和肥胖症等疾病的发生和发展密切相关。黑大豆曲(BSK)是由黑豆与泡盛曲霉发酵而成。先前的研究表明,BSK提取物具有抗氧化和多功能的生物活性,然而,BSK在能量代谢调节中的作用仍不清楚。我们旨在研究葡萄糖利用对BSK治疗的分化型脂肪细胞中胰岛素抵抗性3T3-L1前脂肪细胞和脂肪形成相关蛋白表达的影响。细胞毒性试验表明,在浓度高达200μg/ mL的水平下,BSK不会对细胞活力产生不利影响。响应BSK处理,胰岛素抵抗性3T3-L1细胞中葡萄糖转运蛋白1(GLUT1),GLUT4和蛋白激酶B(AKT)蛋白表达增加,从而增加了葡萄糖利用的潜力。同时,BSK抑制分化的3T3-L1细胞中脂质滴的积累。脂肪生成的抑制作用与过氧化物酶体增殖物激活受体γ(PPARγ)水平下调和Acrp30蛋白表达上调有关。我们的结果表明BSK提取物可以通过调节3T3-L1胰岛素抵抗细胞模型中的GLUT1和GLUT4表达来改善葡萄糖摄取。此外,BSK抑制了成熟的3T3-L1脂肪细胞的分化和脂质蓄积,这可能表明其可能通过补充食品来预防肥胖症和相关的代谢异常。

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