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Chlorella modulates insulin signaling pathway and prevents high-fat diet-induced insulin resistance in mice

机译:小球藻可调节胰岛素信号通路并防止高脂饮食诱导的小鼠胰岛素抵抗

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Aims The search for natural agents that minimize obesity-associated disorders is receiving special attention. In this regard, the present study aimed to evaluate the prophylactic effect of Chlorella vulgaris (CV) on body weight, lipid profile, blood glucose and insulin signaling in liver, skeletal muscle and adipose tissue of diet-induced obese mice. Main methods Balb/C mice were fed either with standard rodent chow diet or high-fat diet (HFD) and received concomitant treatment with CV for 12 consecutive weeks. Triglyceride, free fatty acid, total cholesterol and fractions of cholesterol were measured using commercial assay. Insulin and leptin levels were determined by enzyme-linked immunosorbent assay (ELISA). Insulin and glucose tolerance tests were performed. The expression and phosphorylation of IRβ, IRS-1 and Akt were determined by Western blot analyses. Key findings Herein we demonstrate for the first time in the literature that prevention by CV of high-fat diet-induced insulin resistance in obese mice, as shown by increased glucose and insulin tolerance, is in part due to the improvement in the insulin signaling pathway at its main target tissues, by increasing the phosphorylation levels of proteins such as IR, IRS-1 and Akt. In parallel, the lower phosphorylation levels of IRS-1ser307 were observed in obese mice. We also found that CV administration prevents high-fat diet-induced dyslipidemia by reducing triglyceride, cholesterol and free fatty acid levels. Significance We propose that the modulatory effect of CV treatment preventing the deleterious effects induced by high-fat diet is a good indicator for its use as a prophylactic-therapeutic agent against obesity-related complications.
机译:目的寻求将与肥胖相关的疾病减至最少的天然药物受到特别关注。在这方面,本研究旨在评估小球藻(CV)对饮食诱导的肥胖小鼠肝脏,骨骼肌和脂肪组织的体重,脂质分布,血糖和胰岛素信号传导的预防作用。主要方法对Balb / C小鼠喂以标准啮齿动物饮食或高脂饮食(HFD),并连续12周接受CV伴随治疗。使用商业测定法测量甘油三酸酯,游离脂肪酸,总胆固醇和胆固醇分数。胰岛素和瘦素水平通过酶联免疫吸附测定(ELISA)确定。进行胰岛素和葡萄糖耐量测试。通过蛋白质印迹分析确定IRβ,IRS-1和Akt的表达和磷酸化。关键发现在此,我们首次在文献中证明,通过CV预防肥胖小鼠的高脂饮食诱导的胰岛素抵抗(如葡萄糖和胰岛素耐受性增加所表明的)部分是由于胰岛素信号通路的改善通过增加蛋白质(例如IR,IRS-1和Akt)的磷酸化水平来达到目标​​。同时,在肥胖小鼠中观察到较低的IRS-1ser307磷酸化水平。我们还发现,静脉给药可降低甘油三酸酯,胆固醇和游离脂肪酸水平,从而防止高脂饮食诱导的血脂异常。重要性我们认为,CV治疗的调节作用可防止高脂饮食诱导的有害作用,是将其用作预防肥胖相关并发症的预防性治疗剂的良好指标。

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