论文部分内容阅读
试验探索了植物提取的没食子酸(GA)在胰岛素抵抗细胞培养模型中发挥的作用及对高果糖饮食(HFD)诱发糖尿病小鼠肝脏碳水化合物代谢的影响。GA可能通过抑制肝脏炎症来减轻胰岛素抵抗情况,从而使高血糖情况减轻,并通过增强肝糖原合成,抑制肝糖质新生来改善HFD诱发糖尿病的小鼠的肝脏碳水化合物代谢异常。在胰岛素抵抗的FL8313小鼠肝细胞中添加GA 6.25μg·m L~(-1),可使其吸收葡萄糖量增加19.2%。在口服葡萄糖耐受试验中,GA极大缓解了HFD诱导糖尿病小鼠的高血糖症状,减少了葡萄糖曲线下面积值,并降低内稳态模型中胰岛素抵抗指数。饲喂GA的HFD小鼠的血清果糖肽、果糖胺水平和心血管风险指数评分均显著降低。此外,GA促进HFD小鼠胰岛素上游信号分子表达,包括胰岛素受体、胰岛素受体底物1、磷脂酰肌醇-3激酶,Akt/蛋白激酶B和葡萄糖转运蛋白。抑制HFD小鼠体内糖质新生相关蛋白表达,例如果糖-1,6-二磷酸酶,而促进肝糖原合成酶表达和糖酵解相关蛋白表达,包括己糖激酶、磷酸果糖激酶和醛缩酶。研究结果表明,GA作为1种健康的食品成分,有一定的预防糖尿病作用。
The experiment explored the role of plant-derived gallic acid (GA) in the model of insulin resistance cell culture and the effect on hepatic carbohydrate metabolism in high fructose diets (HFD) -induced diabetic mice. GA may reduce insulin resistance by inhibiting liver inflammation, thereby reducing hyperglycemia and improving hepatic carbohydrate metabolism abnormalities in HFD-induced diabetic mice by enhancing hepatic glycogen synthesis and inhibiting hepatic glucogenesis. Adding 6.25 μg · mL -1 of GA to insulin-resistant FL8313 mouse hepatocytes increased the amount of glucose uptake by 19.2%. In oral glucose tolerance test, GA greatly ameliorates the symptoms of hyperglycemia in HFD-induced diabetic mice, decreases the area under the glucose curve, and decreases the insulin resistance index in the homeostasis model. HFD mice fed GA had significantly lower serum fructosyl peptide, fructosamine levels, and cardiovascular risk index scores. In addition, GA promotes the expression of insulin upstream signal molecules in HFD mice, including insulin receptor, insulin receptor substrate 1, phosphatidylinositol 3-kinase, Akt / protein kinase B and glucose transporter. Inhibits the expression of glycoproteins such as fructose-1,6-bisphosphatase in HFD mice and promotes the expression of glycogen synthase and glycolysis-related proteins including hexokinase, phosphofructokinase and aldose Enzymes. The results show that GA as a healthy food ingredients, have a certain role in the prevention of diabetes.