Huang Da-Wei, Chang Wen-Chang, Wu James Swi-Bea, Shih Rui-Wen, Shen Szu-Chuan
Department of Food and Beverage Management, China University of Science and Technology, Taipei 11581, Taiwan.
Graduate Institute of Food Science and Technology, National Taiwan University, Taipei 10672, Taiwan.
Nutr Res. 2016 Feb;36(2):150-60. doi: 10.1016/j.nutres.2015.10.001. Epub 2015 Oct 14.
Herein, we investigated the hypoglycemic effect of plant gallic acid (GA) on glucose uptake in an insulin-resistant cell culture model and on hepatic carbohydrate metabolism in rats with a high-fructose diet (HFD)-induced diabetes. Our hypothesis is that GA ameliorates hyperglycemia via alleviating hepatic insulin resistance by suppressing hepatic inflammation and improves abnormal hepatic carbohydrate metabolism by suppressing hepatic gluconeogenesis and enhancing the hepatic glycogenesis and glycolysis pathways in HFD-induced diabetic rats. Gallic acid increased glucose uptake activity by 19.2% at a concentration of 6.25 μg/mL in insulin-resistant FL83B mouse hepatocytes. In HFD-induced diabetic rats, GA significantly alleviated hyperglycemia, reduced the values of the area under the curve for glucose in an oral glucose tolerance test, and reduced the scores of the homeostasis model assessment of insulin resistance index. The levels of serum C-peptide and fructosamine and cardiovascular risk index scores were also significantly decreased in HFD rats treated with GA. Moreover, GA up-regulated the expression of hepatic insulin signal transduction-related proteins, including insulin receptor, insulin receptor substrate 1, phosphatidylinositol-3 kinase, Akt/protein kinase B, and glucose transporter 2, in HFD rats. Gallic acid also down-regulated the expression of hepatic gluconeogenesis-related proteins, such as fructose-1,6-bisphosphatase, and up-regulated expression of hepatic glycogen synthase and glycolysis-related proteins, including hexokinase, phosphofructokinase, and aldolase, in HFD rats. Our findings indicate that GA has potential as a health food ingredient to prevent diabetes mellitus.
在此，我们研究了植物没食子酸（GA）在胰岛素抵抗细胞培养模型中对葡萄糖摄取的降血糖作用，以及在高果糖饮食（HFD）诱导的糖尿病大鼠中对肝脏碳水化合物代谢的影响。我们的假设是，GA通过抑制肝脏炎症减轻肝脏胰岛素抵抗来改善高血糖，并通过抑制肝脏糖异生以及增强HFD诱导的糖尿病大鼠的肝脏糖原合成和糖酵解途径来改善异常的肝脏碳水化合物代谢。在胰岛素抵抗的FL83B小鼠肝细胞中，没食子酸在浓度为6.25μg/mL时使葡萄糖摄取活性提高了19.2%。在HFD诱导的糖尿病大鼠中，GA显著减轻了高血糖，降低了口服葡萄糖耐量试验中葡萄糖曲线下面积的值，并降低了胰岛素抵抗指数的稳态模型评估得分。用GA治疗的HFD大鼠的血清C肽、果糖胺水平和心血管风险指数得分也显著降低。此外，GA上调了HFD大鼠肝脏胰岛素信号转导相关蛋白的表达，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2。没食子酸还下调了HFD大鼠肝脏糖异生相关蛋白如果糖-1,6-二磷酸酶的表达，并上调了肝脏糖原合酶和糖酵解相关蛋白如己糖激酶、磷酸果糖激酶和醛缩酶的表达。我们的研究结果表明，GA作为预防糖尿病的健康食品成分具有潜力。
