Background Type 2 diabetes (T2D) is hallmarked by insulin resistance and pancreatic gradual islet β-cell dysfunction and hyperglycemia. Consumption of large quantities of high-fat diet (HFD) activates the caspase-pathway. This leads to apoptotic degradation of pancreatic β-cell and eventually progression to T2D or worsening of diabetes. Aims We aimed to assess the antidiabetic effects of aspirin when administered at low doses on insulin sensitivity and glucose uptake. Materials and methods A rat model fed HFD has been reported as an approved model of T2D. A total of 40 animals were assigned into four groups: controlled diet, HFD, controlled diet with aspirin, and HFD with aspirin. Hyperglycemia was confirmed by estimating the blood glucose levels. The diabetic rats were orally treated with low dose of aspirin 20 mg/kg body weight, for 70 days. At the end of the experiment, some biochemical parameters, the oxidative stress, and gene expression levels were quantified. Results Current data indicated that aspirin improved different physiological and immunological parameters. These include reduction of low-density lipoprotein and total cholesterol and improved glucose uptake via up-regulation of GLUT4 expression. Moreover, aspirin reduced fat peroxidation and obliterated hemeoxygenase-1-dependent fat down-regulation and reestablished the expression of LUT4 and hemeoxygenase-1 to the basal level. Conclusions In conclusion, this study confirmed the anti-inflammatory effect of aspirin and suggested that low-dose aspirin enhanced the metabolism of glucose and increased insulin sensitivity by suppression of inflammation and oxidative stress.
)
View on SCiNiTO