Recent reports suggest that salidroside protects cardiomyocytes from oxidative injury and stimulates glucose uptake by skeletal muscle cells. Despite these findings, the therapeutic potential of salidroside in the treatment of obesity and insulin resistance remains uncertain and requires further investigation. In the present study, the treatment effect of salidroside on the onset and development of the obese phenotype and insulin resistance as well as the underlying mechanisms was investigated using long-term high-fat diet-induced obese mice supplemented with salidroside. We used biochemical kits to determine serum biochemical parameters (including triacylglycerol, total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, fasting glucose, and insulin). The results show that salidroside-supplemented animals showed better glucose tolerance and insulin sensitivity, decreased blood lipids, and weight gain (p < .05). Protein expression of p-Nrf2 and Nrf2 was analyzed by western blotting, and the mRNA levels of thermogenic-related genes (Ucp1, Pgc1a, Prdm16, and Cidea) were detected by quantitative RT-PCR. The results show an improvement in lipid peroxidation and Nrf2/ARE signaling, as well as an increased expression of the Ucp1, Pgc1a, Prdm16, and Cidea (p < .05). Our evidence suggests that salidroside alleviates diet-induced obesity and insulin resistance potentially by activating Nrf2/ARE pathway and enhancing the thermogenesis of adipose tissues. This induction represents a potential technique for the management of comorbidities related to obesity and its prevention.
Keywords: Nrf2; insulin resistance; obesity; salidroside; thermogenesis.
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