This study investigated the effects of telmisartan on insulin resistance in high-fat diet-treated rats and the possible mechanism.A total of 40 male Sprague-Dawley rats enrolled in the study were divided into 4 groups at random:ND group(n=10) and HD group(n=10),in which the rats were given a normal chow diet or a high-fat diet for 20 weeks following a one-week adaptation;ND+telmisartan(n=10) group and HD+telmisartan group(n=10),in which the rats were initially administered in the same way as the ND or HD group,and then they were orally gavaged with telmisartan(5 mg/kg daily) additionally for 5 weeks.Related inflammatory factors were measured by ELISA.Monocyte chemotactic protein 1(MCP-1),phosphorylated JNK and IκB-α expressions in both adipose and liver were detected by Western blotting.CRP and angiotensin Ⅱ receptor 1(AT1) mRNA expressions in both adipose and liver were determined by RT-PCR.The results showed that telmisartan administration in vivo reversed insulin resistance as evidenced by a decrease in plasma fasting glucose levels,plasma fasting insulin levels and homeostasis model of assessment-insulin resistance(HOMA-IR).Furthermore,telmisartan administration significantly reduced serum CRP,TNF-α and IL-1β levels,and elevated serum IL-10 levels.It was also found to hamper the high-fat diet-induced increase in CRP mRNA,AT1 mRNA and MCP-1,and decrease in IκB-α in both adipose and liver.It was concluded that telmisartan administration in vivo may improve insulin resistance through attenuated inflammatory response pathways. This study investigated the effects of telmisartan on insulin resistance in high-fat diet-treated rats and the possible mechanism. A total of 40 male Sprague-Dawley rats enrolled in the study were divided into 4 groups at random: ND group (n = 10 ) and HD group (n = 10), in which the rats were given a normal chow diet or a high-fat diet for 20 weeks following a one-week adaptation; ND + telmisartan (n = 10) group and HD + telmisartan group (n = 10), in which the rats were initially administered in the same way as the ND or HD group, and then were were orally gavaged with telmisartan (5 mg / kg daily) further for 5 weeks. Both mRNA and protein expressions of phosphorylated JNK and IκB-α in both adipose and liver were detected by Western blotting. The mRNA expression of both mRNA and protein in both adipose and liver were determined by RT -PCR.The results showed that telmisartan administration intically reversed insulin resistance as e videnced by a decrease in plasma fasting glucose levels, plasma fasting insulin levels and homeostasis model of assessment-insulin resistance (HOMA-IR) .Furthermore, telmisartan administration significantly reduced serum CRP, TNF-α and IL-1β levels, and elevated serum IL -10 levels. It was also found to hamper the high-fat diet-induced increase in CRP mRNA, AT1 mRNA and MCP-1, and decrease in IκB-α in both adipose and liver. It was certified that telmisartan administration in vivo improve insulin resistance through attenuated inflammatory response pathways.