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Telmisartan protects against insulin resistance by attenuating inflammatory response in rats

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Summary

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.

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Correspondence to Ling Tu  (凃 玲).

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This project was partially supported by a grant from National Natural Sciences Foundation of China (No. 30971247).

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Xu, X., Yin, X., Feng, W. et al. Telmisartan protects against insulin resistance by attenuating inflammatory response in rats. J. Huazhong Univ. Sci. Technol. [Med. Sci.] 31, 317–323 (2011). https://doi.org/10.1007/s11596-011-0374-7

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  • DOI: https://doi.org/10.1007/s11596-011-0374-7

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