Telmisartan Protects against Insulin Resistance by Attenuating Inflammatory Response in Rats
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...
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Veröffentlicht in: | Journal of Huazhong University of Science and Technology. Medical sciences 2011-06, Vol.31 (3), p.317-323 |
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Sprache: | eng |
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Zusammenfassung: | 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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ISSN: | 1672-0733 1993-1352 |
DOI: | 10.1007/s11596-011-0374-7 |