Rosuvastatin may Modulate Insulin Signaling and Inhibit Atherogenesis Beyond its Plasma Cholesterol-Lowering Effect in I
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Rosuvastatin may Modulate Insulin Signaling and Inhibit Atherogenesis Beyond its Plasma Cholesterol-Lowering Effect in Insulin-Resistant Mice Hangyuan Guo & Haitao Lv & Weiliang Tang & Jufang Chi & Longbin Liu & Fukang Xu & Zheng Ji & Xiaoya Zhai & Fang Peng Published online: 24 August 2012 # Springer Science+Business Media, LLC 2012
Abstract Objectives To provide evidence that rosuvastatin may improve insulin-resistance and inhibit atherogenesis by modulating insulin signaling, and whether this effect occurs beyond its plasma cholesterol-lowering effect. Methods Thirty-two 6-week-old low-density lipoprotein receptor deficient mice were randomized into 4 groups (n0 8 in each group): Normal control group (NC); High fat and high fructose diet group (HFF); HFF plus rosuvastatin group (HFFR); HFFR plus mevalonic acid group (HFFRMA). After 12 weeks, we measured fasting blood sugar, fasting insulin and cholesterol levels; the morphological concentrations of the aorta and aortic sinus; the expression of insulin receptor substrate 2, phosphorylated insulin receptor substrate 2, protein kinase B, phosphorylated protein kinase B and the glucose transporter 4 in the liver. Results Compared with other groups, fasting blood sugar and fasting insulin increased significantly in HFF group. Furthermore, HFF group had an increase in the morphological concentrations of the aorta and aortic sinus, but there was a significant decrease in the HFFRMA group and the HFFR group. Moreover, there was a high expression of insulin receptor substrate 2, phosphorylated insulin receptor substrate 2, protein kinase B, phosphorylated protein kinase B and the
Hangyuan Guo, Haitao Lv and Weiliang Tang contributed equally to this work. H. Guo (*) : H. Lv : W. Tang : J. Chi : L. Liu : F. Xu : Z. Ji : X. Zhai : F. Peng Department of Cardiology, Shaoxing People’s Hospital, Shaoxing Hospital of Zhejiang University, Shaoxing City, Zhejiang 312000, China e-mail: [email protected] H. Lv : Z. Ji : X. Zhai Wenzhou Medical College, Wenzhou City, Zhejiang 325000, China
glucose transporter 4 in the HFFRMA and HFFR groups, but a low expression in the HFF group. No significant differences regarding each afore-mentioned index was observed in the HFFR and HFFRMA groups. Conclusions Our data show that rosuvastatin may improve insulin-resistance and inhibit atherogenesis in HFF-fed mice by partially reversing the decrease in the insulin stimulated insulin receptor substrate 2/Phosphatidylinositol 3-kinase/protein kinase B/glucose transporter 4 pathway in the liver, and that this effect is independent of its cholesterol-lowering effect. Key words Rosuvastatin . Atherogenesis . Insulin signaling . Insulin resistance Abbreviations LDL Low-density lipoprotein LDLR−/− Low-density lipoprotein receptor deficient NC Normal control group HFF High fat and high fructose diet group HFFR HFF plus rosuvastatin group HFFRMA HFFR plus mevalonic acid group HMG-CoA 3-hydroxy-3-methylglutaryl coenzyme A FBS Fasting blood sugar TG Triglycerides TC Total cholesterol LDL-C Low-density l
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