【摘 要】
：
Background To provide evidence that rosuvastatin could improve insulin-resistance and inhibit atherogenesis by modulating insulin signaling,and whether this effect beyond its plasma cholesterol-loweri
【机 构】
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Shaoxing People's Hospital,Zhejiang,China
【出 处】
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第十二届中国介入心脏病学大会(CIT2014)
论文部分内容阅读
Background To provide evidence that rosuvastatin could improve insulin-resistance and inhibit atherogenesis by modulating insulin signaling,and whether this effect beyond its plasma cholesterol-lowering effect.Methods Thirty-two 6-week-old low-density lipoprotein receptor deficient (LDLR-/-) mice were randomized into four groups (n=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,2 weeks,we measured the fasting blood sugar (FBS),fasting insulin (FINS) and total cholesterol (TC);the morphological concentrations of the aorta artery and aorta sinus;the expression of insulin receptor substrate 2 (IRS-2),phosphorylated insulin receptor substrate 2 (P-IRS-2),protein kinase B (AKT,also known as PKB) and phosphorylated protein kinase B (P-AKT) in liver.
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