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IRS-1 deficiency causes hypertension, hypertriglyceridemia, and impaired endothelium-dependent vascular relaxation in mice.
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Insulin resistance is often associated with atherosclerotic diseases in subjects with obesity and impaired glucose tolerance. This study examined the effects of insulin resistance on coronary risk factors in IRS-1 deficient mice, a nonobese animal model of insulin resistance. Blood pressure and plasma triglyceride levels were significantly higher in IRS-1 deficient mice than in normal mice. Impaired endothelium-dependent vascular relaxation was also observed in IRS-1 deficient mice. Furthermore, lipoprotein lipase activity was lower than in normal mice, suggesting impaired lipolysis to be involved in the increase in plasma triglyceride levels under insulin-resistant conditions. Thus, insulin resistance plays an important role in the clustering of coronary risk factors which may accelerate the progression of atherosclerosis in subjects with insulin resistance.
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Abe et al. (1998) studied Insulin resistance. Insulin receptor substrate-1 (IRS-1) deficiency vs. Normal wild-type mice was evaluated on Blood pressure, plasma triglyceride levels, endothelium-dependent vascular relaxation, and lipoprotein lipase activity. IRS-1 deficiency in mice caused significantly higher blood pressure and plasma triglycerides, impaired endothelium-dependent vascular relaxation, and reduced lipoprotein lipase activity vs normal mice.
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