Table 3.

Important liable mechanisms for metabolic syndrome related to cardiovascular diseases

Hypertension	Dyslipidemia	Proinflammatory cytokines	Insulin resistance	Microalbuminuria
Insulin resistance stimulates sympathetic nervous system	Enhancement of lipolysis in adipocytes	Elevation of plasma concentrations of IL-6, TNF-α, C-reactive protein, and resistin	Overabundance of circulating fatty acids by lipolysing of triacylglycerol by insulin	Glomerular hyperfiltration
Insulin resistance mediates hyperadrenergic state	Insulin drives lipogenesis in the liver	Reduction of anti-inflammatory adipokines such as adiponectin	Inhibition of antilipolytic effect of insulin by circulating fatty acids	Over-production of ROS
Insulin resistance stimulates renal sodium absorption	Increase CETP activity and lipolysis of HDL-c		Impairment activation of protein kinase Ce-_ and protein kinase C-by Fatty acids	Insulin resistance, inflammation and altered renal hemodynamics
Insulin can cause upregulation of angiotensin II type I receptors	Enhancement of triglyceride synthesis in the liver		Defect in insulin stimulated IRS-1 and IRS-2 tyrosine phosphorylation
Low levels of plasma natriuretic peptides			Activation of protein kinase Ce-_ and c-Jun N-terminal kinase-1.41
Insulin resistance increases endothelin 1impairment of NO-mediated vasodilation			Fatty acids increase hepatic glucose production and diminish inhibition of glucose production by insulin
Hyperuricemia			Defect in mitochondrial oxidative phosphorylation
Production of endogenous digoxin-like factor			Deficient in the endoplasmic reticulum X-box binding protein-1, hyperactivation of c-Jun N-terminal kinase-1 increases serine phosphorylation of IRS-1

NO: nitric oxide, CETP: cholesteryl ester transfer protein, HDL-c: high density lipoprotein cholesterol, IL-6: interlukin 6, TNF-α: tumor necrosis factor α, ROS: reactive oxygen species, IRS: insulin receptor substrate