A common characteristic of the metabolic syndrome is insulin resistance， and hyperinsulinemia. Insulin resistance plays an important role in the pathogenesis of type 2 diabetes. Recent studies have suggested that insulin resistance in vascular tissues and the heart might contribute in part to the cardiovascular complications that are associated with insulin resistance and the metabolic syndrome.  

Insulin Resistance in Non Vascular Tissues and Cardiovascular Risk
Insulin resistance in the liver is associated with increased production of triglycerides and secretion of very low-density lipoproteins (VLDL) leading to hypertriglyceridemia. Production of high-density lipoprotein (HDL) is also reduced and this is due in part to increased secretion of and decreased clearance of apolipoprotein B. Insulin resistance in liver cells and adipocytes is also associated with increased production of plasminogen activator inhibitor (PAI-1). Insulin resistance in adipocytes is associated with increased secretion of inflammatory cytokines， which could represent another mechanism linking atherosclerosis with insulin resistance. Secretion of adiponectin by adipose tissue is reduced in obesity and insulin resistant states. Insulin resistance and obesity is associated with increased generation of angiotensinogen thereby promoting activation of the renin angiotensin system and hyperinsulinemia increases renal absorption of sodium. 

Consequences of Impaired Insulin Signaling in the Vasculature
Moreover in insulin resistant states， insulin resistance at the cellular level is characterized by impaired insulin signaling to PI3K/PKB， while signaling to MAPK is relatively preserved. In the vasculature， insulin-mediated activation of PI3K/PKB leads to activation of endothelial nitric oxide synthase. Thus in insulin resistant states that are associated with hyperinsulinemia， nitric oxide generation is reduced， but endothelin production is increased because of persistent insulin-mediated activation of MAPK signaling. Multiple mechanisms lead to impaired insulin signaling in the vasculature in the metabolic syndrome， and include increased metabolism of glucose and fatty acids by endothelial cells， which promote oxidative stress.

Consequences of Impaired Insulin Signaling in the Heart
Insulin resistance at the whole body level increases the delivery of fatty acids (FA) to the heart， which augments myocardial FA metabolism. Increased FA utilization leads to oxidative stress and mitochondrial dysfunction. Hearts with impaired insulin signaling are unable to maintain normal cardiac function in response to hypertrophic and ischemic insults. This is due in part to increased myocyte and vascular endothelial apoptosis and necrosis leading to an increase in myocardial fibrosis.
Summary/Conclusion
The greater challenge for the future is to demonstrate that improving insulin resistance in humans will lead to long-term reductions in cardiovascular complications of the metabolic syndrome. Results from clinical trials have thus far been mixed. The basis for these differences in outcome is unclear but clearly justify the need for additional studies. The results of A number of clinical trials should hopefully shed important insight into the relationship between insulin sensitizing therapies and cardiovascular outcomes in humans. 

（中文摘要）
胰岛素抵抗与心血管疾病的关系
代谢综合征、肥胖和2型糖尿病全球发病率的急剧升高大大增加了心血管疾病的风险。而胰岛素抵抗和高胰岛素血症是代谢综合征的常见特征。本文讨论了非血管组织中胰岛素抵抗与血管风险，及血管和心脏中胰岛素信号传导受损的后果。胰岛素抵抗通过多种机制导致心血管功能障碍，有研究提示增强胰岛素敏感性将改善心脏和血管功能障碍。关于强化血糖控制对长期心血管预后影响的众多临床研究目前正在进行，其预期结果可望为洞察人类胰岛素增敏治疗和心血管预后关系提供证据。