Introduction

Type 2 diabetes mellitus (T2DM) is an important independent risk factor for cardiovascular and cerebrovascular diseases.1Insulin has been widely used in the treatment of T2DM patients, and it has made obvious effect on improving blood glucose level. But, according to several research conclusions published recently, both insulin treated DM and non-insulin treated DM patients have greater risk of major adverse cardiovascular events (MACE) and mortality compared with non-DM patients, and insulin treated DM suffered greater risk than non-insulin treated DM,2-7 including short-term and long-term risks.3, 7, 8 Nevertheless, it is unclear about any causality suggestion between insulin treatment and outcomes. As well known, Insulin has antiplatelet effect as well as hypoglycemic effect,9, 10 normally, it should reduce the occurrence of MACE, but the fact is opposite. Therefore, the relationship between insulin therapy and platelet function has gradually become an important research direction. In a randomized trial, Vivas et al thought that intensive glucose control with insulin in patients with an acute coronary syndrome reduced platelet reactivity during hospitalization.11 Nevertheless, after 12 months of follow-up, platelet aggregation following adenosine diphosphate stimulation showed no differences between optimized glucose control with insulin and conventional control groups.12 Westerbacka et al found that platelet-inhibitory actions of insulin under conditions mimicking thrombus formation are blunted or absent in obese or insulin resistance subjects.13 In order to further explore the relationship between insulin therapy and platelet function, this study was carried out.