LAUSR

Type 1 diabetes (T1D) is a chronic autoimmune disease characterized by absence of insulin secretion due to destruction of the pancreatic beta-cells. Patients with T1D exhibit an increased risk for cardiovascular disease (CVD) compared with non-diabetic subjects. It has been established that low concentration of high-density lipoprotein cholesterol (HDL-C), an independent risk marker of CVD, coincides with a reduced protective capacity against oxidative stress. However, conflicting results have been reported on the prevalence of low HDL-C levels in T1D. Interestingly, changes in composition and function of HDL particles (abnormal ratio of cholesteryl ester-to-triglyceride, reduction in the phospholipid content, reduced capacity to promote cholesterol efflux from macrophages, impaired anti-inflammatory and anti-oxidant activities) have been described in patients with T1D. Hence, exploring HDL function, even in the presence of normal HDL-C levels, might provide additional insight into the underlying pathophysiology associated with increased CV risk in T1D. In the current review, we will provide a detailed overview of the current evidence for a role of HDL function as independent risk factor for the development of CVD in T1D.