The risk of cardiovascular disease (CVD) in persons with type 2 diabetes mellitus (DM2) increases two to four times. One of the main factors increasing cardiovascular risk is dyslipidemia, which includes abnormalities in all lipoproteins, including high-density lipoproteins (HDL). The development of DM2 is accompanied not only by a decrease in the level of HDL, but also by significant changes in their structure. This leads to the transformation of native HDL into so-called dysfunctional or diabetic HDL, which loses their antiatherogenic, cardioprotective, anti-inflammatory and anti-diabetic properties. In poorly controlled diabetes mellitus HDL can not only lose its beneficial functions, but also acquire proatherogenic, proinflammatory ones. Diabetic HDL can contribute to the accumulation of such unfavorable qualities as increased proliferation, migration, and invasion of cancer cells. Given that HDL, in addition to participation in cholesterol transport, performs important regulatory functions in the body, there is reason to assume that structural modifications of HDL (oxidation, glycation, triglyceride enrichment, loss of HDL-associated enzymes, etc.) are one of the causes of vascular complications of diabetes.