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Dyslipidemia in Type 2 Diabetes: Prevalence, Pathophysiology, and Management


Dyslipidemia is one of the key risk factors for cardiovascular disease (CVD) in diabetes mellitus. Despite the mounting clinical trial data, the management of dyslipidemia other than lowering the low density lipoprotein cholesterol (LDL-c) continues to be controversial. The characteristic features of diabetic dyslipidemia are high plasma triglyceride concentration, reduced high density lipoprotein cholesterol (HDL-c) concentration, and increased concentration of small dense LDL particles. These changes are caused by increased free fatty acid flux secondary to insulin resistance and aggravated by increased inflammatory adipokines. The availability of several lipid-lowering drugs and nutritional supplements offers novel and effective options for achieving target lipid levels in people with diabetes. While initiation of drug therapy based on differences in the lipid profile is an option, most practice guidelines recommend statins as first-line therapy. Although the evidence for clinical utility of combination of statins with fibrates or nicotinic acid in reducing cardiovascular events remains inconclusive, the preponderance of evidence suggests that a subgroup who have high triglycerides and low HDL-c levels may benefit from combination therapy of statins and fibrates. The goal of therapy is to achieve at least 30–40 % reduction in LDL-c levels. Preferably the LDL-c should be less than 100 mg/dL in low-risk people and less than 70 mg/dL in those at high risk, including people with established CVD.

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The authors thank the nursing and pharmacy staff and the residents and students training in the Division of Endocrinology, for their valuable discussions.

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Correspondence to Arshag D. Mooradian.

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Chehade, J.M., Gladysz, M. & Mooradian, A.D. Dyslipidemia in Type 2 Diabetes: Prevalence, Pathophysiology, and Management. Drugs 73, 327–339 (2013).

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  • Statin
  • High Density Lipoprotein Cholesterol
  • Fenofibrate
  • Ezetimibe
  • Cholesteryl Ester Transfer Protein