Published online Apr 15, 2014. doi: 10.4239/wjd.v5.i2.165
Revised: March 8, 2014
Accepted: March 17, 2014
Published online: April 15, 2014
Hypertriglyceridaemia (HTG) is a risk factor for cardiovascular disease (CVD) in type 2 diabetes and is caused by the interaction of genes and non-genetic factors, specifically poor glycaemic control and obesity. In spite of statin treatment, residual risk of CVD remains high in type 2 diabetes, and this may relate to HTG and atherogenic dyslipidemia. Treatment of HTG emphasises correcting secondary factors and adverse lifestyles, in particular, diet and exercise. Pharmacotherapy is also required in most type 2 diabetic patients. Statins are the first-line therapy to achieve recommended therapeutic targets of plasma low-density lipoprotein cholesterol and non-high-density lipoprotein cholesterol. Fibrates, ezetimibe and n-3 fatty acids are adjunctive treatment options for residual and persistent HTG. Evidence for the use of niacin has been challenged by non-significant CVD outcomes in two recent large clinical trials. Further investigation is required to clarify the use of incretin-based therapies for HTG in type 2 diabetes. Extreme HTG, with risk of pancreatitis, may require insulin infusion therapy or apheresis. New therapies targeting HTG in diabetes need to be tested in clinical endpoint trials. The purpose of this review is to examine the current evidence and provide practical guidance on the management of HTG in type 2 diabetes.
Core tip: Diabetic dyslipidemia relates collectively to hyperglycaemia, insulin resistance, hyperinsulinaemia, abdominal visceral adipose disposition, increased liver fat content, and dysregulated fatty acid metabolism. Insulin resistance in diabetes induces hypertriglyceridaemia by increasing the enterocytic production of chylomicrons and an impaired clearance capacity is also involved. Usual care for diabetic dyslipidemia is statin treatment, but a significant proportion of patients have residual dyslipidemia, related to hypertriglyceridaemia and atherogenic dyslipidemia. Current evidence supports the use of fenofibrate in type 2 diabetics with high triglyceride levels.