Postprandial lipemia: an under-recognized atherogenic factor in patients with diabetes mellitus.
Atherosclerotic disease is the leading cause of both morbidity and mortality in patients with type 2 diabetes. In these patients, postprandial dyslipidemia include not only quantitative but also qualitative abnormalities of lipoproteins which are potentially atherogenic and seems to be a significant risk factor for cardiovascular disease since there is evidence that it results in endothelial dysfunction and enhanced oxidative stress. The most common pattern of postprandial dyslipidemia in diabetes consists of high concentrations of triglycerides, higher VLDLs production by the liver and a decrease in their clearance, a predominance of small dense LDL particles, and reduced levels of HDL. The cause of this postprandial dyslipidemia in diabetes is complex and involves a variety of factors including hyperinsulinemia, insulin resistance, hyperglycemia and disturbed fatty acid metabolism. Numerous clinical studies have shown that postprandial dyslipidemia is associated with endothelial dysfunction in type 2 diabetes and with alterations in other surrogate markers in the cascade of atherosclerosis. Current published guidelines indicate that in diabetics the primary lipid target is LDL<100 mg/dL (70 mg/dL in very high-risk patients) and the most appropriate class of drugs are statins although the issue of postprandial dyslipidemia has not been specifically addressed so far. Moreover, several other classes of medications (fibrates, niacin and antidiabetic drugs) as well as non-pharmacological interventions (i.e. diet, smoking cessation and exercise) can be used to treat lipid and lipoprotein abnormalities associated with insulin resistance and type 2 diabetes. These type of interventions may be more appropriate to ameliorate postprandial dyslipidemia. However, this remains to be confirmed on clinical grounds.
Pastromas
Socrates
S
First Department of Cardiology, Evagelismos General Hospital of Athens, Greece. spastromas@yahoo.gr
Terzi
Angela-Beth
AB
Tousoulis
Dimitris
D
Koulouris
Spyridon
S
D050197:Atherosclerosis / Q000097:blood / Q000188:drug therapy / Q000209:etiology*; D048909:Diabetes Complications / Q000097:blood / Q000150:complications / Q000188:drug therapy; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000150:complications* / Q000188:drug therapy; D006801:Humans; D006949:Hyperlipidemias / Q000097:blood / Q000188:drug therapy / Q000209:etiology*; D000960:Hypolipidemic Agents / Q000097:blood / Q000627:therapeutic use; D050356:Lipid Metabolism / Q000187:drug effects / Q000502:physiology*; D019518:Postprandial Period / Q000187:drug effects / Q000502:physiology*
D000960:Hypolipidemic Agents