Published online Oct 15, 2014. doi: 10.4239/wjd.v5.i5.577
Revised: March 19, 2014
Accepted: July 17, 2014
Published online: October 15, 2014
Processing time: 205 Days and 8.3 Hours
Peripheral arterial disease, manifested as intermittent claudication or critical ischaemia, or identified by an ankle/brachial index < 0.9, is present in at least one in every four patients with type 2 diabetes mellitus. Several reasons exist for peripheral arterial disease in diabetes. In addition to hyperglycaemia, smoking and hypertension, the dyslipidaemia that accompanies type 2 diabetes and is characterised by increased triglyceride levels and reduced high-density lipoprotein cholesterol concentrations also seems to contribute to this association. Recent years have witnessed an increased interest in postprandial lipidaemia, as a result of various prospective studies showing that non-fasting triglycerides predict the onset of arteriosclerotic cardiovascular disease better than fasting measurements do. Additionally, the use of certain specific postprandial particle markers, such as apolipoprotein B-48, makes it easier and more simple to approach the postprandial phenomenon. Despite this, only a few studies have evaluated the role of postprandial triglycerides in the development of peripheral arterial disease and type 2 diabetes. The purpose of this review is to examine the epidemiology and risk factors of peripheral arterial disease in type 2 diabetes, focusing on the role of postprandial triglycerides and particles.
Core tip: Peripheral arterial disease is highly prevalent in type 2 diabetes; traditional risk factors contribute to the disease. Interestingly, postprandial lipidaemia is increased in both conditions. However, one study showed that only subjects with both type 2 diabetes and peripheral arterial disease had elevation of postprandial lipids; subjects with type 2 diabetes and a normal ankle-brachial index had a normal postprandial response. Because most of the triglycerides of chylomicrons are extracted in muscle and adipose cells in the legs, the authors speculate on whether arteriosclerosis in the legs may contribute to greater postprandial lipidaemia.