TRIGLYCERIDE-RICH LIPOPROTEINS IN NON-INSULIN-DEPENDENT DIABETES-MELLITUS - POSTPRANDIAL METABOLISM AND RELATION TO PREMATURE ATHEROSCLEROSIS

Citation
Fhaf. Deman et al., TRIGLYCERIDE-RICH LIPOPROTEINS IN NON-INSULIN-DEPENDENT DIABETES-MELLITUS - POSTPRANDIAL METABOLISM AND RELATION TO PREMATURE ATHEROSCLEROSIS, European journal of clinical investigation, 26(2), 1996, pp. 89-108
Citations number
267
Categorie Soggetti
Medicine, Research & Experimental","Medicine, General & Internal
ISSN journal
00142972
Volume
26
Issue
2
Year of publication
1996
Pages
89 - 108
Database
ISI
SICI code
0014-2972(1996)26:2<89:TLIND>2.0.ZU;2-H
Abstract
Non-insulin-dependent diabetes mellitus is frequently associated with premature atherosclerosis. Abnormalities in lipid and lipoprotein meta bolism contribute to the increased risk of coronary heart disease. One of the most common lipid abnormalities in non-insulin-dependent diabe tes mellitus is hypertriglyceridaemia. In the present paper, the autho rs review the metabolism of triglyceride-rich lipoproteins, with speci al emphasis on the post-prandial state. Several studies have demonstra ted that levels of atherogenic post-prandial lipoproteins are increase d in patients with non-insulin-dependent diabetes mellitus. An increas ed supply of glucose and free fatty acids contributes to overproductio n of very low-density lipoproteins, increasing the burden of triglycer ide-rich lipoproteins on the common lipolytic pathway at the level of lipoprotein lipase. Low lipoprotein lipase activity and increased amou nts of lipolysis-inhibiting free fatty acids further impair lipolysis of post-prandial lipoproteins. The clearance of atherogenic remnants i s also delayed in non-insulin-dependent diabetes mellitus. There is ev idence that a relative hepatic removal defect exists, secondary to imp aired remnant-receptor interaction and increased competition with very low density lipoprotein remnants. Correction of the increased post-pr andial lipaemia in non-insulin-dependent diabetes mellitus is advisabl e, as it may contribute to attenuation of the risk on premature athero sclerosis. When dietary measures and hypoglycaemic agents have failed to achieve acceptable lipid levels, lipid-lowering drugs should be adv ised. Fibric acids and hydroxymethylglutaryl coenzyme A (HMG CoA) redu ctase inhibitors are the drugs of choice.