Reverse cholesterol transport in diabetes mellitus

✍ Scribed by Eder C. R. Quintão; Wilson L. Medina; Marisa Passarelli

• Publisher: John Wiley and Sons
• Year: 2000
• Tongue: English
• Weight: 232 KB
• Volume: 16
• Category: Article
• ISSN: 1520-7552
• DOI: 10.1002/1520-7560(200007/08)16:4<237::aid-dmrr127>3.0.co;2-9

✦ Synopsis

There are epidemiological data and experimental animal models relating the development of premature atherosclerosis with defects of the reverse cholesterol transport (RCT) system. In this regard, the plasma concentrations of the high density lipoprotein (HDL) subfractions, of cholesteryl ester transfer protein (CETP), as well as the activity of the enzyme lecithincholesterol acyl transferase (LCAT) play critical roles. However, there has been plenty of evidence that atherosclerosis in diabetes mellitus (DM) is ascribed to a greater arterial wall cell uptake of modi®ed apoB-containing lipoproteins whereas a primary or predominant defect of the RCT system is still a subject of debate. In other words, in spite of the fact that in DM the composition and rates of metabolism of the HDL particles are greatly altered and display a diminished in vitro ef®ciency to remove cell cholesterol, de®nitive in vivo demonstration of the importance of this fact in atherogenesis is lacking. Furthermore, the roles played by LCAT and CETP in RCT in DM are dif®cult to interpret because the in vitro procedures of measurement utilized have either been inadequate, or inappropriately interpreted. Knock-out or transgenic mice are much needed models to investigate the roles of LCAT, CETP, phospholipid transfer protein (PLTP), and of a CETP inhibitor in the development of atherosclerosis of experimental DM.