Abstract
BackgroundTo evaluate the relationship between the low-density lipoprotein cholesterol (LDL-C)/high-density lipoprotein cholesterol (HDL-C) ratio and HDL subclass distribution and to further examine and discuss the potential impact of LDL-C and HDL-C together with TG on HDL subclass metabolism.ResultsSmall-sized preβ1-HDL, HDL3b and HDL3a increased significantly while large-sized HDL2a and HDL2b decreased significantly as the LDL-C/HDL-C ratio increased. The subjects in low HDL-C level (< 1.03 mmol/L) who had an elevation of the LDL-C/HDL-C ratio and a reduction of HDL2b/preβ1-HDL regardless of an undesirable or high LDL-C level. At desirable LDL-C levels (< 3.34 mmol/L), the HDL2b/preβ1-HDL ratio was 5.4 for the subjects with a high HDL-C concentration (≥ 1.55 mmol/L); however, at high LDL-C levels (≥ 3.36 mmol/L), the ratio of LDL-C/HDL-C was 2.8 in subjects, and an extremely low HDL2b/preβ1-HDL value although with high HDL-C concentration.ConclusionWith increase of the LDL-C/HDL-C ratio, there was a general shift toward smaller-sized HDL particles, which implied that the maturation process of HDL was blocked. High HDL-C concentrations can regulate the HDL subclass distribution at desirable and borderline LDL-C levels but cannot counteract the influence of high LDL-C levels on HDL subclass distribution.
Highlights
Lipid abnormalities have long been suspected to contribute to atherosclerosis (As); there is overwhelming evidence [1,2] that an elevated low-density lipoprotein cholesterol (LDL-C) concentration in plasma is atherogenic, whereas a higher high-density lipoprotein cholesterol (HDL-C) level is cardioprotective [2,3,4]
It has been postulated that reverse cholesterol transport (RCT) is the smallest preb1-HDL that adsorbs free cholesterol efficiently from the cell membrane, is transformed by the action of lecithin-cholesterol acyltransferase (LCAT), and is remodeled further by the activities of other plasma factors, such as hepatic lipase (HL), cholesterol ester transfer protein (CETP), and lipoprotein lipase (LPL), such that the nascent lipid-poor preb1HDL is converted into mature, cholesterol-rich, spherical HDL2, following the pathway of preb1-HDL ® preb2-HDL ® preb3-HDL ® HDL3 ® HDL2 [7,8,9]
We have previously investigated the impact of plasma lipids together with their ratios on HDL subclass distribution and found that the particle size of HDL became smaller with the rise in plasma triglyceride (TG), TC, LDL-C levels, and TG/HDL-C along with total cholesterol (TC)/HDL-C ratios or with the fall of HDL-C levels [14,15,16,17]
Summary
Lipid abnormalities have long been suspected to contribute to atherosclerosis (As); there is overwhelming evidence [1,2] that an elevated low-density lipoprotein cholesterol (LDL-C) concentration in plasma is atherogenic, whereas a higher high-density lipoprotein cholesterol (HDL-C) level is cardioprotective [2,3,4]. The cardioprotective effect of HDL has been largely attributed to its role in reverse cholesterol transport (RCT), wherein excessive cholesterol is conveyed from peripheral tissues to the liver and steroidogenic organs. The distribution of HDL subclasses can effectively reflect the efficiency of RCT and may directly impact the atherogenic progress. To evaluate the relationship between the low-density lipoprotein cholesterol (LDL-C)/high-density lipoprotein cholesterol (HDL-C) ratio and HDL subclass distribution and to further examine and discuss the potential impact of LDL-C and HDL-C together with TG on HDL subclass metabolism
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