The relationship between high density lipoprotein subclass profile and plasma lipids concentrations

Abstract

HDL particles posses multiple antiatherogenic activities and the identification and differentiation of individual HDL subclasses may be useful in documentation and understanding of metabolic changes of different HDL subclasses. The major plasma lipids exist and are transported in the form of lipoprotein complexes. Hence, alterations in plasma lipids levels can interfere with the composition, content, and distribution of plasma lipoprotein subclasses that affect atherosclerosis risk. The research review major discussed the relationship between plasma lipids levels and HDL subclasses distribution. The general shift toward smaller size of HDL particle size in HTG, HCL and MHL subjects, and the changes were more prominent with the elevation of TG and TC levels which imply that HDL maturation might be abnormal and RCT pathway might be weaken, and these changes were more seriously in MHL subjects. Plasma contents of small sized HDL particles significantly higher, whereas those of large sized HDL particles were significantly lower with elevation of TG/HDL-C and TC/HDL-C ratios. Increased in the TC/HDL-C ratio alone did not influence the distributions of HDL subclasses significantly when the TG/HDL-C ratio was low (TG/HDL-C ≤ 2.5). Hence, the TG/HDL-C ratio might be more sensitive to reflect the alteration of HDL subclass distribution than the TC/HDL-C ratio. In LDL-C/HDL-C ≤ 2.3 group, the pattern of distribution in HDL subclass was in agreement with the normolipidemic subjects. Moreover, considering the relative ease of measuring TC/HDL-C, TG/HDL-C and LDL-C/HDL-C ratios, as opposed to measuring HDL subclasses, these 3 ratios together may be a good indicator of HDL subclass distribution. The protective effect of increased apoA-I levels against the reduction of HDL2b caused by elevated TG concentration. On one hand, plasma HDL-C and apoA-I appear to play a coordinated role in the assembly of HDL particles and the determination of their contents among the total subjects. On the other hand, the apoA-I level might be a more powerful factor than HDL-C to influence the distribution of HDL subclasses in hyperlipidemic subjects. At the same time, from point of HDL subclasses distribution, the plasma lipids, apos concentrations and apos ratios should be considered while assessing the CHD risk. Abnormality of HDL subclasses distribution may result in accelerated atherosclerosis, therapeutic normalization of attenuated antiatherogenic HDL function in terms of both particle number and distribution of HDL particles is the target of innovative pharmacological approaches to large-sized HDL particles rising, including enhanced apoA-I levels.

Are hsCRP Levels and LDL/HDL Ratio Better and Early Markers to Unmask Onset of Dyslipidemia and Inflammation in Asymptomatic Subclinical Hypothyroidism?

“…The LDL-C/HDL-C is a better predictor for risk of heart disease than LDL-C alone. The LDL-C/HDL-C reflects the two way traffic of cholesterol entering and leaving the arterial intima [42]. An ideal ratio of LDL-C/HDL-C at 3.5 has been used as marker of coronary atherosclerosis.…”

Intake of Fatty Fish Alters the Size and the Concentration of Lipid Components of HDL Particles and Camelina Sativa Oil Decreases IDL Particle Concentration in Subjects with Impaired Glucose Metabolism

“…However, HDL and LDL are not homogeneous groups of particles, but have subfractions differing in size and density as well as in lipid and apolipoprotein compositions . These subfractions have different impact on the risk of CVD; large HDL particles may be more atheroprotective than small HDL particles . Conversely, small LDL particles may be more atherogenic than large LDL particles …”

The Changing Face of HDL and the Best Way to Measure It

“…When HDL is fractionated by density, the small, dense forms of HDL, known as HDL 3 , are converted into larger and less-dense forms, called HDL 2 , by LCAT. Large HDL 2 can be further remodeled by cholesteryl ester transfer protein (CETP), which exchanges HDL-associated cholesteryl esters for triglycerides (TGs) from TG-rich lipoproteins (e.g., verylow-VLDL and LDL) (13,14 ). Additionally, VLDL can transfer associated apoC and apoE, as well as phospholipid, to HDL via the phospholipid-transfer protein (11 ).…”