Small HDL subclasses become cholesterol-poor during postprandial period after a fat diet intake in subjects with high triglyceridemia increases

CETP and LCAT Gene Polymorphisms Are Associated with High‐Density Lipoprotein Subclasses and Acute Coronary Syndrome

“…Since CETP Taq1B A5454G polymorphism is associated with an altered CETP activity (Ordovas et al, ), we suggest that its impact is more important on the HDL structure than in the plasma lipid profile. In this context, HDL structure has been proposed to be related with CHD risk rather than HDL‐C plasma levels (Perez‐Mendez et al, ); the selective increase or decrease of cholesterol associated to certain HDL subclasses is likely the result of an impaired metabolism of lipoproteins (Perez‐Mendez et al, , ; Quintanilla‐Cantu et al, ; Toledo‐Ibelles et al, ), which in turn may represent an increased risk of CAD (Perez‐Mendez et al, ). This idea is consistent with the potential role of the AGA haplotype conformed by CETP‐971 A/G , CETP Taq1B A/G, and LCAT A21892G SNP in the CETP–LCAT genetic region; in fact, this haplotype may be related to the quality of HDL derived from the coordinated activity of both proteins.…”

Hypertriglyceridemia and atherosclerosis

“…TRLs can also impact HDL levels and its particle size. At the setting of the higher TG levels, the greater exchange between TG of apoB-containing lipoproteins and cholesterol ester (CE) of HDL via CETP results in the TG-rich and CE-poor HDL particles which can be catabolized faster and more rapidly than large and CE-rich HDL, and the process brings the consequence with lower levels of HDL-C. And, a recent study also revealed that high postprandial triglyceridemia induced a shift of HDL size towards large particles, and cholesterol depletion with TG enrichment of HDL3 subclasses [ 73 ]. The change of HDL structure is related with their antioxidant capacity that may be affected by HDL remodeling [ 74 ].…”

“…Whether the TG-rich and CE-poor HDL particles contain different content of PON1 or the change of PON1 activity, by which contribute to atherosclerosis. However, a study found that PON-1 activity did not decrease and significantly increase along the postprandial stage [ 73 ]. And, the further studies will undoubtedly need to be conducted to investigate the roll of such structural modifications (other components or proteins, i.e.…”

High Density Lipoproteins: Metabolism, Function, and Therapeutic Potential

“…Of note, HDLs play an important role in uptake from the gut and transport into the systemic circulation of antioxidants, such as carotenoids and vitamins of dietary origin (18). Indeed, HDL structure and lipidome are modified post-prandially and in relation to the magnitude of post-prandial triglyceridemia HDL may acquire larger size and a triglyceride rich phenotype (19). Along this evidence, it has been suggested that non-fasting HDL concentrations may be more appropriate predictors of cardiovascular events than fasting levels (20,21).…”

“…Along this evidence, it has been suggested that non-fasting HDL concentrations may be more appropriate predictors of cardiovascular events than fasting levels (20,21). The underlying Abbreviations: ABCA1, ATP-Binding Cassette Transporter 1; apoA1, Apolipoprotein A1; ApoA2, Apolipoprotein A2; CD36, Cluster of Differentiation 36; CETP(i), Cholesteryl Ester Transfer Protein (inhibitor); eNOS, Endothelial Nitric Oxide Synthase; EPC, Endothelial Progenitor Cells; FMD, Flow Mediated Vasodilation; HDL, High Density Lipoproteins; HDL-C, HDL cholesterol; HDL-TG, HDL triglycerides; LDL, Low Density Lipoprotein; miRNA, Micro Ribonucleic Acid; NO, Nitric Oxide; NMR, nuclear magnetic resonance; PL, Phospholipid; PON-1, Paraoxonase-1; RCT, Reverse Cholesterol Transport; rHDL, Reconstituted HDL; RYGB, Roux-en-Y Gastric Bypass; S1P, Sphingosine-1-Phosphate; S1PR, Sphingosine-1-Phosphate Receptor; SM, Sphingomyelin; S-rHDL, Reconstituted HDL encapsulated statin; T2DM, Type 2 Diabetes Mellitus; TNF-α, Tumor Necrosis Factor α; TG, Triglycerides; VEGF-A, Vascular Endothelial Growth Factor A; VEGFR2, Vascular Endothelial Growth Factor Receptor 2; VLDL, Very Low-Density Lipoproteins biological explanation is still unclear as for instance, a major HDL antioxidant enzyme, paraoxonase-1 (PON-1) activity may not decrease along the postprandial stage (19). The post-prandial metabolism of HDL is still poorly detailed and would benefit from additional investigations in larger groups of individuals in health and disease conditions.…”