Thematic review series: Patient-Oriented Research. What have we learned about HDL metabolism from kinetics studies in humans?

Abstract

Plasma measurements of lipids, lipoproteins, and apolipoproteins provide information on the static levels of these fractions without providing key information on the dynamic fluxes of lipoproteins in the circulation. Kinetics studies, in contrast, provide additional information on the production and clearance rates of lipoproteins and the flow of lipids and apolipoproteins through lipoprotein fractions. This information is crucial in accurately delineating the metabolism of HDL in plasma, because plasma concentrations of HDL are the net result of the de novo production and catabolism of HDL as well as the recycling of HDL particles and the contribution to HDL from components of other lipoproteins. Studies aimed at measuring the metabolism of HDL particles have shown that HDL metabolism in vivo is complex and consists of multiple components. Kinetics studies provide a window into the metabolism of HDL, allowing us to better understand the mechanisms of HDL decrease in human conditions and the functionality of HDL particles. Here, we review the progress in our understanding of HDL metabolism derived from in vivo kinetics studies, focusing primarily on studies in humans but also reviewing key studies in animal models.-Rashid, S

Therapeutic effect of high-dose green tea extract on weight reduction: A randomized, double-blind, placebo-controlled clinical trial

“…Therefore, cellulose treatment might not be able to reverse the trend of exacerbated insulin resistance without diet restriction or other treatment. According to a previous study, patients with insulin resistance exhibit increased HDL catabolism, which might explain the abnormal trend in HDL levels we observed in the cellulose group [32]. The influence of cellulose on sugar metabolism warrants further exploration.…”

Reduction of paraoxonase-1 activity may contribute the qualitative impairment of HDL particles in patients with type 2 diabetes

“…In the insulinresistant diabetic state, CETP and hormone-sensitive lipase modify HDL composition to triglyceride-rich HDL and then ApoA-I dissociates from HDL [48]. Released apoA-I can be filtered by the renal glomerulus and then degraded by proximal renal tubular cells [49]. However, if the HDL particle releases ApoA-I in patients with diabetes, Efflux-hdl in this study was underestimated, because applied HDL (which was adjusted for 5 mg/mL ApoA-I) would contain a greater number of HDL molecules in the fraction.…”

Sex-specific interaction between APOE genotype and carbohydrate intake affects plasma HDL-C levels: the Strong Heart Family Study

“…Beyond its putative role of sequestering and transporting cholesterol and other detrimental products back to the liver for disposal, HDL is believed to inhibit endothelial inflammation and promote production of endothelial nitric oxide (NO) and prostacyclins [39]. Variation in HDL levels is believed to be primarily associated with variation in clearance, except in dietary studies which have identified that fat intake affects HDL production or transport rates [61]. Although we cannot identify the specific metabolic effects on HDL-C variation here, as plasma levels of APOA-1 are not associated with carbohydrate intake, our findings suggest that catabolism may be the more likely mechanism affecting HDL-C variation in this study.…”

“…Kataoka et al [32] study examining the relationship of APOE polymorphisms to plasma lipids in the original Strong Heart Study individuals (n = 4,410), reported sexspecific variation associated with APOE polymorphisms. Genotype was not significantly associated with HDL-C variation in males (ages [45][46][47][48][49][50][51][52][53][54][55][56][57][58][59][60][61][62][63][64], however, in females, a significant trend for HDL-C levels was noted in all female subgroups studied: normal and diabetic, premenopausal and menopausal. HDL-C was higher in females carrying an e2 and lower in individuals carrying an e4 than for females with e3/3 genotypes.…”