Reverse Cholesterol Transport: Molecular Mechanisms and the Non-medical Approach to Enhance HDL Cholesterol

Abstract

Dyslipidemia (high concentrations of LDL-c and low concentrations of HDL-c) is a major cause of cardiovascular events, which are the leading cause of death in the world. On the other hand, nutrition and regular exercise can be an interesting strategy to modulate lipid profile, acting as prevention or treatment, inhibiting the risk of diseases due to its anti-inflammatory and anti-atherogenic characteristics. Additionally, the possibility of controlling different training variables, such as type, intensity and recovery interval, can be used to maximize the benefits of exercise in promoting cardiovascular health. However, the mechanisms by which exercise and nutrients act in the regulation of cholesterol and its fractions, such as reverse cholesterol transport, receptors and transcription factors involved, such as PPARs and their role related to exercise, deserve further discussion. Therefore, the objective of this review is to debate about non-medical approaches to increase HDL-c, such as nutritional and training strategies, and to discuss the central mechanisms involved in the modulation of lipid profile during exercise, as well as that can be controlled by physical trainers or sports specialists in attempt to maximize the benefits promoted by exercise. The search for papers was performed in the databases: Medline (Pubmed), Science Direct, Scopus, Sport Discus, Web of Science, Scielo and Lilacs until February 2016.

Comprehensive amelioration of high-fat diet-induced metabolic dysfunctions through activation of the PGC-1α pathway by probiotics treatment in mice

“…RCT is the major route for removal of excess cholesterol from peripheral tissues and its transport to the liver, by which HDL protects against atherosclerotic cardiovascular disease [37]. In RCT, excess cholesterol from macrophage foam cells is transferred and carried by HDL to the liver for excretion as bile acids or free cholesterol into the feces, including ApoA1-activated LCAT-mediated HDL maturation, HDL cholesterol uptake via SR-BI, and biliary cholesterol secretion by ABCG5 and ABCG8 [38]. Our results showed an increased hepatic expression of SR-B1, ABCG5, ABCG8, LCAT, and ApoA1 in L. plantarum treated mice (Fig 2H), from which it is indicated that L. plantarum treatment contributes to prevent elevated cholesterol levels by promoting RCT.…”

Exercise intensity and physical fitness modulate lipoproteins profile during acute aerobic exercise session

“…training, especially at moderate intensity protocols, is associated with the regulation of the lipid profile, decreasing concentrations of total cholesterol, LDL-c, triacylglycerol, and increasing HDL-c, being this process facilitated by reverse cholesterol transport mediated by enzymatic modulation of lecithin-cholesterol acyltransferase (L-CAT) and cholesteryl ester transfer protein (CETP) 9 .…”

The causal pathway effects of a physical activity intervention on adiposity in children: The KISS Study cluster randomized clinical trial

“…The indirect impact of the intervention on adiposity via HDL/cholesterol might be due to the positive relationship between aerobic capacity and lipid profile regulation. This relationship is associated with the enzymatic modulation of lecithin‐cholesterol acyltransferase (L‐CAT), which is involved in the esterification of cholesterol 27 . In addition, cholesteryl ester transfer protein (CETP) is one of the facilitators of the transport of cholesterol ester particles of HDL‐c to other lipoproteins, 28,29 since both L‐CAT and CETP are part of the mechanism in which the excess of cholesterol is removed from the peripheral tissues and both pathways are stimulated by physical activity 27 .…”

“…This relationship is associated with the enzymatic modulation of lecithin‐cholesterol acyltransferase (L‐CAT), which is involved in the esterification of cholesterol 27 . In addition, cholesteryl ester transfer protein (CETP) is one of the facilitators of the transport of cholesterol ester particles of HDL‐c to other lipoproteins, 28,29 since both L‐CAT and CETP are part of the mechanism in which the excess of cholesterol is removed from the peripheral tissues and both pathways are stimulated by physical activity 27 . Moreover, aerobic exercise has been shown to activate the hydrolysis of the triacylglycerols (TAG) from very low‐density lipoprotein (VLDL) by lipoprotein lipase (LPL), which partly results, in the production of beneficial HDL‐c particles 30,31 .…”