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Atherosclerosis and Coronary Heart Disease
Published in Victor A. Bernstam, Pocket Guide to GENE LEVEL DIAGNOSTICS in Clinical Practice, 2019
The recognized genetic defects of reverse cholesterol transport are few in number. A homozygous form of apo A-I deficiency resulting in defective HDL production leads to severe premature CHD and corneal opacities. Heterozygotes have half-normal HDL levels, and three types of mutations are associated with this condition: in type I (apo A-I/C-III), both apo A-I and C-III are deficientdeletion of the entire locus leads to the type II mutation, in which apo A-I, C-III, and C-IV are all deficientin type III, apo A-I is deficient due to a small insertion in the apo A-I gene leading to premature termination of translation of the apo A-I mRNA
Cardiometabolic comorbidities
Published in M. Alan Menter, Caitriona Ryan, Psoriasis, 2017
Dyslipidemia, commonly referred to as high cholesterol, is highly prevalent in people with psoriasis. Dyslipidemia is based on measurement of serum or plasma cholesterol concentration, which is then fractionated for the commonly reported elements. Total cholesterol, triglycerides (TGs), and high-density lipoprotein (HDL) are directly measured in most clinical laboratories. This then permits calculation of low-density lipoprotein (LDL) by the Friedewald formula. LDL total cholesterol and TGs contain apolipoprotein B, which is atherogenic. HDL contains apolipoprotein A and has been referred to as “good cholesterol” due to its beneficial activity of removing cholesterol from the body in a process called “reverse cholesterol transport.” In psoriasis, dyslipidemia also remains one of the most underdiagnosed CV risk factors,17 which is highly modifiable by lifestyle changes and medical therapy. Patterns of dyslipidemia observed in psoriasis resemble diabetes, whereby HDL is low, TGs are high, and LDL particles are small and dense.18,19 Finally, recent efforts have demonstrated that psoriasis severity directly relates to a decrement in the ability of HDL to perform “reverse cholesterol transport,” which may accelerate atherosclerosis in these patients.20
Plasma lipids and lipoproteins
Published in Martin Andrew Crook, Clinical Biochemistry & Metabolic Medicine, 2013
The transport of cholesterol from non-hepatic cells to the liver involves HDL particles, in a process called reverse cholesterol transport (Fig. 13.8). The HDL is synthesized in both hepatic and intestinal cells and secreted from them as small, nascent HDL particles rich in free cholesterol, phospholipids, apoA and apoE. This cholesterol acquisition is stimulated by adenosine triphosphate-binding cassette protein 1 (ABC1). If the plasma concentration of VLDL or chylomicrons is low, apoC is also carried in HDL, but as the plasma concentrations of these lipoproteins rise, these particles take up apoC from HDL. In addition, HDL can be formed from the surface coat of VLDL and chylomicrons. Various factors control the rate of HDL synthesis, including oestrogens, thus explaining why plasma concentrations are higher in menstruating women than in menopausal women or men.
The effects of resistance exercise training followed by de-training on irisin and some metabolic parameters in type 2 diabetic rat model
Published in Archives of Physiology and Biochemistry, 2022
Hassan Tavassoli, Ali Heidarianpour, Mehdi Hedayati
This study's results demonstrated that using HFD/STZ model increased TG, LDL-C, and TC levels and reduced irisin level in Wistar rats, but RET could decrease TG and TC levels and increase serum irisin concentration. An increase in skeletal muscle lipoprotein lipase expression is believed to be mediated through exercise-induced production of AMP-activated protein kinase (AMPK) allowing muscle to clear greater quantities of circulating lipids. Furthermore, exercise was observed to improve the “reverse cholesterol transport” that eliminates cholesterol (patel et al.2015). Increased enzymatic activity following exercise training increases the ability of muscle fibers to oxidize plasma fatty acids, VLDL cholesterol or TG (Mann et al. 2014). In addition to, RET resulted to significantly weight loss in HFDR group. It has been reported that weight loss causes a decrease in TG level, which can be attributed to an increase in LPL activity. Also, a small reduction in LDL-C level can be expected upon weight loss due to increased LDL receptor activity (klop et al.2013).
Lower LDL is better – can this be achieved with CETP inhibition therapy?
Published in Expert Review of Cardiovascular Therapy, 2020
In contrast to the decline in LDL levels, the substantial increases in HDL produced by anacetrapib (130%) are not thought to have contributed to CVD benefits achieved. This in and of itself is not a refute of the HDL hypothesis that HDL elevation confers CVD protection as the quality, components, and subtypes of the HDL produced by CETP inhibition – large, CE-enriched, slow-turning HDL particles – are not those necessarily found to be athero-protective in multitude of past studies [20]. Although some CETP inhibitors markedly increased cellular HDL efflux, a function shown to be significantly associated with decreased CHD risk in prior studies, it is difficult to assess whether this translated to enhanced hepatic HDL reverse cholesterol transport and, thereby, reduced CHD with the CETP inhibitors [21]. The effects of CETP inhibition by anacetrapib on HDL, overall, likely played a negligible role in CVD outcomes, whereas the effects on apoB can explain in large part its CVD mitigating effects.
CSL112, a reconstituted, infusible, plasma-derived apolipoprotein A-I: safety and tolerability profiles and implications for management in patients with myocardial infarction
Published in Expert Opinion on Investigational Drugs, 2018
Davide Capodanno, Roxana Mehran, C. Michael Gibson, Dominick J. Angiolillo
CSL112 is a human plasma-derived apoA-I, the primary functional component of HDL [13]. The processes of reverse cholesterol transport and HDL remodeling are schematized in Figure 1 [20]. In the first step of reverse cholesterol transport, lipid-poor apoA-I particles (also known as nascent HDL) interact with the membrane-bound ATP-binding cassette transporter A1 (ABCA1) to accept cholesterol from cells, including macrophages from the arterial wall. The free cholesterol is then esterified by the lecithin–cholesterol acyltransferase enzyme, leading to the formation of mature HDL that can accept cholesterol through other transporters. HDL is then constantly remodeled in the circulation by numerous enzymes and proteins, and cholesterol is finally taken back to the liver for removal. CSL112 acts by promoting cholesterol efflux preferentially through the ABCA1 transporter, which is overexpressed in atherosclerotic plaques.