Plasma lipids and lipoproteins
Martin Andrew Crook in 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.
Atherosclerosis and Coronary Heart Disease
Victor A. Bernstam in 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
Physical Activity, Lipids, and Lipoprotein Metabolism: The Benefit of Exercise and Training in Hyperlipidemia
Ronald R. Watson, Marianne Eisinger in Exercise and Disease, 2020
The results and facts presented support the hypothesis of a multifactorial change in lipid and lipoprotein metabolism induced by increased physical activity. By means of physical exercise, it seems possible to favorably affect the lipid profile of the “still healthy” as well as the atherogenic lipid profile of cardiac risk groups, such as hypercholesterolemic individuals. This effect is achieved either directly, with respect to the currently known factors for atherosclerosis, or indirectly, by circumstances which are coupled with a monitored and physically active lifestyle. Overall, the differences observed in serum lipoprotein profiles between untrained and endurance-trained subjects strongly indicate adaptation mechanisms induced by physical activity. These effects cause the following metabolic processes that oppose possible progression of vascular atherosclerotic processes: Enlargement of the HDL pool responsible for reverse cholesterol transport with an elevation of the HDL-2 subfraction component that is considered cardio-protective.Acceleration of plasma triglyceride cleavage with improved metabolism of the probably atherogenic large triglyceride-rich LDL particles.34Reduction of the LDL pool with decrease in the certainly atherogenic small LDL particles.
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.
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).
Targeted delivery of garcinia glycosides by reconstituted high-density lipoprotein nano-complexes
Published in Journal of Microencapsulation, 2018
Chang Liu, Zijun Zhou, Ye Chen, Ju Liu, Yang Wang, Hongsheng Liu
As human endogenous substance, lipoproteins, especially high density lipoprotein (HDL), are important components of the nanoscale drug delivery systems. HDL consists of cholesterol, a hydrophobic lipid core and an apolipoprotein, especially apoA-1, which is a 28 kDa α-helical poly-peptide that serves as a binding domain for the HDL receptor (Lacko et al., 2002). Previous studies have demonstrated that plasma-derived HDL plays an important role in reverse cholesterol transport (RCT) by promoting the return of excess cholesterol from all the tissues of the body to the liver for degradation (Mo et al., 2016). In addition, HDL has the ability to escape the reticuloendithelial system (RES) so that it exhibits longer residence time in the blood than other drug formulation, such as lipidosome and micelle. Scavenger receptor class B type 1 (SR-B1) is an important receptor that has the ability to mediate the uptake of the drug payload of reconstituted HDL (rHDL) in vivo through the RCT process. Furthermore, SR-B1 is over-expressed in a variety of tumour cells such as hepatocellular carcinoma and ovarian cancer cells and to a lesser extent, in normal tissues (Rigotti et al., 2003, Fenske et al., 2009, Mooberry et al., 2010). Due to the special properties of HDL, it has been studied as a possible vehicle for drug delivery in the nanoscale drug delivery system. HDL has the ability to combine with hydrophobic drugs so as to reduce the toxicity and improve the therapeutic efficacy of the drugs (Ding et al., 2014), making it an ideal drug delivery vehicle.
Related Knowledge Centers
- Abca1
- Cholesteryl Ester
- Enzyme
- Phospholipid
- Cholesterol
- High-Density Lipoprotein
- Atp-Binding Cassette Transporter
- Apolipoprotein Ai
- Lecithin–Cholesterol Acyltransferase
- Cholesteryl Ester Transfer Protein