China
Africa
Explore chapters and articles related to this topic
Atherosclerosis and Coronary Heart Disease
Published in Victor A. Bernstam, Pocket Guide to GENE LEVEL DIAGNOSTICS in Clinical Practice, 2019
Polymorphisms affecting regulatory elements of the apo A–I/C–III/A–IV region do account for hyperalphalipoproteinemia. The strong antiatherosclerotic potential of this type of HDL alteration has been subsequently demonstrated. Polymorphisms in the gene coding for CETP, particularly the TaqI, appear to be related to plasma HDL-cholesterol and transfer protein activity.
Berries and Lipids in Cardiovascular Health
Published in Catherina Caballero-George, Natural Products and Cardiovascular Health, 2018
Arpita Basu, Nancy Betts, Paramita Basu, Timothy J. Lyons
In addition to measuring lipid outcomes related to conventional lipids, findings reported by Qin et al. (2009) and Zhu et al. (2015) provide further mechanistic insights on the hypolipidemic effects of purified berry extracts in adults with independent cardiovascular risks such as dyslipidemia/hyperlipidemia and type 2 diabetes. In a 12-week randomized placebo-controlled trial in adults with dyslipidemia, purified anthocyanins derived from bilberries and black currants were shown to decrease the mass and activity of cholesteryl ester transfer protein (CETP) (Qin et al., 2009). CETP is a plasma protein that mediates the removal of cholesteryl esters from HDL in exchange for a triglyceride molecule derived primarily from either LDL, VLDL or chylomicrons. Thus, CETP inhibition has been shown to be a possible mechanism for the elevation of HDL cholesterol and decrease of LDL cholesterol (Inazu et al., 1990). In another study in participants with type 2 diabetes, supplementation of a similar berry anthocyanin extract was shown to decrease specific plasma apolipoproteins, especially apolipoprotein B and CIII that have been associated with increased risks of atherosclerotic CVD in epidemiological observations (Jiang et al., 2004; Wyler von Ballmoos et al., 2015; Zhu et al., 2015).
Plasma lipids and lipoproteins
Published in Martin Andrew Crook, Clinical Biochemistry & Metabolic Medicine, 2013
The enzyme lecithin–cholesterol acyltransferase (LCAT) is present on HDL and catalyses the esterification of free cholesterol and is activated by apoA1, the predominant apolipoprotein of HDL. Some HDL particles also contain apoA2. Most of this esterified cholesterol is transferred to LDL, VLDL and chylomicron remnants and thus ultimately reaches the liver. Some may be stored within the core of the HDL particle and taken directly to the liver. Cholesterol ester transfer protein (CETP) is involved in these processes.
Heightened risks of cardiovascular disease in South Asian populations: causes and consequences
Published in Expert Review of Cardiovascular Therapy, 2023
Maria Stefil, Jack Bell, Peter Calvert, Gregory YH Lip
The lipid profile of South Asian people is typically characterized by higher triglyceride levels[66], lower high-density lipoprotein (HDL), and lower low-density lipoprotein (LDL) levels compared to non-Asian people [67]. While LDL levels in South Asian people are typically lower than in non-South Asian people, a small study reported that Indian people have a greater prevalence of smaller and denser LDL particles compared to matched White controls [68] which may contribute to ASCVD risk[69]. This lipid pattern of high triglyceride levels, low HDL, and a small dense LDL phenotype is typically thought to be a sequelae of insulin resistance[70], although this pattern is also associated with abnormalities in cholesteryl ester transfer protein (CETP). CETP is a plasma protein that promotes the transfer of cholesteryl esters from HDLs to proatherogenic lipoproteins, such as LDLs, IDLs, and VLDLs[71]. CETP activity has been shown to be 30% higher in South Asians compared to matched Europeans (p < 0.0001) and is associated with higher triglyceride levels, lower HDL, and smaller LDL particle size.
Islamic fasting: cardiovascular disease perspective
Published in Expert Review of Cardiovascular Therapy, 2022
Hifza Naz, Rakhshan Haider, Haroon Rashid, Zargham Ul Haq, Jahanzeb Malik, Syed Muhammad Jawad Zaidi, Uzma Ishaq, Roberto Trevisan
The cardioprotective effect of IF is mainly based on reduced oxidative damage and increased cellular stress resistance. These may also be moderated by the brain-derived neurotrophic factor. These processes are similar to those induced by regular exercise [49]. Furthermore, the enzymatic actions induced by IF, such as decreasing the expression of sterol regulatory element-binding protein 2, which suppresses the action of several enzymes responsible for cholesterol synthesis, lead to cholesterol level reduction [73]. IF may also decrease cholesteryl ester transfer protein (CETP) expression, when associated with fat loss- often seen in RDIF, a protein responsible for transferring cholesterol esters from HDL-C to VLDL-C. This lowers HDL-C levels and increases VLDL-C levels, thus, leading to IF induced CETP-lowering effect leading to an increase in HDL-C [74].
An update on emerging drugs for the treatment of hypercholesterolemia
Published in Expert Opinion on Emerging Drugs, 2021
Adam J Nelson, Kristen Bubb, Stephen J Nicholls
Cholesteryl ester transfer protein (CETP) plays an important role in the regulation of lipid metabolism, promoting transfer of esterified cholesterol from HDL to VLDL and LDL particles, in exchange for triglycerides [62]. CETP inhibitors were originally developed on the basis of their ability to raise HDL cholesterol levels [62] and atheroprotective properties of CETP inhibition in rabbit models [63–66]. However, the clinical development of small molecule CETP inhibitors has proven challenging. The first agent, torcetrapib, was demonstrated to produce an increase cardiovascular events and all-cause mortality [67]. Subsequent analyses revealed that torcetrapib possessed a number of off-target toxicities, including elevation of blood pressure, adrenal synthesis of cortisol and aldosterone and aortic wall expression of endothelin [67–69]. The ability to demonstrate a lack of such effects would permit other CETP inhibitors to proceed in development. However, outcomes trials of the modest CETP inhibitor, dalcetrapib, and the potent CETP inhibitor, evacetrapib, demonstrated clinical futility with no impact on cardiovascular events [70,71]. Anacetrapib, an additional potent CETP inhibitor, was demonstrated to produce a significant reduction in cardiovascular events, with the degree of benefit directly proportional to the extent of lowering levels of atherogenic lipoproteins [72]. Clinical development of this agent was halted due to the finding of adipose tissue accumulation.