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Nutrition and Nutritional Supplements in the Management of Dyslipidemia and Dyslipidemia-Induced Cardiovascular Disease
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
Curcumin is one of the phenolic compounds in turmeric and curry [5,116]. It induces changes in the expression of genes involved in cholesterol synthesis such as LDL receptor mRNA, HMG-CoA reductase, SREBP, cholesterol 7 alpha hydroxylase, peroxisome proliferator-activated receptors (PPARs), liver X receptor (LXR), activated protein kinase (AMPK), ATP-binding cassette transporters (ABCA1 and ABCG1), receptors for RCT, and CEC [5,116]. In one human study of ten patients consuming 500 mg/day of curcumin, the HDL increased 29% and TC fell 12% [5,116]. This needs confirmation in larger randomized clinical trials.
Fenugreek in Management of Primary Hyperlipidaemic Conditions
Published in Dilip Ghosh, Prasad Thakurdesai, Fenugreek, 2022
Subhash L. Bodhankar, Amit D. Kandhare, Amol P. Muthal
Hyperlipidaemia is a chronic, complex condition well characterized by an abnormal increase in lipids including total cholesterol (TC) and triglyceride (TG) as well as lipoproteins such as low-density lipoprotein-cholesterol (LDL-C) and very-low-density lipoprotein-cholesterol (VLDL-C) with a decrease in high-density lipoprotein-cholesterol (HDL-C) levels in serum (Parhofer 2016). These elevated lipid levels are closely associated with increased risk of various disorders such as cardiovascular diseases, diabetes, insulin resistance, obesity, and hepatotoxicity. Furthermore, epidemiological studies have reported several unhealthy lifestyle factors, including cigarette smoking, alcohol consumption, poor diet, physical inactivity, and consumption of a diet with high saturated or trans fats responsible for hyperlipidaemia (Karr 2017; Writing Group et al. 2016). In addition, a genetic factor also plays an essential role in the development of familial hypercholesterolaemia where genetic mutations in the LDL receptor (LDLR) and apolipoprotein (apo) B gene caused significant elevations in TC and LDL-C (Nordestgaard et al. 2013; Sjouke et al. 2015).
Dyslipidemia
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
To reduce LDL, the statins are the treatment of choice. They greatly reduce cardiovascular disease and deaths. The statins inhibit hydroxymethylglutaryl CoA reductase. This is an important enzyme in the synthesis of cholesterol. The statins lead to LDL receptor up-regulation and more clearance of LDL. They reduce LDL by as much as 60% while causing small increases in HDL and moderate decreases in total triglycerides. The statins may decrease systemic inflammation, intra-arterial inflammation, or both. They do this by stimulating endothelial nitric oxide production. Other types of lipid-lowering drugs are not as effective as the statins for decreasing ASCVD. There are high, moderate, and low intensity statin regimens, based on the patient’s age and conditions. Statins are chosen based on comorbidities, other drugs being taken, intolerance to statins, risk factors for adverse outcomes, cost, and the preference of the patient.
LDR-adapted liver-derived cytokines have potential to induce atherosclerosis
Published in International Journal of Radiation Biology, 2023
Eunguk Shin, Dahye Kim, You Yeon Choi, HyeSook Youn, Ki Moon Seong, BuHyun Youn
LDL receptor deficient (Ldlr−/−) mouse model is very similar to the human lipoprotein profile and thus has been employed as a platform to assess the role of a large variety of genes in atherosclerosis as a suitable model to study atherosclerosis (Getz and Reardon 2016). Ldlr−/− mice fed a normal diet have slightly elevated plasma cholesterol levels from an accumulation of LDL resulting in minimal atherosclerotic lesions in the proximal aortic root, whereas a high-fat diet increases the severity of atherosclerotic lesions and hypercholesterolemia in Ldlr−/− mice (Knowles and Maeda 2000). Therefore, Ldlr−/− mice have helped a great deal understand the biology of atherosclerosis because they made it possible to investigate numerous effects on atherosclerosis without resorting to a diet containing high levels of fat and cholesterol (Zhao et al. 2018).
Evolocumab, a PCSK9 inhibitor, protects human endothelial cells against H2O2-induced oxidative stress
Published in Archives of Physiology and Biochemistry, 2022
Leila Safaeian, Mina Mirian, Shahryar Bahrizadeh
The proprotein convertase subtilisin/kexin type 9 (PCSK9) is a member of the family of proprotein convertases. This family of proteins comprises 9 members with wide expression in different organs and several important biological activities (Seidah et al. 2013). Over the past decade, PCSK9 has received special attention as a therapeutic goal in the treatment of lipid disorders. This enzyme binds to the low density lipoprotein (LDL) receptor in the liver and reduces the presentation of LDL receptor on the cells surface for eliminating LDL particles from extracellular medium. Therefore, inhibition of PCSK9 results in lesser serum LDL level and lower risk of cardiovascular disorders (Cohen et al. 2006). PCSK9 may also accelerate the development of atherosclerosis through several non-LDL receptor-dependent mechanisms such as inflammation, raising blood pressure, diabetes and impairment of endothelial function (Urban et al. 2013). In addition to the liver, PCSK9 is broadly expressed in many tissues and also in the vascular system including endothelial cells, macrophages and smooth muscle cells (Poyner 1992).
Proprotein convertase subtilisin/kexin type 9 is associated with atherosclerosis in patients with Behcet’s disease
Published in Clinical and Experimental Hypertension, 2022
Rabia Aydogan Baykara, Pinar Diydem Yilmaz, Mevlüt Hakan Göktepe, Cengiz Kadiyoran, Mustafa Ogul, Adem Kucuk, Medine Cumhur Cüre, Erkan Cüre
Proprotein convertase subtilisin/kexin type 9 (PCSK9) is an enzyme, the 9th member of the proprotein converting protein family, encoded by the gene located on chromosome 1, found in many tissues and cell types (7). PCSK9 binds to the receptor for low-density lipoprotein particles (LDL) that carry fat molecules in the extracellular fluid (8). The LDL receptor (LDLR) found on many cells initiates the uptake of LDL particles from the extracellular fluid into cells, thereby reducing LDL particle concentrations (9). PCSK9 binds to the LDLR and induces lysosomal degradation of LDLR in cells. The increase in PCSK9 leads to an increase in the LDL level by lowering the number of LDLRs (10). Therefore, there is a strong relationship between PCSK9 and subclinical atherosclerosis and coronary artery disease (11).