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Diabetes Mellitus, Obesity, Lipoprotein Disorders and other Metabolic Diseases
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Overproduction of apolipoprotein B-containing lipoproteins by the liver results in high cholesterol and/or triglycerides, reduced HDL, raised apo B and increased small, dense (atherogenic) LDL. Obesity and insulin resistance are more common in familial combined hyperlipidaemia (FCH) and contribute to the phenotypic variation.
Dyslipidaemia in Hypertension
Published in Giuseppe Mancia, Guido Grassi, Konstantinos P. Tsioufis, Anna F. Dominiczak, Enrico Agabiti Rosei, Manual of Hypertension of the European Society of Hypertension, 2019
Massimo Volpe, Giovanna Gallo, Giuliano Tocci
In a study including 16,130 adult normotensive women, after a 10-year follow up the incidence of hypertension was increased by 14% and 25% in patients with high concentrations of total cholesterol and non-HDL cholesterol, respectively, and decreased by 19% in subjects with high HDL-cholesterol (10). Another study demonstrated that high concentrations of apolipoprotein-B were associated with a 1.4-fold higher risk of hypertension.
Plasma lipids and lipoproteins
Published in Martin Andrew Crook, Clinical Biochemistry & Metabolic Medicine, 2013
This condition is due to a mutation in the apoB gene resulting in a substitution of arginine at the 3500 amino acid position for glutamine. Apolipoprotein B is the ligand upon the LDL particle for the LDL receptor. It may be indistinguishable clinically from FH and is also associated with hypercholesterolaemia and premature coronary artery disease. The treatment is similar to that for heterozygote FH. The apoB gene is located upon chromosome 2.
The Effect of Hesperidin and Diosmin Individually or in Combination on Metabolic Profile and Neuropathy among Diabetic Patients with Metabolic Syndrome: A Randomized Controlled Trial
Published in Journal of Dietary Supplements, 2023
Hasnaa Osama, Ehdaa O. Hamed, Muhammed A. Mahmoud, Mohamed E. A. Abdelrahim
Lipid metabolism abnormalities are well known in patients with T2DM. Clinically relevant animal models and randomized controlled trials revealed the positive effect of hesperidin (34, 35) and diosmin (36) on lipid profile. Notably, 12-week supplementation of both hesperidin and diosmin, either individually or in combination has shown a consistent serum LDL and TGs-lowering effect among type 2 diabetic patients with MetS in the present study. However, although hesperidin and diosmin consumption during 12-week trial increased HDL level, this increase was non-significant in the study groups, which agreed with the results obtained in previous studies (19, 32, 34). This favorable effect on lipid profile partially could be explained by the reduction of the enzymatic activities involved in cholesterol metabolism and the net secretion of apolipoprotein B (apoB) which constitutes the LDL protein (35).
Colesevelam – a bile acid sequestrant for treating hypercholesterolemia and improving hyperglycemia
Published in Expert Opinion on Pharmacotherapy, 2022
Oluwayemisi Esan, Adie Viljoen, Anthony S. Wierzbicki
Cardiovascular disease (CVD) is one of the leading causes of morbidity and mortality. A substantial component is caused by lipids with associations shown with total cholesterol and its easily measured subfractions low-density lipoprotein-cholesterol (LDL-C) [1] and high-density lipoprotein-cholesterol (HDL-C) [2]. Non-high density lipoprotein cholesterol (nHDL-C [2]; which adds the contribution of triglyceride (TG)-rich lipoproteins; (TGRLs) [3,4] to LDL-C is a better predictor of CVD than LDL-C alone. Studies also find a strong association of CVD with apolipoprotein B100 levels. As there is one molecule of apoB per very low density lipoprotein (VLDL) or LDL particle this translates to an association with the cholesterol content of nHDL-C particles . Statins and other LDL-C reducing drugs reduce the 5 year incidence of major coronary events, coronary revascularisation and stroke by about 21% per 1 mmol/L reduction in LDL-C [5]. Treatment options beyond statins are only considered as add-on treatment, when these drugs are not tolerated or when hypertriglyceridemia is present. Bile acid sequestrants (BAS) are one of the classes of traditional lipid-lowering therapies now viewed as third line agents for reducing LDL-C. This article reviews the mechanism of action, pharmacokinetics, pharmacodynamics, safety and efficacy of the BAS colesevelam in CVD and patients with type 2 diabetes (T2DM) focusing on their effects on glycemic control. Other reviews have addressed the role of colesevelam in reducing LDL-C [6,7]
Current and emerging drugs for the treatment of atherosclerosis: the evidence to date
Published in Expert Review of Cardiovascular Therapy, 2022
Ali A. Rizvi, Djordje S. Popovic, Nikolaos Papanas, Anca Pantea Stoian, Wael Al mahmeed, Amirhossein Sahebkar, Andrej Janez, Manfredi Rizzo
Although proper and comprehensive cardiovascular risk prevention is available, a considerable amount of residual risk exists and a large proportion of patients continue to suffer from major cardiovascular events. This has led research to identify new risk biomarkers as well as novel therapeutic approaches. In this context, the apolipoprotein B/apolipoprotein AI ratio, a surrogate of dyslipidemia, had the highest calculated population attributable risk, thus suggesting that blood lipid represent the leading risk factor for acute myocardial infarction [17]. The lowering of LDL-C and other apolipoprotein B-containing lipoproteins reduces the risk of future cardiovascular events [18]. Beyond LDL, low concentrations of high-density lipoproteins (HDL) are also associated with increased cardiovascular risk [19] and, in recent years, it has became evident that subjects with a specific form of dyslipidemia, the so-called lipid triad or atherogenic lipoprotein phenotype, are those exposed to much higher risk [20,21]; this type of dyslipidemia is constituted by three plasma lipid alterations, namely high triglycerides, low HDL-cholesterol and increased levels of atherogenic small, dense LDL.