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Bile Acid Sequestrants
Published in Charles Theisler, Adjuvant Medical Care, 2023
Prescription bile acid sequestrants such as cholestyramine (Cholybar, Questran) and cholestipol (Colestid) are used to reduce low-density lipoprotein (LDL) cholesterol levels. After oral administration, the sequestrants are not absorbed but instead bind to bile acids (which contain cholesterol) in the intestine and prevent their reabsorption into the body.1 Drugs that sequester bile acids can result in deficiencies of iron, folic acid, and fat-soluble vitamins (A, D, E, and K).1
Dyslipidemia
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Very low-density lipoproteins (VLDL) are rich in triglycerides, and are produced by the liver. They are similar to chylomicrons in size, also varying based on the amount of triglyceride being carried. With increased triglyceride production in the liver, the secreted VLDL particles are larger. The IDL are VLDL remnants. Removal of triglycerides from VLDL is done by the adipose tissue and muscle tissue. Lipoprotein (α) is an LDL particle with apolipoprotein (α) attached to Apo B-100 with a disulfide bond. The apolipoproteins play a structural role, serve as ligands for lipoprotein receptors, regulate formation of lipoproteins, and are important activators or inhibitors of enzymes involved in lipoprotein metabolism. Insulin resistance and type 2 diabetes mellitus are related to plasma lipid and lipoprotein abnormalities, increasing the risk for cardiovascular disease.
Components of Nutrition
Published in Christopher Cumo, Ancestral Diets and Nutrition, 2020
Among fats, attention focuses on cholesterol, mentioned earlier, as contributor to heart disease. In this context, medical practitioners distinguish between good and bad cholesterol. This language causes confusion because “good cholesterol” is more than cholesterol—also having protein, triglycerides, and phospholipids (a lipid with phosphorus)—and is known as high-density lipoproteins (HDL).56 Doctors praise HDL for removing excess cholesterol from the blood whereas low-density lipoproteins (LDL)—having different ratios of the same components—are deemed bad because they carry cholesterol to cells. Cells depend on LDL for it, though problems arise when LDL bring too much. Criticisms of cholesterol should not discount its role in manufacturing cell membranes, acids that help digest food, vitamin D from sunlight, and five types of steroid hormones: progestins, glucocorticoids, mineralocorticoids, estrogens, and androgens, all of which the body requires.
Secretory autophagy: a turn key for understanding AMD pathology and developing new therapeutic targets?
Published in Expert Opinion on Therapeutic Targets, 2022
Janusz Blasiak, Kai Kaarniranta
Lipoproteins are categorized into five classes according to their density and apolipoprotein composition: HDL, high-density lipoprotein; LDL, low-density lipoprotein; IDL, intermediate-density lipoprotein and VLDL, very-low-density lipoprotein. The cellular uptake of lipoprotein occurs via the specific LDL-receptors (LDL-R). Once the lipoprotein binds to an LDL-R, it is endocytosed along with the receptor. The gradual cytosolic acidification enables the dissociation of the lipoprotein from the receptor and finally the lipoprotein may be degraded in the lysosome [42]. Acid lipase hydrolyzes triglycerides and cholesterol esters, resulting in the release of fatty acids and free cholesterol [43]. The released free lipids can then be transferred to the plasma membrane or the endoplasmic reticulum membrane (ER) to create a lipoprotein complex after covalent binding with proteins. In drusen, the major ultrastructural components are large apolipoprotein B,E-containing cholesterol-rich lipoproteins that are secreted by the RPE [44]. The interplay between cholesterol oxidation products and Aβ, as well as Schiff-base formation by Aβ and aldehyde-bearing lipid products increase Aβ amyloidogenicity with oxidation products of cholesterol [45]. Aβ is an example of how drusen lipoproteins are linked to secretory autophagy since they do not have ER-leader sequence [9]. Proteins having such a sequence in their amino-terminal tail are canonically secreted outside of the cell via the Golgi apparatus [46].
Associations of serum monocyte-to-high-density lipoprotein cholesterol ratio with digital ulcers and skin fibrosis in patients with systemic sclerosis
Published in Scandinavian Journal of Rheumatology, 2021
H-B Kim, A Kim, Y Kim, G-T Kim, E Ahn, MW So, DH Sohn, S-G Lee
Monocytes/macrophages play an important role in the immune response through releasing proinflammatory and pro-oxidant cytokines. High-density lipoprotein cholesterol (HDL) can inhibit the recruitment and migration of monocytes/macrophages and accumulation of vascular cholesterol (8). Thus, the monocyte-to-high-density lipoprotein cholesterol ratio (MHR) may reflect the pathogenesis of atherosclerosis and has emerged as a novel prognostic indicator in CVDs (8, 9). The MHR was also found to be a marker for inflammation (8), oxidative stress (10), and endothelial dysfunction (11), all of which could contribute to the pathogenesis of fibrosis and vasculopathy in SSc (7, 12). Monocytes/macrophages have been reported to be activated in SSc (13) and contribute to its pathogenesis by secreting transforming growth factor-β (TGF-β), a major fibrogenic cytokine (14, 15). Taken together, it is assumed that the MHR may function as a potential biomarker in SSc; however, few studies have investigated the clinical implications of utilizing this marker in patients with SSc. Thus, the purposes of this study were to compare serum MHR values between patients with SSc and healthy controls and to investigate its potential relationship with clinical manifestations and organ involvement in SSc.
Rationale for screening selected patients for asymptomatic carotid artery stenosis
Published in Current Medical Research and Opinion, 2020
Kosmas I. Paraskevas, Hans-Henning Eckstein, Dimitri P. Mikhailidis, Frank J. Veith, J. David Spence
A little-recognized reason for performing carotid ultrasound in patients with known vascular disease is that showing patients images of their carotid plaque improves preventive care. In a study in Wisconsin, this increased by four-fold their intention to take statins, and visualization of plaque increased by seven-fold the likelihood that physicians would prescribe statins36. In a recent randomised trial in Sweden, patients who were shown images of their carotid plaques had significantly reduced Framingham Risk scores over 1 year, whereas risk scores increased in the control group37. Measuring carotid plaque burden improves medical therapy and reduces the risk of both stroke and MI5. Reduction of low-density lipoprotein cholesterol (LDL-C) levels with any combination of lipid-lowering interventions reduces stroke risk proportional to the extent of cholesterol reduction38. However, treating LDL-C to consensus target levels is not sufficient; many patients have plaque progression despite LDL-C below 1.8 mmol/L39. Treating atherosclerosis without measuring plaque would be like treating hypertension without measuring blood pressure40.