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Liver Function Tests in the Differential Diagnosis of Hepatotoxicity
Published in Robert G. Meeks, Steadman D. Harrison, Richard J. Bull, Hepatotoxicology, 2020
It is not surprising that a variety of changes in the levels of various lipids and lipoproteins occur in hepatobiliary disorders since the liver is so intimately involved in lipid metabolism. Serum triglycerides, phospholipids, fatty acid acids, and total cholesterol and its ester are occasionally used to differentiate cholestatic from necrotic processes (Bass et al., 1976). Although changes in triglycerides and total cholesterol levels are not liver-specific, the percent of cholesterol ester (CE) or the occurrence of a unique “lipoprotein-X” (LP-X) can suggest hepatocellular deficiencies or cholestasis, respectively, may be present (Kaplowitz et al., 1982). In hepatocellular disorders, less CE is formed due to low lecithin cholesterol acyltransferase (LCAT) activity in the liver. Elevated levels of both total cholesterol and LP-X are observed in animals with biliary obstruction (Sabesin, 1982). Normal lipoproteins are spherical bodies, while the abnormal LP-X is spherical in structure (Monzato et al., 1976). After the elimination of extrahepatic obstruction in animals, LP-X quickly disappears from the plasma and hepatic LCAT activity returns (Ritland and Bergan, 1975). Although LP-X is not more sensitive than other tests to detect cholestasis, it is another useful test that could be used. The density classes of lipoproteins (VLDL; LDL; HDL; HDL2) are also occasionally measured and are altered significantly in hepatobiliary disorders (Cooper, 1982). There is a need for investigations on such lipids in laboratory animals.
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.
Molecular Imaging of Atherosclerosis with Magnetic Resonance
Published in Michel M. J. Modo, Jeff W. M. Bulte, Molecular and Cellular MR Imaging, 2007
Karen C. Briley-Saebo, Willem J. Mulder, Fabien Hyafil, Venkatesh Mani, Vardan Amirbekian, Juan Gilberto S. Aguinaldo, James F. Rudd, Silvia H. Aguiar, Zahi A. Fayad
HDLs may provide protection against cardiovascular events by decreasing cholesterol accumulation in atherosclerotic plaque.79,80 Additionally, HDL also may reduce atherosclerosis by decreasing LDL oxidation, a critical step in foam cell formation.79,80 The apolipoprotein (ApoA-I), associated with HDL, allows for receptor-mediated uptake of the material within the lesion. Once inside the plaque, the HDL sequesters the free cholesterol via ATP-binding cassette transporter 1 (ABACA1) and lecithin-cholesterol acyltransferase. Once HDL sequesters the cholesterol, the shape of the particle changes from a discoid form (β-form) to spherical α-HDL.79,80 Due to the therapeutic advantages associated with HDL, contrast agents based upon this platform (as opposed to LDL) may be desirable, as shown in Figure 9.7. Studies using gadolinium-labeled a-LDL have shown that these particles penetrate the plaque, allowing for detection by MRI.33 Additionally, these studies indicate that the labeled HDL was primarily localized within the intima layer, with some accumulation in macrophages, as shown in Figure 9.8.
Antihyperlipidemic effect of tyrosol, a phenolic compound in streptozotocin-induced diabetic rats
Published in Toxicology Mechanisms and Methods, 2021
Ramasamy Chandramohan, Leelavinothan Pari
Lecithin cholesterol acyltransferase (LCAT) is a crucial enzyme and plays a significant role in removing free cholesterol from tissues via assisting HDL-C maturation, and its activity has been proposed as the primary indicator of HDL-C function. Therefore, if LCAT is impaired, mature HDL generation would presumably be decreased, resulting in augmentation of atherosclerosis (Kripa et al. 2011). In this study, we observed reduced activity of LCAT in plasma signifies the impairment of HDL-C synthesis as well as cholesterol and triglycerides transport and metabolism in STZ-induced diabetic rats. Similarly, our observations coincide with those reported in the study by Pari et al. (2014). Treatment with tyrosol to STZ-induced diabetic rats increases insulin secretion and prevents the accumulation of cholesterol by stimulating the activity of lipid metabolizing enzyme LCAT and catabolic enzymes of cholesterol degradation.
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.
Hypercholesterolemia due to lipoprotein-X manifesting as pseudohyponatremia in a patient with cholestasis
Published in Baylor University Medical Center Proceedings, 2023
Farhan Azad, Norah Abu Mughaedh, Abdurahman Alloghbi, Ibrahim Tawhari
Symptomatic hyponatremia presents with headache, nausea, vomiting, and feared complications of seizures. Patients can also be asymptomatic if hyponatremia is chronic.4 Before treating, it is important to exclude pseudohyponatremia to avoid complications associated with using isotonic or hypertonic saline. Cholestasis is a common complication of a liver transplant. Given our patient’s recent transplantation and elevated bilirubin and alkaline phosphatase, biliary obstruction and Lp-X–mediated pseudohyponatremia was suspected. Testing for lecithin-cholesterol acyltransferase deficiency, a genetic defect that can raise Lp-X level, was not pursued with the evidence of biliary stricture and cholestasis 2 years after transplantation.5