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Changes in Sertoli Cell Structure and Function
Published in Tom O. Abney, Brooks A. Keel, The Cryptorchid Testis, 2020
David M. de Kretser, Gail P. Risbridger
Subsequently increased vacuolization of Sertoli cells was noted which consisted of two types; the first type resulted from the dilatation of cisternae of smooth endoplasmic reticulum whereas the second specifically involves a dilation of the intercellular space at the sites of the inter-Sertoli cell junctions (see Figure 1). Despite these changes in the inter-Sertoli cell junctional complexes, the function of the blood-testis barrier appeared to be intact.17 It seems likely that the increased lipid in Sertoli cells is not the result of phagocytosis of degenerating germ cells since, when tests without germ cells are made cryptorchid, a similar lipid accumulation occurs.18 Analysis of the lipid showed an increase in cholesterol and cholesterol esters.19
Atherosclerosis
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
Enzymes for cholesteryl ester synthesis and degradation and phospholipases also are found in the arterial wall.548 The development of the atherosclerotic plaque is characterized by the accumulation of free and esterified cholesterol. Oleate esters largely accumulate in smooth muscle cells forming inclusions. As the severity of the lesion is enhanced, the cholesteryl esters show similarity to those of LDL.600 Although smooth muscle produces cholesterol de novo, the major part comes from LDL. Inside the cell, lipids and apoproteins are metabolized also by monolysosomal acid hydrolases. Free cholesterol enters the cell and becomes esterified by microsomal enzymes predominantly to oleate and synthesized de novo. The synthesis of cholesterol esters follows three pathways (Figure 9). Of these pathways, acyl Co A: cholesterol acyl transferase is the most active and responsible for most cholesteryl ester synthesis in atherogenesis. The esters are insoluble in water and they aggregate to form a separate phase. This process continues with continuing influx of cholesterol until cell death. During regression cholesteryl esters are hydrolyzed, and the free cholesterol leaves the cell by direct exchange with serum lipoproteins. The exchange with HDL represent the principal mechanism for the elimination of cholesterol from foam cells.623
Radioiodinated Cholesterol as A Radiotracer in Biochemical Studies
Published in William C. Eckelman, Lelio G. Colombetti, Receptor-Binding Radiotracers, 2019
Raymond E. Counsell, Nancy Korn
Lipoproteins provide cells with the bulk of cholesterol circulating in the plasma. Detailed studies by Brown and Goldstein31 have shown that human fibroblasts as well as a variety of other cell types obtain their cholesterol by binding LDL to a specific high affinity receptor site (LDL receptor) on the cell membrane followed by internalization of the intact lipoprotein by adsorptive endocytosis. The uptake of cholesterol by this process is followed by a prompt inhibition of intracellular cholesterol biosynthesis and an enhancement in the conversion of cholesterol to cholesterol esters.
Hepatoprotective effects of ethyl pyruvate against carbon tetrachloride-induced oxidative stress, biochemical and histological alterations in rats
Published in Archives of Physiology and Biochemistry, 2021
The liver plays a fundamental role in the metabolism of lipids. In the present study, serum levels of cholesterol, triglycerides, HDL, and LDL indicated deterioration in hepatic function due to parenchymal injury after CCl4 administration. However, treatment with EP in CCl4-induced group of rats significantly lessened the CCl4-induced liver damage as evidenced by decreased serum levels of cholesterol, triglycerides, LDL and the increase in serum HDL levels. These findings suggest that EP is effective in reversing hyperlipidaemia caused by the CCl4. The mechanism of lipid-lowering effects of EP may be due to an inhibitory activity on microsomal acyl-coenzyme A: cholesterol acyltransferase enzyme. This enzyme is responsible for cholesterol ester formation in tissues in the liver (Matsuda 1994). Similarly, a significant decrease in the triglyceride and free fatty acid concentrations of mice with alcoholic liver disease has been found after the administration of EP (Shen et al.2018).
Platelet-lymphocyte ratio (PLR) and all-cause mortality in general population: insights from national health and nutrition education survey
Published in Platelets, 2019
Kanupriya Mathur, Nargiza Kurbanova, Rehan Qayyum
Platelet and lymphocyte counts were reported in 1000 cells/µL. PLR was calculated by dividing the platelet count by the lymphocyte count. The hazard ratio with 95% confidence intervals (CIs) were reported for difference from the lowest PLR quartile. Serum creatinine was measured using the Jaffe rate method (kinetic alkaline picrate) and glomerular filtration rate (GFR) was calculated using Chronic Kidney Disease Epidemiology Collaboration equation and was reported in ml/min/1.73 m2. Total cholesterol was measured enzymatically in serum or plasma in a series of coupled reactions that hydrolyze cholesteryl esters. Serum c-reactive protein (CRP) was quantified using latex-enhanced nephelometry. Serum glucose level was measured using the Beckman Synchron LX20 test (Beckman Coulter, Fullerton, CA, USA) on refrigerated specimens. Diabetes was defined as random glucose >200 mg/dL, HbA1c >7%, self-report of diabetes diagnosis, or taking diabetes medications.
Association of carotid intima media thickness with atherogenic index of plasma, apo B/apo A-I ratio and paraoxonase activity in patients with non-alcoholic fatty liver disease
Published in Archives of Physiology and Biochemistry, 2019
Reza Fadaei, Reza Meshkani, Hossein Poustchi, Soudabeh Fallah, Nariman Moradi, Ghodratollah Panahi, Shahin Merat, Taghi Golmohammadi
Inflammation, dysregulation of lipoprotein metabolism and oxidative stress lead to an accumulation of cholesterol ester in macrophages of arterial wall in the pathogenesis of atherosclerosis (Mahmoudi et al. 2017). PON enzyme has several anti-atherogenic roles such as, reducing LDL and HDL oxidation, reducing cellular oxidative stress and inhibiting endothelial cells apoptosis (Litvinov et al. 2012). Also, PON deficient mice are more prone to development of atherosclerosis when compared with control mice (Rozenberg et al. 2003). Also, several studies have shown a significant association between PON activity and atherosclerosis (Yu et al. 2013). In line with this concept, the results of the present study indicated a weak negative correlation of cIMT and ARE and PON activities. Regarding atheroprotective roles of PON, decreased PON activity could be a weak underlying mechanism for increased atherosclerosis risk in NAFLD patients.