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Atherosclerosis
Published in George Feuer, Felix A. de la Iglesia, Molecular Biochemistry of Human Disease, 2020
George Feuer, Felix A. de la Iglesia
The elimination of cholesterol metabolites takes place entirely through the stool, either as unchanged cholesterol, or bile acids produced in the liver, or coprostanol formed from cholesterol by bacterial action (Figure 13). Small amounts of cholesterol are converted to steroid hormones. The excreted cholesterol mixes with dietary cholesterol and probably limited amounts reenter the pool. Bile acids are reabsorbed efficiently via the enterohepatic circulation into the liver, and only small quantities leave the body (Figure 14). A fraction of cholesterol is excreted through the skin and in the milk during lactation. In the production of bile acids, the conversion of cholesterol to 7α-hydroxycholesterol is the rate-limiting step. The enzyme is located in the microsomal fraction of the hepatocyte and has a short halflife of 2.5 to 3.0 h. Bile salts returning to the liver via the portal circulation exercise a feedback control on 7α-hydroxylase.521,576
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
Cholic and chenodeoxycholic acid are the primary bile acids formed in man and most mammalian species (Figure 3). These bile acids are conjugated with glycine or taurine to form the bile salts and excreted into the bile. The initial and rate-limiting step in bile acid formation is the formation of 7α-hydroxycholesterol via 7α-OHase. Further oxidation of the steroid nucleus precedes degradation of the side-chain and ultimate formation of the C-24 bile acids.11
The Controlling Nutritional Status (CONUT) Score and Prognosis in Malignant Tumors: A Systematic Review and Meta-Analysis
Published in Nutrition and Cancer, 2022
Junhao Chen, Pan Song, Zhufeng Peng, Zhenghuan Liu, Luchen Yang, Linchun Wang, Jing Zhou, Qiang Dong
Third, cholesterol plays a key role in maintaining cellular function. In addition to being an essential component of the plasma membrane, cholesterol also participates in intracellular signal transduction and the synthesis of steroid hormones (90). Furthermore, cholesterol metabolites have been demonstrated to be connected to cancer development (91). Oxysterol is an oxidation product of cholesterol, and many oxysterols, including 7α-hydroxycholesterol, 7β-hydroxycholesterol and 25- hydroxycholesterol, have been reported to inhibit proliferation in various cancer types (92). Studies have also reported that hypocholesterolemia is significantly associated with poor prognosis of various malignant tumors (93–95). Other immune-inflammatory indicators, such as PNI and mGPS, do not include cholesterol levels, which represent an important component of the CONUT score.
Current insights in the complexities underlying drug-induced cholestasis
Published in Critical Reviews in Toxicology, 2019
Neel Deferm, Tom De Vocht, Bing Qi, Pieter Van Brantegem, Eva Gijbels, Mathieu Vinken, Peter de Witte, Thomas Bouillon, Pieter Annaert
BAs are the main organic solutes in bile and the primary determinants of BA-dependent flow (BADF) (Figure 2). BAs are de novo synthesized from cholesterol via two major pathways: the “neutral” pathway, which involves conversion of cholesterol to 7α-hydroxycholesterol via 7α-hydroxylase (CYP7A1), and the “acidic” pathway, which is initiated by formation of 27-hydroxycholesterol (Axelson and Sjövall et al. 1990; Javitt 1994). Both pathways generate primary BAs namely, chenodeoxycholic acid (CDCA) and cholic acid (CA), although the acidic pathway predominantly produces CDCA (Setchell et al. 1988). The final step of BA synthesis involves conjugation of primary BAs with either glycine or taurine, a process which takes place in peroxisomes and is mediated by two enzymes namely, bile acid:CoA synthase (BACS) and bile acid CoA:amino acid N-acyltransferase (BAAT) (Fuchs 2003). Conjugated and unconjugated BAs can further undergo sulfation or glucuronidation inside hepatocytes, after which they are secreted into bile canaliculi via the bile salt export pump (BSEP/ABCB11) and the multidrug resistance-associated protein 2 (MRP2/ABCC2), located in the canalicular membrane of the hepatocyte (Pauli-Magnus and Meier 2006).