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PET-CT
Published in Anju Sahdev, Sarah J. Vinnicombe, Husband & Reznek's Imaging in Oncology, 2020
Mario Jreige, Marie Nicod-Lalonde, John O Prior, Niklaus Schaefer
Phosphatidylcholine is an essential element of cell membrane phospholipids and choline is its precursor. Neoplastic tissue has elevated levels of phosphatidylcholine. Choline kinase, which catalyses the phosphorylation of choline, has elevated activity in neoplastic tissue. The classical indication for 18F or 11C-choline PET-CT is in suspected recurrence of prostate cancer with rising prostate-specific antigen (PSA) levels (116). However, a recent prospective study shows the superiority of 68Ga-PSMA PET-CT over choline PET-CT (117).
Nature, Function, and Biosynthesis of Surfactant Lipids
Published in Jacques R. Bourbon, Pulmonary Surfactant: Biochemical, Functional, Regulatory, and Clinical Concepts, 2019
Unlike most other enzymes of the CDP-choline pathway, choline kinase is a cytosolic enzyme.215 The activity in the cytosol of type II cells is about fivefold that in whole lung cytosol.181 In the lung as in other tissues, choline phosphate cytidylyltransferase is also located for the most part in the cytosol, but there is substantial microsomal activity, especially in the fetus.175 The role of each form is not known, but it was shown that phosphatidylglycerol, which stimulates CP-CyT activity, also induces an increase in the proportion recovered in cytosol,216 which suggests a major importance of the cytosolic enzyme.
Emerging ergogenic aids for strength/power development
Published in Jay R Hoffman, Dietary Supplementation in Sport and Exercise, 2019
Phosphatidylcholine (PC) is a phospholipid with choline as its head group located in the external leaflet of the cell membrane (Figure 14.6). It is the most abundant phospholipid (~50% of total phospholipid pool) and a major component of cell membranes, assists enzymes in carrying out functions, secretion of plasma lipoproteins and membrane-mediated cell signalling. Skeletal muscle PC is higher in endurance-trained athletes (45), showing a chronic benefit to aerobic training. It is the phospholipid in highest concentrations in lecithin and is the principal phospholipid in circulation. PC may be synthesized in two major ways: 1) the main pathway from choline in a series of reactions involving the enzymes choline kinase and cytidine diphosphate-choline (CDP-choline):1,2-diacylglycerol cholinephosphotransferase; and 2) from methylation of PE via the enzyme PE N-methyltransferase (mostly in the liver). PC supplementation is beneficial for increasing plasma choline concentrations or maintaining it during exercise (33). Choline is a precursor to acetylcholine, a major neurotransmitter in the nervous system. PC supplementation may assist in supporting healthy cholesterol levels, liver and brain function (33). Sources of dietary PC include eggs, chicken breast, salmon, soybeans and other meats (14). Acute exercise has been shown to not affect skeletal muscle PC; however, two hours into recovery muscle PC is acutely reduced in endurance athletes (45).
Functional profiles of coronal and dentin caries in children
Published in Journal of Oral Microbiology, 2018
Christine A Kressirer, Tsute Chen, Kristie Lake Harriman, Jorge Frias-Lopez, Floyd E Dewhirst, Mary A Tavares, Anne CR Tanner
Alcohol dehydrogenase, methylenetetrahydrofolate reductase, and choline kinase genes were detected at higher levels in caries-free compared to coronal or dentin caries. Alcohol dehydrogenase mapped mainly to N. sicca which produces this enzyme [41], Alcohol dehydrogenase can play a role in neutralizing bacterial acid production through reduction of nicotinamide adenine dinucleotide (NAD+ to NADH). This suggests an alternative mechanism to NH3 production to counteract community bacterial acid in health. Genes for methylenetetrahydrofolate reductase, which is involved in methionine production, mapped principally to S. sanguinis and while the gene has been detected in bacteria no specific role in the oral biofilm community was found. Choline kinase genes mapped mainly to S. mitis as previously reported [42] and are considered to play a role in cell wall lysis. It is not clear what their role in caries-free sites would be.
Lipidomics reveal aryl hydrocarbon receptor (Ahr)-regulated lipid metabolic pathway in alpha-naphthyl isothiocyanate (ANIT)-induced intrahepatic cholestasis
Published in Xenobiotica, 2019
Bao-Long Wang, Chang-Wen Zhang, Liang Wang, Kun-Long Tang, Naoki Tanaka, Frank J. Gonzalez, Yong Xu, Zhong-Ze Fang
The alteration of lipid profile induced by ANIT treatment was investigated in the present study, and many lipid components changed, including PC 16:0, 20:4, PC 16:0, 22:6, PC 16:0, 18:2, LPC 18:2, PC 18:2, LPC 18:1, PC 18:1, 14:0, SM 18:1, 16:0, oleoylcarnitine and palmitoylcarnitine. Furthermore, the relevant molecular mechanisms resulting in the alteration of these lipid components were investigated. Choline kinase (Chk) a, a key enzyme catalyzing the first reaction in the choline pathway for biosynthesis of PC (Bansal et al., 2012), was detected to increase in ANIT-induced liver injury, which can explain why the level of many PC components increased in ANIT-treated mice. The elevated level of PC furtherly resulted in the increase of LPC, SM and fatty acid–carnitine conjugate through the biotransformation of PC components towards these components. The alteration of lipid components was furtherly complicated by the altered expression of Smpd3 and Scd1. Sphingomyelin phosphodiesterase (SMPD), a hydrolase enzyme converting SM to PC components (Hannun, 1994), can furtherly increase the levels of PC through biotransformation of SM to PC. Stearoyl-CoA desaturase 1 (SCD1), an endoplasmic reticulum (ER) enzyme is responsible for biosynthesis of oleic acid (18:1) and palmitoleic acid (16:1) from stearic acid (18:0) and palmitic acid (16:0), respectively. The inhibition of SCD1 has been reported to increase the level of saturated LPC and decrease the level of unsaturated LPC (Chen et al., 2008). Therefore, the alteration of lipid components in ANIT-treated mice will be the final results affected by the combined change of all these genes.
Metabolomic profiling for the identification of novel diagnostic markers and therapeutic targets in prostate cancer: an update
Published in Expert Review of Molecular Diagnostics, 2019
Giuseppe Lucarelli, Davide Loizzo, Matteo Ferro, Monica Rutigliano, Mihai Dorin Vartolomei, Francesco Cantiello, Carlo Buonerba, Giuseppe Di Lorenzo, Daniela Terracciano, Ottavio De Cobelli, Carlo Bettocchi, Pasquale Ditonno, Michele Battaglia
In a recent study, using an integrated multi-omics approach, Shao and colleagues revealed that PCa is characterized by the accumulation of metabolic intermediates and an increased expression of genes in the TCA cycle [51]. These findings are in accordance with the reactivation of ACO2, and the restoration of metabolic flux through the Krebs cycle. Interestingly, the existence of potential anaplerotic routes from the metabolism of pyruvate, glutamine, and branched chain amino acids, that replenish metabolites for the TCA cycle, was also shown [51]. Increased lipogenesis for cell signaling, membrane formation, and cellular proliferation is one of the most significant events in cancer metabolism reprogramming [52]. In PCa, an increased expression of choline kinase alpha (CHKA), an enzyme involved in phospholipids bioynthesis, has been demonstrated [53]. In fact, an increased phosphatidylcholine:choline ratio, in association with higher levels of other phospholipids such as phosphatidylethanolamine and glycerophosphocholine, has been demonstrated in PCa, in accordance with an enhanced membrane structural lipids biosynthesis program [53]. Recently, in addition to its well-known function in fueling membrane production through the Kennedy pathway, CHKA has been shown to act as a chaperone that regulates AR signaling, promoting a feed-forward AR-CHKA signaling loop that reinforces AR activity [54]. These findings suggest that CHKA could have a role as a therapeutic target and prognostic marker especially in advanced PCa. In this perspective, a CHKA inhibitor for the treatment of solid tumors is under investigation (ClinicalTrial.gov identifier NCT01215864).