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Journal articles on the topic 'Desmosterol'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 April 2022

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1

Rodríguez-Acebes, Sara, Paloma de la Cueva, Carlos Fernández-Hernando, Antonio J. Ferruelo, Miguel A. Lasunción, Robert B. Rawson, Javier Martínez-Botas, and Diego Gómez-Coronado. "Desmosterol can replace cholesterol in sustaining cell proliferation and regulating the SREBP pathway in a sterol-Δ24-reductase-deficient cell line." Biochemical Journal 420, no. 2 (May 13, 2009): 305–18. http://dx.doi.org/10.1042/bj20081909.

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Cholesterol homoeostasis is critical for cell viability and proliferation. The SREBP (sterol regulatory element-binding protein) pathway is crucial for the maintenance of cholesterol homoeostasis. This pathway is controlled by cholesterol and cholesterol-derived oxysterols. J774 cells cannot convert desmosterol into cholesterol, a defect resulting from the absence of mRNA for sterol-Δ24-reductase. Using J774 cells, we addressed the capacity of desmosterol to replace cholesterol in sustaining cell proliferation and regulating the SREBP pathway. J774 cells were able to grow indefinitely after the virtually total replacement of cholesterol by desmosterol (J774-D cells). Inhibition of sterol biosynthesis with lovastatin suppressed J774-D cell proliferation. Desmosterol prevented this effect, but its analogue, cholest-5,22-trans-dien-3β-ol, did not. Addition of desmosterol inhibited processing of SREBP-1 and -2 and also reduced the expression of SREBP-targeted genes. As occurs in cholesterol-containing cells, 25-hydroxycholesterol was more potent than desmosterol or cholesterol in suppressing these processes. Moreover, desmosterol addition enhanced the expression of Abca1 and Srebf1c, two LXR (liver X receptor)-targeted genes. To test the ability of endogenously produced desmosterol to regulate gene expression, J774-D cells were pretreated with lovastatin to inhibit sterol biosynthesis. After removal of the inhibitor the expression of SREBP-targeted genes decreased and that of an LXR-targeted gene increased, reaching control levels. Our results demonstrate that the virtually complete replacement of cholesterol by desmosterol is compatible with cell growth and the functioning of the SREBP pathway. In these cells, desmosterol suppresses SREBP processing and targeted gene expression, and it is especially effective activating LXR-targeted genes.

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2

Bouthillier, M., G. Bleau, A. Chapdelaine, and K. D. Roberts. "The assay and partial characterization of 3β-hydroxysteroid sulfotransferase of the hamster epididymis." Canadian Journal of Biochemistry and Cell Biology 63, no. 1 (January 1, 1985): 71–76. http://dx.doi.org/10.1139/o85-010.

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Using a partially purified enzyme preparation obtained from hamster epididymis, a simple assay has been developed to measure the sulfurylation of dehydroisoandrosterone (DHA) and desmosterol in the presence of 3′-phosphoadenosine 5′-phospho[35S]sulfate ([35S]PAPS). After stopping the enzymatic reaction with methanol and KCl, the 35S-labelled steroid sulfates are readily extracted into an organic phase. Optimal conditions for the sulfurylation of the two steroids were compared; optimum pH is 8.7 for DHA and 9.8 for desmosterol. Sulfoconjugation of desmosterol increases with magnesium concentrations up to 6 mM, while 40 mM concentrations of the divalent ion are required for the optimal sulfurylation of DHA. Maximum sulfurylation of these steroids requires the presence of 15 mM cysteine. Michaelis–Menten kinetics are observed with DHA which has an apparent Km of 32 μM, while desmosterol inhibits sulfotransferase activity at high concentrations. Saturation of the enzyme with PAPS results in an allosteric behaviour. Only the 3β-hydroxyl function of the steroid nucleus appears to be an appropriate sulfate acceptor for the epididymal hydroxysteroid sulfotransferase.

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3

Tallorin, Lorillee, Valerie A. Villareal, Chih-Yun Hsia, Mary A. Rodgers, Dominique J. Burri, Marc-Philipp Pfeil, Paula Montero Llopis, Brett D. Lindenbach, and Priscilla L. Yang. "Hepatitis C virus NS3-4A protease regulates the lipid environment for RNA replication by cleaving host enzyme 24-dehydrocholesterol reductase." Journal of Biological Chemistry 295, no. 35 (July 8, 2020): 12426–36. http://dx.doi.org/10.1074/jbc.ra120.013455.

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Many RNA viruses create specialized membranes for genome replication by manipulating host lipid metabolism and trafficking, but in most cases, we do not know the molecular mechanisms responsible or how specific lipids may impact the associated membrane and viral process. For example, hepatitis C virus (HCV) causes a specific, large-fold increase in the steady-state abundance of intracellular desmosterol, an immediate precursor of cholesterol, resulting in increased fluidity of the membrane where HCV RNA replication occurs. Here, we establish the mechanism responsible for HCV's effect on intracellular desmosterol, whereby the HCV NS3-4A protease controls activity of 24-dehydrocholesterol reductase (DHCR24), the enzyme that catalyzes conversion of desmosterol to cholesterol. Our cumulative evidence for the proposed mechanism includes immunofluorescence microscopy experiments showing co-occurrence of DHCR24 and HCV NS3-4A protease; formation of an additional, faster-migrating DHCR24 species (DHCR24*) in cells harboring a HCV subgenomic replicon RNA or ectopically expressing NS3-4A; and biochemical evidence that NS3-4A cleaves DHCR24 to produce DHCR24* in vitro and in vivo. We further demonstrate that NS3-4A cleaves DHCR24 between residues Cys91 and Thr92 and show that this reduces the intracellular conversion of desmosterol to cholesterol. Together, these studies demonstrate that NS3-4A directly cleaves DHCR24 and that this results in the enrichment of desmosterol in the membranes where NS3-4A and DHCR24 co-occur. Overall, this suggests a model in which HCV directly regulates the lipid environment for RNA replication through direct effects on the host lipid metabolism.

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4

Wisniewski, Thomas, Kia Newman, and Norman B. Javitt. "Alzheimer's Disease: Brain Desmosterol Levels." Journal of Alzheimer's Disease 33, no. 3 (January 10, 2013): 881–88. http://dx.doi.org/10.3233/jad-2012-121453.

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5

IKUINA, Yoji, Yoko KANZAWA, Yoshinori FUJIMOTO, and Katsumi KAKINUMA. "Preparation of (26-13C)desmosterol." CHEMICAL & PHARMACEUTICAL BULLETIN 37, no. 7 (1989): 1755–57. http://dx.doi.org/10.1248/cpb.37.1755.

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6

Simonen, Marko, Ville Männistö, Joel Leppänen, Dorota Kaminska, Vesa Kärjä, Sari Venesmaa, Pirjo Käkelä, et al. "Desmosterol in human nonalcoholic steatohepatitis." Hepatology 58, no. 3 (July 29, 2013): 976–82. http://dx.doi.org/10.1002/hep.26342.

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7

Chevy, Françoise, Françoise Illien, Claude Wolf, and Charles Roux. "Limb malformations of rat fetuses exposed to a distal inhibitor of cholesterol biosynthesis." Journal of Lipid Research 43, no. 8 (August 2002): 1192–200. http://dx.doi.org/10.1194/jlr.m200082-jlr200.

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Triparanol, an inhibitor of desmosterol Δ24 reductase, produces a high rate of limb malformations in rat fetuses exposed at gestational day 10 (gd 10) to a single oral dose (150–200 mg/kg) given to the pregnant dam. AY9944, another efficient distal inhibitor of cholesterol biosynthesis that blocks dehydrocholesterol Δ7 reductase, produces a similar degree of cholesterol depletion but fewer malformations. Gas liquid chromatography–mass spectrometry (GC-MS) profiling of the sterols in the serum of the dams and in extracted embryos shows that in addition to desmosterol Δ24 reductase inhibition the conversion of Δ8 to Δ7 unsaturated sterols is also blocked by Triparanol. Therefore, the inhibitor induces the accumulation of desmosterol (Δ8 cholesten-3β-ol, 8-dehydrocholesterol) and zymosterol (Δ8, Δ24 cholestadien-3β-ol) in embryo tissues. The high concentration of the teratogenic drug assayed in the embryos at three successive gestational days (10–30 μg/g) is thought to cause the blockade in both Δ24 reductase and Δ8-Δ7 isomerase, which results in the particular profile of aberrant sterols.Comparison of the animal model with human syndromes, including limb osseous and skeleton perturbations, suggests a combination of desmosterol and Δ8 unsaturated sterols as being involved in the deleterious influence on limb bone formation.

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8

Muse, Evan D., Shan Yu, Chantle R. Edillor, Jenhan Tao, Nathanael J. Spann, Ty D. Troutman, Jason S. Seidman, et al. "Cell-specific discrimination of desmosterol and desmosterol mimetics confers selective regulation of LXR and SREBP in macrophages." Proceedings of the National Academy of Sciences 115, no. 20 (April 9, 2018): E4680—E4689. http://dx.doi.org/10.1073/pnas.1714518115.

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Activation of liver X receptors (LXRs) with synthetic agonists promotes reverse cholesterol transport and protects against atherosclerosis in mouse models. Most synthetic LXR agonists also cause marked hypertriglyceridemia by inducing the expression of sterol regulatory element-binding protein (SREBP)1c and downstream genes that drive fatty acid biosynthesis. Recent studies demonstrated that desmosterol, an intermediate in the cholesterol biosynthetic pathway that suppresses SREBP processing by binding to SCAP, also binds and activates LXRs and is the most abundant LXR ligand in macrophage foam cells. Here we explore the potential of increasing endogenous desmosterol production or mimicking its activity as a means of inducing LXR activity while simultaneously suppressing SREBP1c-induced hypertriglyceridemia. Unexpectedly, while desmosterol strongly activated LXR target genes and suppressed SREBP pathways in mouse and human macrophages, it had almost no activity in mouse or human hepatocytes in vitro. We further demonstrate that sterol-based selective modulators of LXRs have biochemical and transcriptional properties predicted of desmosterol mimetics and selectively regulate LXR function in macrophages in vitro and in vivo. These studies thereby reveal cell-specific discrimination of endogenous and synthetic regulators of LXRs and SREBPs, providing a molecular basis for dissociation of LXR functions in macrophages from those in the liver that lead to hypertriglyceridemia.

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9

Mack, Yin Shan Isa, Masatoshi Dehari, Nobukatsu Morooka, and Shinji Nagata. "Identification and Characterization of 24-Dehydrocholesterol Reductase (DHCR24) in the Two-Spotted Cricket, Gryllus bimaculatus." Insects 12, no. 9 (September 1, 2021): 782. http://dx.doi.org/10.3390/insects12090782.

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Arthropods, including insects, convert sterols into cholesterol due to the inability to synthesise cholesterol de novo. 24-dehydrocholesterol reductase (DHCR24) plays an important role in the conversion. Not only involving the cholesterol biosynthesis in vertebrates, DHCR24 is required for the conversion of desmosterol into cholesterol in phytophagous insects. The current study extensively examined DHCR24 in omnivorous insects, which feed on both plants and animals, using Gryllus bimaculatus as the experimental model. We identified cDNAs encoding two homologues of DHCR24 from G. bimaculatus, which were designated as GbDHCR24-1 and GbDHCR24-2. Both homologues contained the flavin adenine dinucleotide binding domain, which is a feature of DHCR24. Quantitative polymerase chain reaction revealed that among tissues of adult crickets, fat body and anterior midgut expressed high levels of GbDHCR24s. Both fat body and anterior midgut demonstrated DHCR24 activities in which one of the functions is the conversion of desmosterol into cholesterol in vitro. Knockdown of GbDHCR24-1 significantly reduced the conversion activity in the anterior midgut while knockdown of the GbDHCR24-2 did not. Additionally, the accumulation of desmosterol was detected in a feeding experiment with a specific DHCR24 inhibitor, azacosterol. We finally concluded that GbDHCR24-1 is the major enzyme that facilitates the desmosterol-to-cholesterol-conversion in crickets.

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10

Slotte, J. P., and E. L. Bierman. "Movement of plasma-membrane sterols to the endoplasmic reticulum in cultured cells." Biochemical Journal 248, no. 1 (November 15, 1987): 237–42. http://dx.doi.org/10.1042/bj2480237.

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The spontaneous turnover of plasma-membrane sterols, as measured by their transfer to the endoplasmic reticulum, was measured in quiescent cultured human skin fibroblasts and monkey arterial smooth-muscle cells. The plasma-membrane sterol pool was pulse-labelled with trace amounts of either [3H]desmosterol or [3H]cholesterol. We then measured the enzymic conversion of [3H]desmosterol into [3H]cholesterol and of [3H]cholesterol into [3H]cholesteryl esters in intact cells. Depending on the probe used, markedly different transfer or conversion rates were found in these cells. In quiescent human skin fibroblasts, incubated in a serum-free medium, about 1.1% of the plasma-membrane [3H]desmosterol was converted into [3H]cholesterol/h, whereas in monkey arterial smooth-muscle cells the corresponding rate was 0.4%. Under similar experimental conditions, these cells esterified less than 0.02% (fibroblasts) and 0.12% (smooth-muscle cells) of the plasma-membrane [3H]cholesterol/h. The movement of sterols from the plasma membrane to the endoplasmic reticulum, as measured by the conversion of [3H]desmosterol into [3H]cholesterol was not blocked by colchicine, but was markedly enhanced by 3% (w/v) dimethyl sulphoxide. In all, these results indicate that plasma-membrane sterols of cultured cells are continuously transferred to the interior of the cell at a rate substantially higher than previously appreciated. This turnover of plasma-membrane sterol molecules took place even when there was no mass transfer of sterols into the cells.

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11

Zhang, Shuo, Eiji Sakuradani, and Sakayu Shimizu. "Identification of a Sterol Δ7 Reductase Gene Involved in Desmosterol Biosynthesis in Mortierella alpina 1S-4." Applied and Environmental Microbiology 73, no. 6 (January 12, 2007): 1736–41. http://dx.doi.org/10.1128/aem.02425-06.

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ABSTRACT Molecular cloning of the gene encoding sterol Δ7 reductase from the filamentous fungus Mortierella alpina 1S-4, which accumulates cholesta-5,24-dienol (desmosterol) as the main sterol, revealed that the open reading frame of this gene, designated MoΔ7SR, consists of 1,404 bp and codes for 468 amino acids with a molecular weight of 53,965. The predicted amino acid sequence of MoΔ7SR showed highest homology of 51% with that of sterol Δ7 reductase (EC 1.3.1.21) from Xenopus laevis (African clawed frog). Heterologous expression of the MoΔ7SR gene in yeast Saccharomyces cerevisiae revealed that MoΔ7SR converts ergosta-5,7-dienol to ergosta-5-enol (campesterol) by the activity of Δ7 reductase. In addition, with gene silencing of MoΔ7SR gene by RNA interference, the transformant accumulated cholesta-5,7,24-trienol up to 10% of the total sterols with a decrease in desmosterol. Cholesta-5,7,24-trienol is not detected in the control strain. This indicates that MoΔ7SR is involved in desmosterol biosynthesis in M. alpina 1S-4. This study is the first report on characterization of sterol Δ7 reductase from a microorganism.

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12

Simonen, P., J. Lehtonen, A. M. Lampi, V. Piironen, U. H. Stenman, M. Kupari, and H. Gylling. "Desmosterol accumulation in users of amiodarone." Journal of Internal Medicine 283, no. 1 (September 21, 2017): 93–101. http://dx.doi.org/10.1111/joim.12682.

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13

Okumura, Kazuo, Yutaka Nakamura, Seiji Takeuchi, Isao Kato, Yoshinori Fujimoto, and Nobuo Ikekawa. "Formal Synthesis of Squalamine from Desmosterol." CHEMICAL & PHARMACEUTICAL BULLETIN 51, no. 10 (2003): 1177–82. http://dx.doi.org/10.1248/cpb.51.1177.

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14

FERNÁNDEZ, Carlos, Yajaira SUÁREZ, Antonio J. FERRUELO, Diego GÓMEZ-CORONADO, and Miguel A. LASUNCIÓN. "Inhibition of cholesterol biosynthesis by Δ22-unsaturated phytosterols via competitive inhibition of sterol Δ24-reductase in mammalian cells." Biochemical Journal 366, no. 1 (August 15, 2002): 109–19. http://dx.doi.org/10.1042/bj20011777.

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Dietary phytosterols are cholesterol-lowering agents that interfere with the intestinal absorption of cholesterol. In the present study, we have studied their effects on cholesterol biosynthesis in human cells, particularly in the sterol-conversion pathway. For this, both Caco-2 (intestinal mucosa) and HL-60 (promyelocytic) human cell lines were incubated with [14C]acetate, and the incorporation of radioactivity into sterols was determined using HPLC and radioactivity detection online. Sterols containing a double bond at C-22 in the side chain (stigmasterol, brassicasterol and ergosterol) dramatically inhibited the activity of sterol Δ24-reductase, as indicated by the decrease in radioactivity incorporation into cholesterol and the accumulation of its precursors (mainly desmosterol). Phytosterols with the saturated side chain (β-sitosterol and campesterol) were inactive in this regard. The inhibition of sterol 24-reductase was confirmed in rat liver microsomes by using 14C-labelled desmosterol as the substrate. The 22-unsaturated phytosterols acted as competitive inhibitors of sterol 24-reductase, with Ki values (41.1, 42.7 and 36.8μM for stigmasterol, brassicasterol and ergosterol respectively) similar to the estimated Km for desmosterol (26.3μM). The sterol 5,22-cholestedien-3β-ol, an unusual desmosterol isomer that lacks the alkyl groups characteristic of phytosterols, acted as a much stronger inhibitor of 24-reductase (Ki = 3.34μM). The usually low intracellular concentrations of the physiological substrates of 24-reductase explains the strong inhibition of cholesterol biosynthesis that these compounds exert in cells. Given that inhibition of sterol 24-reductase was achieved at physiologically relevant concentrations, it may represent an additional mechanism for the cholesterol-lowering action of phytosterols, and opens up the possibility of using certain 22-unsaturated sterols as effective hypocholesterolaemic agents.

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15

Li, Zhi-Zhao, Qiong Huang, Xiao-li Yang, Jieqiong Zeng, QI-Hui Wang, Hai-Ming Tang, Zhen-qiu Yu, Yu-Qing Song, and Yang Liu. "Cholesterol Metabolic Markers for Differential Evaluation of Patients with Hyperlipidemia and Familial Hypercholesterolemia." Disease Markers 2022 (April 21, 2022): 1–9. http://dx.doi.org/10.1155/2022/2008556.

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The cholesterol metabolism in humans can be indirectly reflected by measuring cholesterol metabolism marker levels. We aimed to investigate the association of cholesterol homeostasis markers on standard lipid profiling components in familial hypercholesteremia and hyperlipidemia patients. A total of 69 hyperlipidemia patients, 25 familial hypercholesteremia (FHC) patients, and 64 healthy controls were enrolled in this study. We performed routine testing of blood lipid water. Gas chromatography was used to determine the changes in the concentration of cholesterol synthesis (squalene, desmosterol, and lathosterol) and absorption markers (campesterol, sitosterol, and stigmasterol) in the blood. Baseline hyperlipidemia patients displayed significantly higher total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (LDL-C) levels in comparison to the control group, which was reflected in the increased levels of squalene, desmosterol, campesterol, and sitosterol observed ( P < 0.05 ) in the hyperlipidemia patients. The desmosterol, lathosterol, campesterol, stigmasterol, and sitosterol were statistically different in the FHC group than the hyperlipidemic group ( P < 0.05 ). The proportions of squalene/cholesterol, lathosterol/cholesterol, stigmasterol/cholesterol, and sitosterol/cholesterol in the FHC group were lower than those in the hyperlipidemic group; only desmosterol/cholesterol was higher than that in the hyperlipidemic group. Correlation studies between lipid metabolic factors showed that the proportion of moderate and strong correlations was much higher in the FHC group than in the other two groups (76.92% vs. 32.50% and 31.25%). Logistic regression analysis showed that the concentrations of glucose, LDL-C, lactosterol, and sitosterol were all independent risk factors for developing hyperlipidemia. This result was further confirmed by the ROC curve. These results indicated that the study of cholesterol synthesis and decomposition markers can serve as a reference index for related diseases caused by changes in its concentration.

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16

Huster, Daniel, Holger A. Scheidt, Klaus Arnold, Andreas Herrmann, and Peter Müller. "Desmosterol May Replace Cholesterol in Lipid Membranes." Biophysical Journal 88, no. 3 (March 2005): 1838–44. http://dx.doi.org/10.1529/biophysj.104.048926.

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17

Chen, Wei, Baogen Su, Huabin Xing, Yiwen Yang, and Qilong Ren. "Solubility of Desmosterol in Five Organic Solvents." Journal of Chemical & Engineering Data 53, no. 11 (November 13, 2008): 2715–17. http://dx.doi.org/10.1021/je8006088.

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18

Maruoka, Keiji, Ronan Bureau, and Hisashi Yamamoto. "Biogenetic-Type Synthesis of Halosterol from Desmosterol." Synlett 1991, no. 04 (1991): 363–64. http://dx.doi.org/10.1055/s-1991-20731.

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19

Maruoka, Keiji, Ronan Bureau, and Hisashi Yamamoto. "Biogenetic-Type Synthesis of Halosterol from Desmosterol." Synlett 1991, no. 05 (1991): 363–64. http://dx.doi.org/10.1055/s-1991-34739.

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20

Muse, Evan, Shan Yu, Chantle Edillor, Jenhan Tao, Nathan Spann, Katherine Ozeki, Jeffrey McDonald, et al. "CELL-SPECIFIC DISCRIMINATION OF DESMOSTEROL AND DESMOSTEROL MIMETICS CONFERS SELECTIVE REGULATION OF LXR AND SREBP PATHWAYS IN MACROPHAGES." Journal of the American College of Cardiology 69, no. 11 (March 2017): 2556. http://dx.doi.org/10.1016/s0735-1097(17)35945-4.

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21

Stevenson, Julian, and Andrew J. Brown. "How essential is cholesterol?" Biochemical Journal 420, no. 2 (May 13, 2009): e1-e4. http://dx.doi.org/10.1042/bj20090445.

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Cholesterol is an apparently indispensable lipid for numerous processes required for cell proliferation. Levels of this molecule are primarily regulated at the transcriptional level by the SREBPs (sterol-regulatory-element-binding proteins) and LXR (liver X receptor). In this issue of the Biochemical Journal, Rodríguez-Acebes et al. show that a cholesterol precursor, desmosterol, can support cell proliferation in the absence of cholesterol in a murine macrophage-like model (J774-D cells). These cells are defective in DHCR24 (sterol-Δ24-reductase, or 3β-hydroxysterol Δ24-reductase), leading to desmosterol accumulation, and yet sterol homoeostasis appears to be normal with respect to SREBP processing and LXR activation. Other potentially cholesterol-dependent processes which were not the focus of this study are briefly discussed, such as lipid-raft-dependent cell signalling.

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22

Yoder, Christi A., Michael L. Avery, Kandy L. Keacher, and Eric A. Tillman. "Use of DiazaCon™ as a reproductive inhibitor for monk parakeets (Myiopsitta monachus)." Wildlife Research 34, no. 1 (2007): 8. http://dx.doi.org/10.1071/wr06069.

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Feral monk parakeet (Myiopsitta monachus) populations have become established in the United States and other countries around the world, and can cause damage to electrical facilities. Because the monk parakeet is a highly visible species and there is often public opposition to lethal control measures, non-lethal methods, such as contraception, are being developed to help control the spread of feral populations. Two gavage studies and one ad libitum nesting study were conducted to assess the efficacy of DiazaCon™ as a potential contraceptive for the monk parakeet. The first gavage study compared daily dose levels of 0, 50, 75, and 100 mg DiazaCon™ (kg bodyweight)–1 administered for 10 consecutive days. Cholesterol concentrations decreased significantly concomitant with a significant increase in desmosterol concentrations in the treated groups, but did not vary between sexes. Cholesterol and desmosterol concentrations did not differ significantly among DiazaCon™ groups, and cholesterol remained significantly suppressed 12 weeks after treatment. On the basis of these results, the second gavage study compared 5 or 10 consecutive days of DiazaCon™ administration at 50 mg kg–1 bird–1 day–1. Cholesterol concentrations decreased significantly concomitant with a significant increase in desmosterol concentrations in the treated groups, but did not vary between sexes. Cholesterol and desmosterol concentrations did not differ significantly between DiazaCon™ groups, and cholesterol remained significantly suppressed 11 weeks after treatment. Parakeets in the nesting study were fed hulled sunflower seeds treated with a target dose of 50 mg DiazaCon™ kg–1 bird–1 day–1. Birds consumed enough to receive an average dose of 34 mg kg–1 pair–1 day–1, or 17 mg kg–1 bird–1 day–1. Birds in the treated group laid an average of 1.6 ± 0.7 eggs per clutch compared with 3.9 ± 1.1 eggs per clutch in the untreated control group. None of the eggs laid by treated birds hatched compared with 1.1 ± 0.6 eggs per clutch hatching in the control group. Reproductive inhibition was effective for the length of the breeding season, at which time the study was stopped and no more data were collected. DiazaCon™ is a promising avian oral contraceptive that should be further investigated in a field setting with monk parakeets.

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23

Goh, Edward H., Scott M. Colles, and Kimberly D. Otte. "HPLC analysis of desmosterol, 7-dehydrocholesterol, and cholesterol." Lipids 24, no. 7 (July 1989): 652–55. http://dx.doi.org/10.1007/bf02535083.

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24

Saucier, SE, AA Kandutsch, AK Gayen, JA Nelson, and TA Spencer. "Oxygenation of desmosterol and cholesterol in cell cultures." Journal of Lipid Research 31, no. 12 (December 1990): 2179–85. http://dx.doi.org/10.1016/s0022-2275(20)42104-2.

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25

Pinto, Raphael S., Guilherme S. Ferreira, Gina Camillo R. Silvestre, Monique de Fátima M. Santana, Valéria S. Nunes, Lucas Ledesma, Paula R. Pinto, et al. "Plasma advanced glycation end products and soluble receptor for advanced glycation end products as indicators of sterol content in human carotid atherosclerotic plaques." Diabetes and Vascular Disease Research 19, no. 2 (March 2022): 147916412210852. http://dx.doi.org/10.1177/14791641221085269.

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Advanced glycation end products (AGEs) are independently related to cardiovascular disease (CVD) and favor cholesterol and oxysterol accumulation in macrophage foam cells. Soluble RAGE (sRAGE) impairs cellular AGE signaling alleviating the deleterious effects of AGE in atherogenesis. The association between plasma AGEs and sRAGE with the content of cholesterol, markers of cholesterol synthesis and absorption, and oxysterols in atherosclerotic plaques was evaluated in subjects undergoing carotid endarterectomy. Plasma and carotid plaques were obtained from symptomatic ( n = 23) and asymptomatic subjects ( n = 40). Lipids from plaques were extracted and sterols (oxysterols, cholesterol, desmosterol, lathosterol, sitosterol, and campesterol) were determined by using gas chromatography/mass spectrometry. Plasma total AGEs and pentosidine were measured by using fluorimetry and sRAGE by using ELISA. In symptomatic subjects´ atherosclerotic plaques, an increased amount of cholesterol (3x) and oxysterols [7 α-hydroxycholesterol (1.4x); 7 β−hydroxycholesterol (1.2x); 25-hydroxycholesterol (1.3x); 24-hydroxycholesterol (2.7x), and 27-hydroxycholesterol, (1.15x)], with exception to 7 ketocholesterol, were found in comparison to asymptomatic individuals. Plasma total AGEs and pentosidine significantly and positively correlated to sterols accumulated in the atherosclerotic lesion, including cholesterol, desmosterol, campesterol, sitosterol, and oxysterols. On the other hand, sRAGE inversely correlated to total AGEs and pentosidine in plasma, and with major species of oxysterols, cholesterol, and markers of cholesterol synthesis and absorption in the atherosclerotic lesion. In multiple regression analyses, it was observed a significant inverse correlation between sRAGE and 24-hydroxycholesterol and desmosterol, and a positive significant correlation between pentosidine and 24-hydroxycholesterol, 27-hydroxycholesterol, and campesterol. In conclusion, the plasma concentration of AGEs and sRAGE is a tool to predict the accumulation of sterols in atherosclerotic lesions in symptomatic and asymptomatic individuals, helping to prevent and improve the management of acute cardiovascular complications.

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26

Stuper-Szablewska, Kinga, Tomasz Rogoziński, and Juliusz Perkowski. "Contamination of pine and birch wood dust with microscopic fungi and determination of its sterol contents." Archives of Industrial Hygiene and Toxicology 68, no. 2 (June 27, 2017): 127–34. http://dx.doi.org/10.1515/aiht-2017-68-2924.

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Abstract Wood compounds, especially sterols, are connected with the level of contamination with microscopic fungi. Within this study, tests were conducted on wood dust samples collected at various work stations in a pine and birch timber conversion plant. Their contamination with mycobiota was measured as the concentration of ergosterol (ERG) by ultra performance liquid chromatography (UPLC). Another aim of this study was to assess the effect of contamination with microscopic fungi on the sterol contents in wood dusts. Analyses were conducted on five sterols: desmosterol, cholesterol, lanosterol, stigmasterol, and β-sitosterol using UPLC and their presence was confirmed using gas chromatography/mass spectrometry (GC/MS). The results of chemical analyses showed the greatest contamination with mycobiota in birch wood dust. We also observed varied contents of individual sterols depending on the wood dust type. Their highest concentration was detected in birch dust. The discriminant analysis covering all tested compounds as predictors showed complete separation of all tested wood dust types. The greatest discriminatory power was found for stigmasterol, desmosterol, and ergosterol.

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Lin, DS, WE Connor, DP Wolf, M. Neuringer, and DL Hachey. "Unique lipids of primate spermatozoa: desmosterol and docosahexaenoic acid." Journal of Lipid Research 34, no. 3 (March 1993): 491–99. http://dx.doi.org/10.1016/s0022-2275(20)40740-0.

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Allen, Luke B., Thiago C. Genaro‐Mattos, Ned A. Porter, Károly Mirnics, and Zeljka Korade. "Desmosterolosis and desmosterol homeostasis in the developing mouse brain." Journal of Inherited Metabolic Disease 42, no. 5 (April 8, 2019): 934–43. http://dx.doi.org/10.1002/jimd.12088.

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Phillips, Jane Ellen, Wendi V. Rodrigueza, and William J. Johnson. "Basis for rapid efflux of biosynthetic desmosterol from cells." Journal of Lipid Research 39, no. 12 (December 1998): 2459–70. http://dx.doi.org/10.1016/s0022-2275(20)33326-5.

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Flesch, Peter, and Michael Schaefer. "Untersuchungen zur Sterinsynthese des Ascomyceten Aureobasidium (Dematium) pullulans / Studies of the Sterolsynthesis in the Fungus Aureobasidium (Dematium) pullulans." Zeitschrift für Naturforschung C 40, no. 5-6 (June 1, 1985): 309–12. http://dx.doi.org/10.1515/znc-1985-5-604.

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Abstract Isolation and identification of sterols from culture extracts of the fungus Aureobasidium (Dematium) pullulans yielded metabolites with key function in sterol synthesis. By proof of squalene, lanosterol/dihydrolanosterol, desmosterol, ergosterol, cholesterol, stigmasterol and β-sitosterol it was possible to work out a general synthesis-scheme for the building-up of sundry sterols in Ascomycetes.

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Stránský, Karel, Antonín Trka, Miloš Buděšínský, and Milan Streibl. "Lipidic compounds from the extract of the springtail Tetrodontophora bielanensis (WAGA)." Collection of Czechoslovak Chemical Communications 51, no. 4 (1986): 948–55. http://dx.doi.org/10.1135/cccc19860948.

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Surface and internal lipidic compounds from the springtail Tetrodontophora bielanensis (WAGA) were investigated. Using chromatographic and spectroscopic methods the following compounds were detected: n-alkanes (C15 - C35), lycopane (C40H82), olefin C40H80, seven groups of esters (including sterol esters), secondary alcohol C40H82O, triacyl glycerols, free saturated and unsaturated fatty acids (C12 - C22) and free sterols (cholesterol and desmosterol).

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Tabernero, A., J. P. Bolaños, and J. M. Medina. "Lipogenesis from lactate in rat neurons and astrocytes in primary culture." Biochemical Journal 294, no. 3 (September 15, 1993): 635–38. http://dx.doi.org/10.1042/bj2940635.

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The rate of synthesis of phospholipid and sterol species from L-lactate in neurons and astrocytes in primary culture was studied. Both types of cells actively utilized lactate as lipid precursor, although the rate of lipogenesis was about 2-fold greater in astrocytes than in neurons. The incorporation of lactate into phospholipids was significantly higher than that into sterols in both types of cells, but the ratio of phospholipid/sterol synthesis was much higher in astrocytes than in neurons. Phosphatidylcholine (PC) was the main phospholipid synthesized in both types of cells, followed by phosphatidylethanolamine (PE), phosphatidylserine and phosphatidylinositol. No detectable synthesis of sphingomyelins was observed. The ratio of PC/PE synthesis was about 2-fold higher in astrocytes than in neurons. The main sterol synthesized in neurons was lanosterol, followed by desmosterol. However, the main sterol synthesized in astrocytes was desmosterol, followed by lanosterol and cholesterol. The different ratios of phospholipid/sterol and PC/PE synthesis found in neurons and astrocytes may result in different membrane fluidity being higher in astrocytes than in neurons. This may be associated with differences in the functionality of both types of cells.

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Connor, William E., Don S. Lin, and Martha Neuringer. "Biochemical Markers for Puberty in the Monkey Testis: Desmosterol and Docosahexaenoic Acid1." Journal of Clinical Endocrinology & Metabolism 82, no. 6 (June 1, 1997): 1911–16. http://dx.doi.org/10.1210/jcem.82.6.4001.

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Abstract We previously reported that the sperm of rhesus monkeys and humans uniquely contain large amounts of desmosterol not found in other tissues and have a high concentration of the highly polyunsaturated n-3 fatty acid, docosahexaenoic acid (22:6 n-3). However, the lipid composition of the testis, from which sperm originate, is unknown. During puberty, the testis undergoes remarkable morphological changes as testosterone levels rise and sperm production begins. We hypothesized that testicular maturation might also involve dramatic changes in lipid composition. Accordingly, we characterized the sterol and fatty acid composition of the testis of rhesus monkeys throughout the lifespan, from birth to old age. Although the cholesterol content in the testis remained relatively unchanged throughout life, the desmosterol content first decreased from 59 μg/g in infants to 6 μg/g in prepubertal monkeys, increased to 83 μg/g during puberty, and reached a plateau of 248 μg/g in the young adult, where it remained into old age. The polyunsaturated fatty acid composition of the testis also changed markedly. Docosahexaenoic acid (22:6 n-3) increased from 5.1% of total fatty acids in infants and juveniles to 18.1% in postpubertal young adults. Although some n-6 fatty acids, arachidonic (20:4 n-6) and linoleic (18:2 n-6), decreased from 16.0% and 10.0% in prepubertal juveniles, respectively, to 7.1% and 3.3% in young adults; dihomogamma-linolenic acid (20:3 n-6), the precursor of 1 series PGs, increased greatly from 1.8% to 10.3%. Similar changes occurred in both membrane and storage lipids (phospholipids and triglycerides), respectively. After puberty, the testicular fatty acid pattern remained stable into old age. Our data demonstrated that puberty is accompanied by substantial changes in the lipid composition of the primate testis. These changes suggest that desmosterol and both n-3 and n-6 polyunsaturated fatty acids may have important roles in sexual maturation.

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Amorim, E. A. M., J. K. Graham, M. Meyers, and B. Spizziri. "67 DELIVERING CHOLESTANOL OR DESMOSTEROL TO BULL SPERM MEMBRANES IMPROVES CRYOSURVIVAL." Reproduction, Fertility and Development 20, no. 1 (2008): 114. http://dx.doi.org/10.1071/rdv20n1ab67.

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Altering the lipid composition of sperm plasma membranes affects sperm cryosurvival. Cryopreservation induces many stresses on the spermatozoa, including destabilization of the plasma membrane, which results in the loss of sperm motility and function. Treating bull spermatozoa with cholesterolloaded cyclodextrin (CLC) prior to cryopreservation increases sperm cryosurvival rates. This study compared the effect of adding other sterols, which should incorporate into the membrane and increase membrane fluidity at low temperatures, thereby increasing cryosurvival. Ejaculates from four bulls were divided into two experiments (E). In E1, ejaculates were extended with Tris, and then subdivided into four treatments: No additive (control), 1.5 mg CLC/120 million sperm (positive control), and 1.5 mg/120 million sperm in cyclodextrin pre-loaded with either cholestanol or desmosterol. Spermatozoa were incubated for 15 min at 22�C after which both the ability of fresh spermatozoa to bind to the zona pellucida (ZP) and chicken egg perivitelline membrane (EPM) and their osmotic tolerance were evaluated. In E2, sperm were diluted to 120 million cells mL–1 in a Tris diluent and treated as described for E1. Then, samples were diluted 1:1 (v:v) in Tris with 20% Egg Yolk (EY) and cooled to 5�C. After dilution 1:1 (v:v) with Tris containing 10% EY and 16% glycerol, samples were allowed to equilibrate for 15 min, and then were packaged into 0.5-mL straws, frozen in static liquid nitrogen vapor for 20 min, and plunged into liquid nitrogen for storage. Straws were thawed and the motility and zona-binding ability were determined using a Hamilton Thorne Motility Analyzer (Hamilton Thorne Biosciences, Beverly, MA, USA) and epifluorescence microscopy, respectively. Treatment differences for sperm motility, osmotic tolerance, and zona binding were determined using analysis of variance. Treating spermatozoa with CLC resulted in more fresh bull spermatozoa binding to the EPM and ZP compared to cholestanolor desmosterol-loaded cyclodextrin-treated spermatozoa or control cells (P < 0.05). No differences were observed between EPM and ZP binding (P > 0.05). The percentages of total and progressively motile spermatozoa were higher for fresh samples treated with cholesterol-, cholestanol-, or desmosterol-loaded cyclodextrin than for control cells (P < 0.05) when spermatozoa were exposed to anismotic conditions, and then returned to isosmolality. After cryopreservation, the percentages of motile spermatozoa and number of spermatozoa binding to ZP were similar for spermatozoa treated with CLC (56% and 115 sperm/ZP) and cholestanol (53% and 108 sperm/ZP) compared to spermatozoa treated with desmosterol (42% and 86 sperm/ZP; P < 0.05). All treatments provided higher motility and binding efficiency than control spermatozoa (32% and 62 sperm/ZP; P < 0.05). Therefore, adding cholesterol or cholestanol to bull sperm membranes improved cell cryosurvival. Studies to determine if cholestanol affects sperm capacitation need to be conducted.

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35

Villareal, Valerie A., Dan Fu, Deirdre A. Costello, Xiaoliang Sunney Xie, and Priscilla L. Yang. "Hepatitis C Virus Selectively Alters the Intracellular Localization of Desmosterol." ACS Chemical Biology 11, no. 7 (May 6, 2016): 1827–33. http://dx.doi.org/10.1021/acschembio.6b00324.

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36

Costello, Deirdre A., Valerie A. Villareal, and Priscilla L. Yang. "Desmosterol Increases Lipid Bilayer Fluidity during Hepatitis C Virus Infection." ACS Infectious Diseases 2, no. 11 (August 25, 2016): 852–62. http://dx.doi.org/10.1021/acsinfecdis.6b00086.

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37

XU, Qing-Qing, Li-Yun KONG, Min LI, Bao-Gen SU, Yi-Wen YANG, and Qi-Long REN. "Separation and Purification of Desmosterol by Simulated Moving Bed Chromatography." CHINESE JOURNAL OF ANALYTICAL CHEMISTRY (CHINESE VERSION) 41, no. 6 (2013): 851. http://dx.doi.org/10.3724/sp.j.1096.2013.20853.

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38

Jansen, Maurice, Wei Wang, Dario Greco, Gian Carlo Bellenchi, Umberto Porzio, Andrew J. Brown, and Elina Ikonen. "What dictates the accumulation of desmosterol in the developing brain?" FASEB Journal 27, no. 3 (December 10, 2012): 865–70. http://dx.doi.org/10.1096/fj.12-211235.

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39

Gale, Douglas J., Raymond I. Logan, and Donald E. Rivett. "Detection of Desmosterol in the Internal Lipids of Wool Fibers." Textile Research Journal 57, no. 9 (September 1987): 539–42. http://dx.doi.org/10.1177/004051758705700909.

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40

Simonsen, Adam C., Luis A. Bagatolli, Lars Duelund, Olav Garvik, John Ipsen, and Ole G. Mouritsen. "Effects of seaweed sterols fucosterol And desmosterol on lipid membranes." Biophysical Journal 96, no. 3 (February 2009): 606a. http://dx.doi.org/10.1016/j.bpj.2008.12.3204.

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41

Mouritsen, Ole G., Luis A. Bagatolli, Lars Duelund, Olav Garvik, John H. Ipsen, and Adam Cohen Simonsen. "Effects of seaweed sterols fucosterol and desmosterol on lipid membranes." Chemistry and Physics of Lipids 205 (June 2017): 1–10. http://dx.doi.org/10.1016/j.chemphyslip.2017.03.010.

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42

Sato, Yoshiaki, Yasukazu Yamanaka, Ikumi Suzuki, Mamoru Yanagimachi, Francois Bernier, Ken Aoshima, Yoshiya Oda, Akinori Miyashita, Takeshi Ikeuchi, and Ryozo Kuwano. "P1-230: Desmosterol: A new plasma biomarker for Alzheimer's disease." Alzheimer's & Dementia 9 (July 2013): P236—P237. http://dx.doi.org/10.1016/j.jalz.2013.05.454.

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43

Hąc-Wydro, Katarzyna, Karolina Węder, Marzena Mach, Michał Flasiński, and Paweł Wydro. "The influence of cholesterol precursor – desmosterol – on artificial lipid membranes." Biochimica et Biophysica Acta (BBA) - Biomembranes 1848, no. 8 (August 2015): 1639–45. http://dx.doi.org/10.1016/j.bbamem.2015.04.017.

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44

Hoai, Nguyen Thi. "TRITERPENE AND STEROL COMPOUNDS ISOLATED FROM ANODENDRON PANICULATUM (ROXB.) A.DC." Hue University Journal of Science: Natural Science 126, no. 1B (August 21, 2017): 155. http://dx.doi.org/10.26459/hueuni-jns.v126i1b.4447.

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<p>Phytochemical study on the aerial parts of <em>Anodendron paniculatum</em> led to the isolation of three triterpenes, including ursolic acid (<strong>1</strong>), esculentic acid (<strong>2</strong>), cycloartenol (<strong>3</strong>), and one sterol, desmosterol (<strong>4</strong>). Their chemical structures were elucidated on the basis of spectroscopic analyses. The cytotoxicity of the isolated compounds against the growth of human cancer cell lines were evaluated using a sulforhodamin B bioassay. Compounds <strong>1</strong> exhibited moderate cytotoxicity against the LU-1 and MKN-7 cell lines with IC<sub>50</sub> values of 44.37 ± 5.40, 30.89 ± 3.60 μg/mL, respectively. Meanwhile, compound <strong>4</strong> possessed moderate cytotoxic effects toward the LU-1, KB, Hep-G2, MKN-7 and SW-480 cell lines with IC<sub>50</sub> values ranging from 28.11 ± 1.95 to 41.41 ± 2.31 μg/mL.</p><p><strong>Key words</strong><em>: Anodendron paniculatum</em>, ursolic acid, esculentic acid, cycloartenol, desmosterol, cytotoxicity.</p>

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45

Hallikainen, Maarit, Henri Tuomilehto, Tarja Martikainen, Esko Vanninen, Juha Seppä, Jouko Kokkarinen, Jukka Randell, and Helena Gylling. "Cholesterol Metabolism and Weight Reduction in Subjects with Mild Obstructive Sleep Apnoea: A Randomised, Controlled Study." Cholesterol 2013 (May 16, 2013): 1–9. http://dx.doi.org/10.1155/2013/769457.

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To evaluate whether parameters of obstructive sleep apnoea (OSA) associate with cholesterol metabolism before and after weight reduction, 42 middle-aged overweight subjects with mild OSA were randomised to intensive lifestyle intervention (N=23) or to control group (N=18) with routine lifestyle counselling only. Cholesterol metabolism was evaluated with serum noncholesterol sterol ratios to cholesterol, surrogate markers of cholesterol absorption (cholestanol and plant sterols) and synthesis (cholestenol, desmosterol, and lathosterol) at baseline and after 1-year intervention. At baseline, arterial oxygen saturation (SaO2) was associated with serum campesterol (P<0.05) and inversely with desmosterol ratios (P<0.001) independently of gender, BMI, and homeostasis model assessment index of insulin resistance (HOMA-IR). Apnoea-hypopnoea index (AHI) was not associated with cholesterol metabolism. Weight reduction significantly increased SaO2and serum cholestanol and decreased AHI and serum cholestenol ratios. In the groups combined, the changes in AHI were inversely associated with changes of cholestanol and positively with cholestenol ratios independent of gender and the changes of BMI and HOMA-IR (P<0.05). In conclusion, mild OSA seemed to be associated with cholesterol metabolism independent of BMI and HOMA-IR. Weight reduction increased the markers of cholesterol absorption and decreased those of cholesterol synthesis in the overweight subjects with mild OSA.

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46

Gylling, H., S. Pyrhönen, E. Mäntylä, H. Mäenpää, L. Kangas, and T. A. Miettinen. "Tamoxifen and toremifene lower serum cholesterol by inhibition of delta 8-cholesterol conversion to lathosterol in women with breast cancer." Journal of Clinical Oncology 13, no. 12 (December 1995): 2900–2905. http://dx.doi.org/10.1200/jco.1995.13.12.2900.

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PURPOSE Long-term effects of tamoxifen and toremifene, a new antiestrogen that closely resembles tamoxifen, were investigated on serum lipids and cholesterol metabolism. PATIENTS AND METHODS The study group consisted of 24 postmenopausal Finnish women with advanced breast cancer from an international multicenter study of 415 patients. Cholesterol metabolism was evaluated by measuring the cholesterol precursor (delta 8-cholestenol, desmosterol, and lathosterol, reflecting cholesterol synthesis) and plant sterol (markers of cholesterol absorption) and cholestanol levels by gas-liquid chromatography. RESULTS Tamoxifen and toremifene lowered significantly serum low-density lipoprotein (LDL) cholesterol levels after 12 months of treatment by 16% and 15%, with no change in high-density lipoprotein (HDL) cholesterol or serum triglyceride levels. Serum delta 8-cholestenol was increased 40- and 55-fold during toremifene and tamoxifen treatment, respectively, while the increase of desmosterol less than doubled and was lacking for lathosterol by toremifene. Plant sterols and cholestanol were only inconsistently increased in serum. CONCLUSION Tamoxifen and toremifene inhibit the conversion of delta 8-cholestenol to lathosterol so that serum total and LDL cholesterol levels are lowered by downregulation of cholesterol synthesis. Thus, inhibition of the delta 8-isomerase may be the major hypolipidemic effect of these agents. Reduced risk of coronary artery disease will probably occur also during long-term toremifene treatment, because the drug reduces cholesterol and its synthesis, similarly to tamoxifen.

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Abuobeid, Roubi, Javier Sánchez-Marco, María J. Felices, Carmen Arnal, Juan Carlos Burillo, Roberto Lasheras, Rebeca Busto, et al. "Squalene through Its Post-Squalene Metabolites Is a Modulator of Hepatic Transcriptome in Rabbits." International Journal of Molecular Sciences 23, no. 8 (April 10, 2022): 4172. http://dx.doi.org/10.3390/ijms23084172.

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Squalene is a natural bioactive triterpene and an important intermediate in the biosynthesis of sterols. To assess the effect of this compound on the hepatic transcriptome, RNA-sequencing was carried out in two groups of male New Zealand rabbits fed either a diet enriched with 1% sunflower oil or the same diet with 0.5% squalene for 4 weeks. Hepatic lipids, lipid droplet area, squalene, and sterols were also monitored. The Squalene administration downregulated 9 transcripts and upregulated 13 transcripts. The gene ontology of transcripts fitted into the following main categories: transporter of proteins and sterols, lipid metabolism, lipogenesis, anti-inflammatory and anti-cancer properties. When the results were confirmed by RT-qPCR, rabbits receiving squalene displayed significant hepatic expression changes of LOC100344884 (PNPLA3), GCK, TFCP2L1, ASCL1, ACSS2, OST4, FAM91A1, MYH6, LRRC39, LOC108176846, GLT1D1 and TREH. A squalene-enriched diet increased hepatic levels of squalene, lanosterol, dihydrolanosterol, lathosterol, zymostenol and desmosterol. Strong correlations were found among specific sterols and some squalene-changed transcripts. Incubation of the murine AML12 hepatic cell line in the presence of lanosterol, dihydrolanosterol, zymostenol and desmosterol reproduced the observed changes in the expressions of Acss2, Fam91a1 and Pnpla3. In conclusion, these findings indicate that the squalene and post-squalene metabolites play important roles in hepatic transcriptional changes required to protect the liver against malfunction.

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Westover, Emily J., and Douglas F. Covey. "First synthesis of ent-desmosterol and its conversion to ent-deuterocholesterol." Steroids 68, no. 2 (February 2003): 159–66. http://dx.doi.org/10.1016/s0039-128x(02)00174-5.

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Brown, A. J., and I. C. Gelissen. "Cholesterol and desmosterol dancing to the beat of a different drug." Journal of Internal Medicine 283, no. 1 (November 26, 2017): 102–5. http://dx.doi.org/10.1111/joim.12710.

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Goyal, Sandeep, Yi Xiao, Ned A. Porter, Libin Xu, and F. Peter Guengerich. "Oxidation of 7-dehydrocholesterol and desmosterol by human cytochrome P450 46A1." Journal of Lipid Research 55, no. 9 (July 13, 2014): 1933–43. http://dx.doi.org/10.1194/jlr.m051508.

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