Готові списки джерел за темами / Metabolism of cholesterol derivatives

Добірка наукової літератури з теми "Metabolism of cholesterol derivatives"

Автор: Grafiati

Опубліковано: 15 червня 2024

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Статті в журналах з теми "Metabolism of cholesterol derivatives":

Zhao, Chunyan, and Karin Dahlman-Wright. "Liver X receptor in cholesterol metabolism." Journal of Endocrinology 204, no. 3 (October 16, 2009): 233–40. http://dx.doi.org/10.1677/joe-09-0271.

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The liver X receptors (LXRs) are nuclear receptors that are activated by endogenous oxysterols, oxidized derivatives of cholesterol. There are two isoforms of LXR, LXRα (NR1H3) and LXRβ (NR1H2). Both LXRα and LXRβ regulate gene expression by binding to DNA sequences associated with target genes as heterodimers with isoforms of the retinoid X receptor (RXR), RXRα (NR2B1), RXRβ (NR2B2), and RXRγ (NR2B3). LXRs act as cholesterol sensors: when cellular oxysterols accumulate as a result of increasing concentrations of cholesterol, LXR induces the transcription of genes that protect cells from cholesterol overload. In this review, we summarize the roles of LXRs in controlling cholesterol homeostasis, including their roles in bile acid synthesis and metabolism/excretion, reverse cholesterol transport, cholesterol biosynthesis and uptake, and cholesterol absorption/excretion in the intestine. The overlapping and distinct roles of the LXRα and LXRβ isoforms, and the potential use of LXRs as attractive targets for treatment of cardiovascular disease are also discussed.

Reboldi, Andrea, and Eric Dang. "Cholesterol metabolism in innate and adaptive response." F1000Research 7 (October 16, 2018): 1647. http://dx.doi.org/10.12688/f1000research.15500.1.

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It has been long recognized that cholesterol is a critical molecule in mammalian cell biology, primarily for its contribution to the plasma membrane’s composition and its role in assuring proper transmembrane receptor signaling as part of lipid rafts. Efforts have also been made to characterize the cholesterol biosynthetic pathway, cholesterol homeostasis, and cholesterol-derived metabolites in order to gain insights into their dysregulation during metabolic diseases. Despite the central role cholesterol metabolism plays in shaping human health, its regulation during immune activation, such as immune response to pathogens or autoimmune/autoinflammatory diseases, is poorly understood. The immune system is composed of several type of cells with distinct developmental origin, life span, molecular requirements, and gene expressions. It is unclear whether the same array of cholesterol metabolism regulators are equally employed by different immune cells and whether distinct cholesterol metabolites have similar biological consequences in different immune cells. In this review, we will describe how cholesterol metabolism is controlled during the adaptive and the innate immune response and the role for intracellular and extracellular receptors for cholesterol and its derivatives.

Bilai, I. M., M. I. Romanenko та D. H. Ivanchenko. "Study on the influence of 7-β-hydroxy-γ-aryloxypropylxanthinyl-8-thioalkanic acid derivatives on the lipid metabolism in experiment". Zaporozhye Medical Journal 23, № 3 (7 червня 2021): 411–16. http://dx.doi.org/10.14739/2310-1210.2021.3.207465.

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Statin side effects are not a rare occurrence, in particular dyspeptic disorders, insomnia, headache, skin erythema, rash are often noted. All of this determines scientists to find new effective and low-toxic hypolipidemic agents. Various natural and synthetic xanthine derivatives have been recognized as therapeutically potential compounds and reported to control various diseases. Therefore, the study of new xanthine derivatives and their hypolipidemic effects, which would have a significant therapeutic effect with minimal side effects, is relevant. The aim of the study was to examine the effect of 7-β-hydroxy-γ-aryloxypropylxanthinyl-8-thioalkanic acid derivatives on lipidogram parameters in experimental laboratory rats. Materials and methods. The objects of the study were 7-β-hydroxy-γ-aryloxypropylxanthinyl-8-thioalkanic acid derivatives. The experiments were performed in white laboratory Wistar rats weighing 180–220 g. Experimental modeling of hyperlipidemia – tween model: intraperitoneal administration of tween-80 at a dose of 200 mg/100 g body weight. The test compounds were administered orally, simultaneously with tween, at a dose of 1/10 of LD50 (previously calculated by Prozorovsky express method) for 6 days. The following indicators of lipidogram were determined: total cholesterol (TC), high-density lipoprotein cholesterol (HDL cholesterol), low-density lipoprotein cholesterol (LDL cholesterol), triglycerides (TG) and atherogenic index of plasma: TC – HDL cholesterol / HDL cholesterol. The experiments were carried out with respect to Bioethical rules and norms. Results. The studies have shown data on the hypolipidemic activity of 7-β-hydroxy-γ-aryloxypropylxanthinyl-8-thioalkane acid derivatives. According to the conditional efficiency index Ʃ, which included the overall percentage of the following indicators – total cholesterol, low-density lipoprotein cholesterol and triglycerides, the leading compounds were 2439 (87.47 %), 6047 (82.30 %). The reference drug atorvastatin had a value of 82.98 %. Conclusions. The major compound was 2439 identified among all compared to the control group. The prospect of further research is a more detailed study on the ability of xanthine derivatives to exhibit hypolipidemic effects and to influence oxidative stress in various hyperlipidemic models.

Nunomura, Satoshi, Makoto Makishima, and Chisei Ra. "Liver X receptors and immune regulation." BioMolecular Concepts 1, no. 5-6 (December 1, 2010): 381–87. http://dx.doi.org/10.1515/bmc.2010.030.

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AbstractRecent studies suggest that homeostasis of lipid metabolism is crucial for the function of various immune cells. Oxygenated derivatives of cholesterol (oxysterols) are well-known regulators of lipid metabolism and have diverse functions, such as inhibition of cholesterol synthesis, efflux of intracellular cholesterol, synthesis of cholesterol esters, and activation of liver X receptors (LXRs). In this review, we introduce novel roles of the oxysterol receptors LXRs in the immune system, including regulation of inflammatory responses, T cell expansion, immunoglobulin production, and antitumor responses. We also discuss lipid-mediated signaling as a potential target for treatment of immune diseases.

Pirmoradi, Leila, Nayer Seyfizadeh, Saeid Ghavami, Amir A. Zeki, and Shahla Shojaei. "Targeting cholesterol metabolism in glioblastoma: a new therapeutic approach in cancer therapy." Journal of Investigative Medicine 67, no. 4 (February 14, 2019): 715–19. http://dx.doi.org/10.1136/jim-2018-000962.

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Glioblastoma multiforme (GBM) is the most aggressive malignant brain tumor known with a poor survival rate despite current advances in the field of cancer. Additional research into the pathophysiology of GBM is urgently needed given the devastating nature of this disease. Recent studies have revealed the unique cellular physiology of GBM cells as compared with healthy astrocytes. Intriguingly, GBM cells are incapable of de novo cholesterol synthesis via the mevalonate pathway. Thus, the survival of GBM cells depends on cholesterol uptake via low-density lipoprotein receptors (LDLRs) in the form of apolipoprotein-E-containing lipoproteins and ATP-binding cassette transporter A1 (ABCA1) that efflux surplus cholesterol out of cells. Liver X receptors regulate intracellular cholesterol levels in neurons and healthy astrocytes through changes in the expression of LDLR and ABCA1 in response to cholesterol and its derivatives. In GBM cells, due to the dysregulation of this surveillance pathway, there is an accumulation of intracellular cholesterol. Furthermore, intracellular cholesterol regulates temozolomide-induced cell death in glioblastoma cells via accumulation and activation of death receptor 5 in plasma membrane lipid rafts. The mevalonate pathway and autophagy flux are also fundamentally related with implications for cell health and death. Thus, via cholesterol metabolism, the mevalonate pathway may be a crucial player in the pathogenesis and treatment of GBM where our current understanding is still lacking. Targeting cholesterol metabolism in GBM may hold promise as a novel adjunctive clinical therapy for this devastating cancer.

Roth, Andrew T., Jennifer A. Philips, and Pallavi Chandra. "The role of cholesterol and its oxidation products in tuberculosis pathogenesis." Immunometabolism 6, no. 2 (April 2024): e00042. http://dx.doi.org/10.1097/in9.0000000000000042.

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Mycobacterium tuberculosis causes tuberculosis (TB), one of the world’s most deadly infections. Lipids play an important role in M. tuberculosis pathogenesis. M. tuberculosis grows intracellularly within lipid-laden macrophages and extracellularly within the cholesterol-rich caseum of necrotic granulomas and pulmonary cavities. Evolved from soil saprophytes that are able to metabolize cholesterol from organic matter in the environment, M. tuberculosis inherited an extensive and highly conserved machinery to metabolize cholesterol. M. tuberculosis uses this machinery to degrade host cholesterol; the products of cholesterol degradation are incorporated into central carbon metabolism and used to generate cell envelope lipids, which play important roles in virulence. The host also modifies cholesterol by enzymatically oxidizing it to a variety of derivatives, collectively called oxysterols, which modulate cholesterol homeostasis and the immune response. Recently, we found that M. tuberculosis converts host cholesterol to an oxidized metabolite, cholestenone, that accumulates in the lungs of individuals with TB. M. tuberculosis encodes cholesterol-modifying enzymes, including a hydroxysteroid dehydrogenase, a putative cholesterol oxidase, and numerous cytochrome P450 monooxygenases. Here, we review what is known about cholesterol and its oxidation products in the pathogenesis of TB. We consider the possibility that the biological function of cholesterol metabolism by M. tuberculosis extends beyond a nutritional role.

Karolczak, Kamil, and Cezary Watala. "The Mystery behind the Pineal Gland: Melatonin Affects the Metabolism of Cholesterol." Oxidative Medicine and Cellular Longevity 2019 (July 10, 2019): 1–8. http://dx.doi.org/10.1155/2019/4531865.

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Melatonin may be considered a cardioprotective agent. Since atherogenesis is partly associated with the metabolism of lipoproteins, it seems plausible that melatonin affects cardiovascular risk by modulating the metabolism of cholesterol and its subfractions. Moreover, cholesterol-driven atherogenesis can be hypothetically reduced by melatonin, mainly due to the minimalization of harmful reactions triggered in the cardiovascular system by the reactive oxygen species-induced toxic derivatives of cholesterol. In this review, we attempted to summarize the available data on the hypolipemizing effects of melatonin, with some emphasis on the molecular mechanisms underlying these reactions. We aimed to attract readers’ attention to the numerous gaps of knowledge present in the reviewed field and the essential irrelevance between the findings originating from different sources: clinical observations and in vitro mechanistic and molecular studies, as well as preclinical experiments involving animal models. Overall, such inconsistencies make it currently impossible to give a reliable opinion on the action of melatonin on the metabolism of lipoproteins.

SHAND, JOHN H., and DAVID W. WEST. "The effect of fibric acid derivatives on cholesterol metabolism in rat liver." Biochemical Society Transactions 22, no. 2 (May 1, 1994): 110S. http://dx.doi.org/10.1042/bst022110s.

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Schroepfer, George J. "Oxysterols: Modulators of Cholesterol Metabolism and Other Processes." Physiological Reviews 80, no. 1 (January 1, 2000): 361–554. http://dx.doi.org/10.1152/physrev.2000.80.1.361.

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Oxygenated derivatives of cholesterol (oxysterols) present a remarkably diverse profile of biological activities, including effects on sphingolipid metabolism, platelet aggregation, apoptosis, and protein prenylation. The most notable oxysterol activities center around the regulation of cholesterol homeostasis, which appears to be controlled in part by a complex series of interactions of oxysterol ligands with various receptors, such as the oxysterol binding protein, the cellular nucleic acid binding protein, the sterol regulatory element binding protein, the LXR nuclear orphan receptors, and the low-density lipoprotein receptor. Identification of the endogenous oxysterol ligands and elucidation of their enzymatic origins are topics of active investigation. Except for 24,25-epoxysterols, most oxysterols arise from cholesterol by autoxidation or by specific microsomal or mitochondrial oxidations, usually involving cytochrome P-450 species. Oxysterols are variously metabolized to esters, bile acids, steroid hormones, cholesterol, or other sterols through pathways that may differ according to the type of cell and mode of experimentation (in vitro, in vivo, cell culture). Reliable measurements of oxysterol levels and activities are hampered by low physiological concentrations (∼0.01–0.1 μM in plasma) relative to cholesterol (∼5,000 μM) and by the susceptibility of cholesterol to autoxidation, which produces artifactual oxysterols that may also have potent activities. Reports describing the occurrence and levels of oxysterols in plasma, low-density lipoproteins, various tissues, and food products include many unrealistic data resulting from inattention to autoxidation and to limitations of the analytical methodology. Because of the widespread lack of appreciation for the technical difficulties involved in oxysterol research, a rigorous evaluation of the chromatographic and spectroscopic methods used in the isolation, characterization, and quantitation of oxysterols has been included. This review comprises a detailed and critical assessment of current knowledge regarding the formation, occurrence, metabolism, regulatory properties, and other activities of oxysterols in mammalian systems.

Gylling, Helena, and Tatu A. Miettinen. "The effect of plant stanol- and sterol-enriched foods on lipid metabolism, serum lipids and coronary heart disease." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 42, no. 4 (July 1, 2005): 254–63. http://dx.doi.org/10.1258/0004563054255605.

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Phytosterols are plant sterols, mainly campesterol and sitosterol, and their respective stanols (5α-saturated derivatives), which chemically resemble cholesterol. They are present in a normal diet and are absorbed proportionally to cholesterol, but to a much lesser extent, such that less than 0.1% of serum sterols are plant sterols. Phytosterols inhibit intestinal cholesterol absorption, and fat-soluble plant stanol esters were introduced as a functional food for lowering serum cholesterol in the early 1990s; plant sterol esters entered the market at the end of the 1990s. Inhibition of the intestinal absorption of cholesterol stimulates cholesterol synthesis, a factor which limits serum cholesterol lowering to about 10% with phytosterols. Enrichment of the diet with plant stanol esters reduces absorption and serum concentrations of both cholesterol and plant sterols, whereas enrichment of the diet with plant sterol esters, especially in combination with statins, lowers serum cholesterol but increases serum plant sterol levels. Recent studies have suggested that high-serum plant sterol levels may be associated with increased coincidence of coronary heart disease. Estimates of coronary heart disease reduction by 20-25% with plant sterols/stanols is based mainly on short-term studies. Long-term cholesterol lowering, needed for the prevention of coronary heart disease, may be successful with plant stanol esters, which lower serum cholesterol in both genders over at least a year.

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Дисертації з теми "Metabolism of cholesterol derivatives":

Norlin, Maria. "Cytochrome P450 Enzymes in the Metabolism of Cholesterol and Cholesterol Derivatives." Doctoral thesis, Uppsala University, Department of Pharmaceutical Biosciences, 2000. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-1086.

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Cholesterol is metabolized to a variety of important biological products in the body including bile acids and vitamin D. The present investigation is focused on enzymes that catalyze 7α-hydroxylation or 27-hydroxylation in the metabolism of cholesterol, oxysterols (side chain-hydroxylated derivatives of cholesterol) and vitamin D₃. The enzymes studied belong to the cytochrome P450 enzyme families CYP7 and CYP27.

The study describes purification of a cytochrome P450 enzyme fraction active in 7α-hydroxylation of 25-hydroxycholesterol, 27-hydroxycholesterol, dehydroepiandrosterone and pregnenolone from pig liver microsomes. Peptide sequence analysis indicated that this enzyme fraction contains an enzyme belonging to the CYP7B subfamily. The purified enzyme was not active towards cholesterol or testosterone. Purification and inhibition experiments suggested that hepatic microsomal 7α -hydroxylation of 27-hydroxycholesterol and dehydroepiandrosterone involves at least two enzymes, probably closely related.

The study shows that recombinantly expressed human and rat cholesterol 7α -hydroxylase (CYP7A) and partially purified pig liver cholesterol 7α -hydroxylase are active towards 20(S)-, 24-, 25- and 27-hydroxycholesterol. CYP7A was previously considered specific for cholesterol and cholestanol. The 7α -hydroxylation of 20(S)-, 25-, and 27-hydroxycholesterol in rat liver was significantly increased by treatment with cholestyramine, an inducer of CYP7A. Cytochrome P450 of renal origin showed 7α -hydroxylase activity towards 25- and 27-hydroxycholesterol, dehydroepiaundrosterone and pregnenolone but not towards 20(S)-, 24-hydroxycholesterol or cholesterol. The results indicate a physiological role for CYP7A as an oxysterol 7α -hydroxylase, in addition to the previously known human oxysterol 7α -hydroxylase CYP7B.

The role of renal sterol 27-hydroxylase (CYP27A) in the bioactivation of vitamin D₃ was studied with cytochrome P450 fractions purified from pig kidney mitochondria. Purification and inhibition experiments and experiments with a monoclonal antibody against CYP27A indicated that CYP27A plays a role in renal 25-hydroxyvitamin D₃ l α -hydroxylation.

The expression of CYP7A, CYP7B and CYP27A during development was studied. The levels of CYP27A in livers of newborn and six months old pigs were similar whereas the levels of CYP7A increased. The expression of CYP7B varied depending on the tissue. The expression of CYP7B increased with age in the liver whereas the CYP7B levels in kidney showed a marked age-dependent decrease.

Patel, Dilipkumar. "Cholesterol metabolism in monocyte-derived macrophages." Thesis, Imperial College London, 1990. http://hdl.handle.net/10044/1/46492.

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Hoang, Van Quyen. "Cholesterol metabolism in cultured hamster hepatocytes." Thesis, Royal Veterinary College (University of London), 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.522583.

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曾紹怡 and Siu-yee Patricia Tsang. "Regulation of cholesterol metabolism in hepatocytes." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31969835.

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Simonen, Piia. "Cholesterol metabolism in type 2 diabetes." Helsinki : University of Helsinki, 2002. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/simonen/.

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Tsang, Siu-yee Patricia. "Regulation of cholesterol metabolism in hepatocytes." Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B22032459.

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Boone, Lindsey R. "Thyroid Hormone Regulation of Cholesterol Metabolism." [Tampa, Fla] : University of South Florida, 2009. http://purl.fcla.edu/usf/dc/et/SFE0003089.

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Sampson, William James. "The intracellular control of cholesterol metabolism." Thesis, University of Edinburgh, 1988. http://hdl.handle.net/1842/26913.

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The liver has a major role in the metabolism of cholesterol, being the main site of lipoprotein assembly and degradation and the only tissue where the metabolism of cholesterol to bile acids occurs. This provides the major pathway for the removal of cholesterol from the body. The results described in this thesis concern the use of specific enzyme inhibitors (58-035, Azacholesterol, Mevinolin) to determine the intracellular use of different sources of cholesterol in monolayers of rat hepatocytes. In particular, the fates of newly synthesized cholesterol from mevalonic acid and cholesterol derived from HDL2 were investigated. Incubation of hepatocyte monolayers with 58-035 resulted in the inhibition of esterification. In the presence of mevalonic acid as a cholesterol source, 58-035 stimulated bile acid synthesis. Azacholesterol inhibited bile acid synthesis, had no effect on cholesterol synthesis, and in the presence of mevalonic acid, stimulated secretion of cholesterol by the hepatocytes; it had no effect on cholesterol esterification. Mevinolin inhibited cholesterol synthesis and as a result inhibited esterification. HDL2, in the presence of mevinolin, was used as a cholesterol source. It stimulated bile acid synthesis and cholesterol esterification. Addition of 58-035 to the system resulted in the inhibition of both esterification and bile acid synthesis. Overall, the results indicated that different intracllular pools of free cholesterol exist and that the inter-relationships of these pools give a complex pattern of flux of intracellular cholesterol between various pathways in the rat hepatocyte.

Jiang, Zhao-Yan. "Studies on cholesterol and bile acid metabolism in Chinese cholesterol gallstone patients." Stockholm, 2010. http://diss.kib.ki.se/2010/978-91-7409-844-0/.

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Skogsberg, Josefin. "PPAR delta : its role in cholesterol metabolism /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-604-9.

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Книги з теми "Metabolism of cholesterol derivatives":

Sabine, John R. Cholesterol. Ann Arbor, Mich: University Microfilms International, 1992.

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Lupovici, Zaharia. Good cholesterol, bad cholesterol, and the most discussed cholesterol-- HDL. New York: Vantage Press, 1992.

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Philip, Yeagle, ed. Biology of cholesterol. Boca Raton, Fla: CRC Press, 1988.

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1939-, Esfahani Mojtaba, and Swaney John B. 1944-, eds. Advances in cholesterol research. Caldwell, N.J: Telford Press, 1990.

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Symposium on Lipoprotein and Cholesterol Metabolism in Steroidogenic Tissues (1984 Laval University). Lipoprotein and cholesterol metabolism in steroidogenic tissues. Philadelphia: Georg F. Stickley Co., 1985.

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Pearce, Jack B. Dietary dairy products and mammalian cholesterol metabolism. Belfast: Food and Agricultural Chemistry Department, Queen's University of Belfast, 1989.

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Myant, N. B. Cholesterol metabolism, LDL, and the LDL receptor. San Diego: Academic Press, 1990.

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1947-, Strauss Jerome F., and Menon K. M. J, eds. Lipoprotein and cholesterol metabolism in steroidogenic tissues. Philadelphia: G. F. STickley, 1985.

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Y, Chang T., and Freeman Dale A, eds. Intracellular cholesterol trafficking. Boston: Kluwer Academic Publishers, 1998.

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Shi-Kaung, Peng, and Morin Robert J, eds. Biological effects of cholesterol oxides. Boca Raton: CRC Press, 1992.

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Частини книг з теми "Metabolism of cholesterol derivatives":

Van Berkel, Theo J. C., Helene Vietsch, and Erik A. L. Biessen. "Lowering of Serum Cholesterol Levels by a Cholesterol Derivative of a New Triantennary Cluster Galactoside." In Drugs Affecting Lipid Metabolism, 531–39. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-0311-1_62.

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Møller, Jens. "Free Fatty Acid Metabolism." In Cholesterol, 8. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71600-3_5.

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Howles, Philip N., and David Y. Hui. "Cholesterol Esterase." In Intestinal Lipid Metabolism, 119–34. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1195-3_7.

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Wüstner, Daniel. "Intracellular Cholesterol Transport." In Cellular Lipid Metabolism, 157–90. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00300-4_6.

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Steinberg, D. "Transport of Cholesterol and Cholesterol Esters by HDL." In Drugs Affecting Lipid Metabolism, 42–47. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71702-4_7.

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Howles, Philip N. "Cholesterol Absorption and Metabolism." In Methods in Molecular Biology, 157–79. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-058-8_10.

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Howles, Philip N. "Cholesterol Absorption and Metabolism." In Methods in Molecular Biology, 177–97. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3661-8_11.

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Mc Auley, Mark T. "Aging and Cholesterol Metabolism." In Encyclopedia of Gerontology and Population Aging, 1–6. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-69892-2_122-1.

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Mc Auley, Mark T. "Aging and Cholesterol Metabolism." In Encyclopedia of Gerontology and Population Aging, 220–25. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-22009-9_122.

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Marinetti, Guido V. "Disorders of Cholesterol Metabolism." In Disorders of Lipid Metabolism, 63–74. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4615-9564-9_5.

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Тези доповідей конференцій з теми "Metabolism of cholesterol derivatives":

Jovanović-Šanta, Suzana S., Aleksandar M. Oklješa, Antos B. Sachanka, Yaraslau U. Dzichenka, and Sergei A. Usanov. "17-SUBSTITUTED STEROIDAL TETRAZOLES – NOVEL LIGANDS FOR HUMAN STEROID-CONVERTING CYP ENZYMES." In 1st INTERNATIONAL Conference on Chemo and BioInformatics. Institute for Information Technologies, University of Kragujevac, 2021. http://dx.doi.org/10.46793/iccbi21.336js.

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In animal and human organisms, there are many enzymes, members of the family of heme- containing proteins, cytochromes P450 (CYPs), included in the biosynthesis and metabolism of many biomolecules, as cholesterol, bile acids, sex, and corticosteroid hormones, as well as in metabolism of drugs and xenobiotics. It is also well-known that different imidazole and triazole derivatives are efficient inhibitors of CYPs activity. In this study, we present in vitro screening of binding of novel androstane derivatives with tetrazole- containing substituents in position 17 to human recombinant steroid-converting CYP enzymes: CYP7A1, CYP7B1, CYP17A1, CYP19, and CYP21. Initial screening was performed using a high throughput screening approach, while the affinity of the ligands was analyzed using spectrophotometric titration. For some among tested compounds type I spectral response (substrate-like binding) for CYP7A1 selectively, while for one compound type II spectral response (inhibitor-like binding) for CYP21 were detected, with micromolar values of Kds. Interestingly, one compound with mixed spectral response was found to bind for CYP7B1, which means that there are two optimal positions of the ligand inside the protein active site. Such results could be useful in CYP-inhibiting drug development, during a fast, high-throughput screening of pharmacological potential of novel compounds, as well as in side- effects recognizing.

Yang, L., Q. Yang, Q. H. Liu, H. Zhang, S. H. Sun, and T. C. Zhuang. "Rice protein level affects cholesterol metabolism." In EM 2011). IEEE, 2011. http://dx.doi.org/10.1109/icieem.2011.6035585.

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Stopsack, Konrad H., Travis A. Gerke, Lorelei A. Mucci, and Jennifer R. Rider. "Abstract 60: PTEN expression, cholesterol metabolism, and lethal prostate cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-60.

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He, Sisi, Georgina Cheng, Edward Roy, Marta Spain, Ronald Kimball, Nikolas Snyder, Melina Salgado, et al. "Abstract 2821: Cholesterol and its metabolism impact ovarian cancer progression." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2821.

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Yue, Shuhua, Junjie Li, Seung Young Lee, Tian Shao, Bing Song, Liang Cheng, Chang-Deng Hu, Xiaoqi Liu, Timothy L. Ratliff, and Ji-Xin Cheng. "Abstract 1893: Spectroscopic imaging unveils altered cholesterol metabolism in prostate cancer ." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-1893.

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Ludescher, M., N. Stamm, T. Fehm, and H. Neubauer. "PGRMC1 interacts with proteins of the cholesterol synthesis pathway resulting in altered cholesterol metabolism in breast cancer cells." In Abstracts of the 10th Scientific Symposium of the Comission for Translational Research of the Working group for Gynecologic Oncology AGO e.V. Georg Thieme Verlag KG, 2018. http://dx.doi.org/10.1055/s-0038-1675447.

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Yoda, Tsuyoshi, Huong Phan Thi Thanh, Mun'delanji C. Vestergaard, Tsutomu Hamada, and Masahiro Takagi. "Thermo-induced dynamics of membranes and liquid crystals containing cholesterol derivatives." In 2012 International Symposium on Micro-NanoMechatronics and Human Science (MHS). IEEE, 2012. http://dx.doi.org/10.1109/mhs.2012.6492459.

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Wang, Sai, Frederik Link, Mei Han, Roohi Chaudhary, Anastasia Asimakopoulos, Roman Liebe, Ye Yao та ін. "Reciprocal Inhibitory Regulation of TGF-β1 Signaling and Cholesterol Metabolism in Hepatocytes". У 40. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag, 2024. http://dx.doi.org/10.1055/s-0043-1777574.

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Verbrugghe, Adronie, and Alexandra Rankovic. "Dietary choline in feline nutrition and its role in obesity prevention and liver health." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/gyun6061.

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In North America, 60% of cats isÂ estimated to be overweight or obese, predisposing cats to obesity-related health consequences, which reduce quality and quantity of life. Weight loss is recommended, yet current protocols are often unsuccessful. Moreover, drastic energy restriction can put overweight and obese cats at risk of developing feline hepatic lipidosis which can be fatal if left untreated.Choline, an essential nutrient, can be found naturally in organ meats, eggs, soybean and wheat germ. Commercial pet foods contain a supplemental source of choline to meet the recommendations set by the Association of American Feed Control Officials. For cats, 2400 mg/kg diet on a dry matter basis or 600 mg/1000 kcal metabolizable energy is recommended for growth and adult maintenance. Choline is a methyl group donor involved in multiple metabolic pathways and plays an important role in fat metabolism and mobilization, particularly in the liver. Choline is a precursor for phosphatidylcholine, an essential component of very-low-density lipoproteins, crucial for exporting triglycerides and cholesterolÂ out of the liver and into circulation. Research in many animal species, including cats, has found that a diet deficient in choline results in hepatic fat accumulation. Similarly in rats, high-fat diet-induced fatty livers were reversed with choline. Choline supplementation studies in the animal nutrition field have largely focused on growth and weight gain in livestock. This research uncovered decreased fat deposition and increased lean carcass composition with supplementation of choline or its derivative betaine. This session will summarize recent choline research in cats. The findings suggest that supplementing choline, above an animalâ€™s recommended allowance, may help to reduce body fat gain in growing kittens after neutering, and help mobilize fats from the liver in overweight and obese cats, proposing a novel nutritional strategy for obesity prevention and liver health in domestic cats.

Muth, Aaron, Veethika Pandey, Xianlin Han, Deborah Altomare, and Otto Phanstiel. "Abstract A108: Targeting sphingolipid metabolism and metastasis with motuporamine derivatives." In Abstracts: AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.panca2014-a108.

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Звіти організацій з теми "Metabolism of cholesterol derivatives":

Min, Byungrok, Il Suk Kim, and Dong U. Ahn. Dietary Cholesterol Affects Lipid Metabolism in Rabbits. Ames (Iowa): Iowa State University, January 2015. http://dx.doi.org/10.31274/ans_air-180814-1348.

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Hung, Hsuan-Yu, Hui-Hsiung Lai, Hui-Chuan Lin, and Chung-Yu Chen. Impact of interferon-free antivirus therapy on lipid profiles in patients with chronic hepatitis C: A network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2022. http://dx.doi.org/10.37766/inplasy2022.7.0055.

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Review question / Objective: P: ("Hepatitis C"[Mesh] AND "Hepacivirus"[Mesh] AND "Hepatitis C, Chronic”[Mesh]) I: (direct acting antiviral OR asunaprevir OR boceprevir OR daclatasvir OR dasabuvir OR elbasvir OR glecaprevir OR grazoprevir OR ledipasvir OR ombitasvir OR paritaprevir OR pibrentasvir OR simeprevir OR sofosbuvir OR telaprevir OR velpatasvir OR voxilaprevir) C: placebo O: ( "Cholesterol, VLDL"[Mesh] OR "Cholesterol, LDL"[Mesh] OR "Cholesterol, HDL"[Mesh] OR "Dyslipidemias"[Mesh] OR "lipoprotein cholesterol ester, human" [Supplementary Concept] OR "lipoprotein cholesterol" [Supplementary Concept] ) OR ((lipoprotein cholesterol) OR ("lipidemia") OR (lipid metabolism) OR (lipid)). Information sources: We conducted a comprehensive literature search of PubMed, Cochrane Library, Embase, and Ovid MEDLINE electronic databases from their inception to May 20, 2022.

Gao, Hui, Chen Gong, Shi-chun Shen, Jia-ying Zhao, Dou-dou Xu, Fang-biao Tao, Yang Wang, and Xiao-chen Fan. A systematic review on the associations between prenatal phthalate exposure and childhood glycolipid metabolism and blood pressure: evidence from epidemiological studies. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2022. http://dx.doi.org/10.37766/inplasy2022.6.0111.

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Review question / Objective: The present systematic review was performed to obtain a summary of epidemiological evidence on the relationships of in utero exposure to phthalates with childhood glycolipid metabolism and blood pressure. Condition being studied: Childhood cardiovascular risk factors including blood pressure, lipid profile (e.g., triglycerides, total cholesterol, HDL−C, LDL−C) and glucose metabolism (e.g., insulin, insulin resistance, insulin sensitivity, glucose) were the interested outcomes. Eligibility criteria: In brief, epidemiological studies including cohort study, case-control study and cross-sectional survey were screened. Studies regarding relationships between human exposure to organophosphate esters and neurotoxicity were possible eligible for the present systematic review. The adverse neurodevelopmental outcomes included development of cognition, behavior, motor, brain change, emotion, etc. Studies that did not meet the above criteria were not included in this systematic review.

yu, luyou, jinping yang, xi meng, and yanhua lin. Effectiveness of the gut microbiota-bile acid pathway (BAS) in the treatment of Type 2 diabetes: A protocol for systematic review and meta analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2022. http://dx.doi.org/10.37766/inplasy2022.7.0117.

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Review question / Objective: To systematically evaluate the efficacy of the intestinal microbiome - bile acid pathway (BAS) in the treatment of T2DM. Condition being studied: Bile acids (BAs), an important component of bile, are also metabolites derived from cholesterol and promote intestinal absorption and transportation of dietary lipids . Studies have shown that bile acid receptor agonists can promote glP-1 secretion and improve glucose metabolism in preclinical mouse models of obesity and insulin resistance , which may become a new therapeutic target for Type 2 diabetes. However, no systematic review and meta-analysis has been found on the treatment of type 2 diabetes by intestinal microbiome - bile acid pathway. Therefore, we conducted a systematic review and meta-analysis to evaluate the safety and effectiveness of intestinal microbiome-bile acid pathway in the treatment of type 2 diabetes.

Meidan, Rina, and Robert Milvae. Regulation of Bovine Corpus Luteum Function. United States Department of Agriculture, March 1995. http://dx.doi.org/10.32747/1995.7604935.bard.

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The main goal of this research plan was to elucidate regulatory mechanisms controlling the development, function of the bovine corpus luteum (CL). The CL contains two different sterodigenic cell types and therefore it was necessary to obtain pure cell population. A system was developed in which granulosa and theca interna cells, isolated from a preovulatory follicle, acquired characteristics typical of large (LL) and small (SL) luteal cells, respectively, as judged by several biochemical and morphological criteria. Experiments were conducted to determine the effects of granulosa cells removal on subsequent CL function, the results obtained support the concept that granulosa cells make a substaintial contribution to the output of progesterone by the cyclic CL but may have a limited role in determining the functional lifespan of the CL. This experimental model was also used to better understand the contribution of follicular granulosa cells to subsequent luteal SCC mRNA expression. The mitochondrial cytochrome side-chain cleavage enzyme (SCC), which converts cholesterol to pregnenolone, is the first and rate-limiting enzyme of the steroidogenic pathway. Experiments were conducted to characterize the gene expression of P450scc in bovine CL. Levels of P450scc mRNA were higher during mid-luteal phase than in either the early or late luteal phases. PGF 2a injection decreased luteal P450scc mRNA in a time-dependent manner; levels were significantly reduced by 2h after treatment. CLs obtained from heifers on day 8 of the estrous cycle which had granulosa cells removed had a 45% reduction in the levels of mRNA for SCC enzymes as well as a 78% reduction in the numbers of LL cells. To characterize SCC expression in each steroidogenic cell type we utilized pure cell populations. Upon luteinization, LL expressed 2-3 fold higher amounts of both SCC enzymes mRNAs than SL. Moreover, eight days after stimulant removal, LL retained their P4 production capacity, expressed P450scc mRNA and contained this protein. In our attempts to establish the in vitro luteinization model, we had to select the prevulatory and pre-gonadotropin surge follicles. The ratio of estradiol:P4 which is often used was unreliable since P4 levels are high in atretic follicles and also in preovulatory post-gonadotropin follicles. We have therefore examined whether oxytocin (OT) levels in follicular fluids could enhance our ability to correctly and easily define follicular status. Based on E2 and OT concentrations in follicular fluids we could more accurately identify follicles that are preovulatory and post gonadotropin surge. Next we studied OT biosynthesis in granulosa cells, cells which were incubated with forskolin contained stores of the precursor indicating that forskolin (which mimics gonadotropin action) is an effective stimulator of OT biosynthesis and release. While studying in vitro luteinization, we noticed that IGF-I induced effects were not identical to those induced by insulin despite the fact that megadoses of insulin were used. This was the first indication that the cells may secrete IGF binding protein(s) which regonize IGFs and not insulin. In a detailed study involving several techniques, we characterized the species of IGF binding proteins secreted by luteal cells. The effects of exogenous polyunsaturated fatty acids and arachidonic acid on the production of P4 and prostanoids by dispersed bovine luteal cells was examined. The addition of eicosapentaenoic acid and arachidonic acid resulted in a dose-dependent reduction in basal and LH-stimulated biosynthesis of P4 and PGI2 and an increase in production of PGF 2a and 5-HETE production. Indomethacin, an inhibitor of arachidonic acid metabolism via the production of 5-HETE was unaffected. Results of these experiments suggest that the inhibitory effect of arachidonic acid on the biosynthesis of luteal P4 is due to either a direct action of arachidonic acid, or its conversion to 5-HETE via the lipoxgenase pathway of metabolism. The detailed and important information gained by the two labs elucidated the mode of action of factors crucially important to the function of the bovine CL. The data indicate that follicular granulosa cells make a major contribution to numbers of large luteal cells, OT and basal P4 production, as well as the content of cytochrome P450 scc. Granulosa-derived large luteal cells have distinct features: when luteinized, the cell no longer possesses LH receptors, its cAMP response is diminished yet P4 synthesis is sustained. This may imply that maintenance of P4 (even in the absence of a Luteotropic signal) during critical periods such as pregnancy recognition, is dependent on the proper luteinization and function of the large luteal cell.

Jander, Georg, and Daniel Chamovitz. Investigation of growth regulation by maize benzoxazinoid breakdown products. United States Department of Agriculture, January 2015. http://dx.doi.org/10.32747/2015.7600031.bard.

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Introduction Previous research had suggested that benzoxazinoids, a class of defensive metabolites found in maize, wheat, rye, and wild barley, are not only direct insect deterrents, but also influence other areas of plant metabolism. In particular, the benzoxazinoid 2,4-dihydroxy-7-methoxy-2H-1,4-benzoxa- zin-3(4H)- one (DIMBOA) was implicated in: (i) altering plant growth by interfering with auxin signaling, and (ii) leading to the induction of gene expression changes and secondary plant defense responses. The overall goal of this proposal was to identify mechanisms by which benzoxazinoids influence other aspects of plant growth and defense. Specifically, the following hypotheses were proposed to be tested as part of an approved BARD proposal: Benzoxazinoid breakdown products directly interfere with auxin perception Global changes in maize and barley gene expression are induced by benzoxazinoid activation. There is natural variation in the maize photomorphogenic response to benzoxazinoids. Although the initial proposal included experiments with both maize and barley, there were some technical difficulties with the proposed transgenic barley experiments and most of the experimental results were generated with maize. Summary of major findings Previous research by other labs, involving both maize and other plant species, had suggested that DIMBOA alters plant growth by interfering with auxin signaling. However, experiments conducted in both the Chamovitz and the Jander labs using Arabidopsis and maize, respectively, were unable to confirm previously published reports of exogenously added DIMBOA effects on auxin signaling. Nevertheless, analysis of bx1 and bx2 maize mutant lines, which have almost no detectable benzoxazinoids, showed altered responses to blue light signaling. Transcriptomic analysis of maize mutant lines, variation in inbred lines, and responses to exogenously added DIMBOA showed alteration in the transcription of a blue light receptor, which is required for plant growth responses. This finding provides a novel mechanistic explanation of the trade-off between growth and defense that is often observed in plants. Experiments by the Jander lab and others had demonstrated that DIMBOA not only has direct toxicity against insect pests and microbial pathogens, but also induces the formation of callose in both maize and wheat. In the current project, non-targeted metabolomic assays of wildtype maize and mutants with defects in benzoxazinoid biosynthesis were used to identify unrelated metabolites that are regulated in a benzoxazinoid-dependent manner. Further investigation identified a subset of these DIMBOA-responsive compounds as catechol, as well as its glycosylated and acetylated derivatives. Analysis of co-expression data identified indole-3-glycerol phosphate synthase (IGPS) as a possible regulator of benzoxazinoid biosynthesis in maize. In the current project, enzymatic activity of three predicted maize IGPS genes was confirmed by heterologous expression. Transposon knockout mutations confirmed the function of the maize genes in benzoxazinoid biosynthesis. Sub-cellular localization studies showed that the three maize IGPS proteins are co-localized in the plastids, together with BX1 and BX2, two previously known enzymes of the benzoxazinoid biosynthesis pathway. Implications Benzoxazinoids are among the most abundant and effective defensive metabolites in maize, wheat, and rye. Although there is considerable with-in species variation in benzoxazinoid content, very little is known about the regulation of this variation and the specific effects on plant growth and defense. The results of this research provide further insight into the complex functions of maize benzoxazinoids, which are not only toxic to pests and pathogens, but also regulate plant growth and other defense responses. Knowledge gained through the current project will make it possible to engineer benzoxazinoid biosynthesis in a more targeted manner to produce pest-tolerant crops without negative effects on growth and yield.