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Dissertationen zum Thema „Cholesterol“
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1
Edington, J. "The relationship of dietary cholesterol to plasma cholesteroll." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.236284.
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2
Malcolmson, Richard Joseph. "Physical studies of cholesterol and cholesteryl esters in model membranes." Thesis, Edinburgh Napier University, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385910.
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3
Velarde, Laos Edmundo, and Ana Gonzalez. "Cholesterol and Cholesterol Oxides in Chicken Meat." Revista de Química, 2012. http://repositorio.pucp.edu.pe/index/handle/123456789/99119.
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Se determinó el contenido de lípidos totales, colesterol yóxidos de colesterol en carne de pollo adquiridos en 3avícolas de Lima. La carne de pollo presentó valores de lípidostotales y colesterol diferentes porpresentó los menores valores demientras que la piel presentó losavícola. La carne de pecholípidos totales y colesterol,mayores valores de estos. Por cromatografía de gases acoplado a espectrómetro demasas (CG-EM) se confirmó la estructura de los siguientes óxidosde colesterol: 7-cetocolesterol, en las 3 avícolas; 7 β -hidroxicolesterol en ala de la avícola 1 y piel de la avícola 2; 7 -hidroxicolesterol y α - epoxicolesterol en piel de la avícola 2.<br>The contents of tota lipids, cholesterol and cholesterol oxides we determined in chicken meat purchased fromen farms in Lima. Chicken meat presented differentvalues of total lipids and cholesterol. Breast chicken presentedthe lowest values of total lipids and cholesterol while the skinpresented the highest values.A gas chromatograph – mass spectrometer (GC – MS) was employed to confirm the structure of theoxides: 7-ketocholesterol was found infarms ; 7- hydroxycholesterol was foundfollowing cholesterolthe three chickenin wing of chickenfarm 1 and in the skin of chicken farm 2; 7-hydroxycholesteroland - epoxycholesterol in the skin of chicken farm 2.
4
Kingdon, Lorraine B. "Speedy Cholesterol." College of Agriculture, University of Arizona (Tucson, AZ), 1990. http://hdl.handle.net/10150/295659.
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5
Famer, Daniel. "Implications of cholesterol and cholesterol-lowering therapy in Alzheimer's disease /." Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-260-6/.
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6
Burkett, Paul A. "Frequent cholesterol feedback as an aid in lowering cholesterol levels." Thesis, Virginia Tech, 1989. http://hdl.handle.net/10919/44704.
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Twenty six male and two female participants in the Cardiac Therapy Program at Virginia Tech were stratified, based upon level of total cholesterol (TC) and length of time in the Cardiac Program, and then randomly assigned to either experimental or control groups. Participants ranged in age from 43 to 68 years and all had baseline TC levels greater than 200 mg/dl. There were no significant
differences between groups in terms of baseline TC (control
M : 248 mg/dl; experimental M = 251 mg/dl), blood pressure
(BP), weight, predicted percent body fat, dietary fat/cholesterol, age, education, or program attendance.<br>Master of Science
7
Alasmi, Mahmood Mohamed. "EFFECTS OF CHOLESTEROL SUPPLEMENTATION ON CHOLESTEROL SYNTHESIS RATES IN INFANTS." University of Cincinnati / OhioLINK, 2000. http://rave.ohiolink.edu/etdc/view?acc_num=ucin974741712.
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8
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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<p>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 D<sub>3</sub>. The enzymes studied belong to the cytochrome P450 enzyme families CYP7 and CYP27.</p><p>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.</p><p>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(<i>S</i>)-, 24-, 25- and 27-hydroxycholesterol. CYP7A was previously considered specific for cholesterol and cholestanol. The 7α -hydroxylation of 20(<i>S</i>)-, 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(<i>S</i>)-, 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.</p><p>The role of renal sterol 27-hydroxylase (CYP27A) in the bioactivation of vitamin D<sub>3</sub> 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 D<sub>3</sub> l α -hydroxylation.</p><p>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.</p>
9
Trevenen, Alexandra H. "Investigations of phospholipid/cholesterol and cholesterol derivative interactions in model membranes." Thesis, Imperial College London, 2010. http://hdl.handle.net/10044/1/5582.
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Multinuclear solid state MAS NMR (1H and 31P), 31P CSA solid state NMR, 2H NMR and x-ray diffraction techniques have been used to compare the structure and properties of DPPC: Andro and DPPC: 4β-hydroxycholesterol with that of the properties known of DPPC: Chol mixtures in excess water. The formation of the Lo phase is known to occur with PC: Chol mixtures with sufficient concentrations of cholesterol. The formation and properties of the Lo phase was looked at with the cholesterol derivatives Andro (lacking in the hydrocarbon tail present in cholesterol) and 4β-hydroxycholesterol (possessing an extra hydroxyl group adjacent to the one present at the headgroup region of cholesterol). The Lo phase shows fluid-fluid immisibility when combined with the disordered Lα phase. It is this heterogeneity that is believed to be important in the formation of lipid rafts, which are thought to play a role in the function of living cells. Cholesterol desorption from DOPC model membranes was examined using methyl-β-cyclodextrin, which has a high affinity for cholesterol and facilitates the mechanism of cholesterol desorption from lipid membranes. By running a number of experiments, measuring cholesterol desorption from MLV’s and LUV’s a cholesterol flip-flop rate within DOPC model membranes was measured using 1H solution state NMR. A number of methods were also attempted to synthesise an asymmetric DOPC: DPPC membranes. These included a split glass slides method and a modified version of an emulsion method as described by Pautot et al. lipid asymmetry with respect to the split glass slides and emulsion methods was to be observed by NMR, where any cholesterol asymmetry formed via desorption by methyl-β- cyclodextrin was to be evaluated via the use of paramagnetic NMR experiments, however no asymmetry was observed in either experiment.
10
Beehler, Kaitlyn. "MiR-1908 Is a Cholesterol Responsive MicroRNA Implicated In Cholesterol Regulation." Thesis, Université d'Ottawa / University of Ottawa, 2020. http://hdl.handle.net/10393/40422.
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Leveraging miRNA-Seq data and the 1000 Genomes imputed genotypes, we identified rs174561-C as a strong miRQTL for circulating miRNA-1908-5p (P=4.8x10-31) which has an inverse relationship with circulating LDL-C, fasting glucose and A1c. Here I investigated the molecular mechanism(s) linking miR1908-5p to cholesterol metabolism. First, by overexpression experiments in HuH-7 cells demonstrate that the presence of the C allele, associated with lower LDL-C levels, significantly increases miR-1908-5p by 2.15-fold relative to the T allele. Further experiments revealed that 72-hour cholesterol depletion increases miR-1908-5p expression (2.11-fold) whereas cholesterol loading decreases miR-1908-5p expression (0.69-fold). Differential miR-1908-5p expression was then used to profile genes involved in lipoprotein signaling and cholesterol metabolism using a PCR array to identify LDLR as a gene of interest. Although total RNA and protein expression of LDLR was unchanged in response to differential miR-1908-5p expression, the ratio of the mature form to the cleaved form of LDLR decreased following miR-1908-5p inhibition (0.85-fold) and conversely, increased with mimic treatment (1.63-fold). Cleavage of the mature LDLR is known to reduce cell surface affinity for LDL. These findings uncover a potential mechanism linking miR-1908-5p to lower LDL-cholesterol levels through reduced LDLR cleavage.
11
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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12
Lubchak, I. V., and A. Koneva. "Inhibitors for cholesterol reduction." Thesis, Sumy State University, 2016. http://essuir.sumdu.edu.ua/handle/123456789/45956.
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Cardiovascular diseases (CVDs) are a group of disorders of the heart and blood vessels. Many of them involve atherosclerosis, which causes most heart attacks and strokes. Cardiovascular diseases are the leading cause of death globally. Nearly 2,200 Americans die of cardiovascular disease daily, with an average of one death occurring every 40 seconds. However, elevated levels of certain forms of cholesterol are some of the primary drivers in the development of some CVDs.
13
Wassif, Christopher A. "Dysregulation of cholesterol homeostasis." Thesis, University of Oxford, 2015. http://ora.ox.ac.uk/objects/uuid:da3374f0-9285-4490-b2e7-af493556d925.
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Cholesterol plays a critical role in the health and normal function of every mammalian cell. Cholesterol has multiple cellular functions including maintenance of cell membrane stability and fluidity, steroid hormone and bile acid synthesis, and membrane receptor signaling. As with any critical metabolite, cholesterol is highly regulated. I will detail my research focusing on the two prevalent disorders of cholesterol homeostasis. The first is a disorder of cholesterol biosynthesis, Smith-Lemli-Opitz syndrome (SLOS), and the second a disorder of cholesterol trafficking, Niemann-Pick disease, type C1 (NPC). I have identified a unique cellular phenotypic overlap between these two previously unrelated disorders. Specifically, increasing concentrations of the precursor sterol present in SLOS, 7-dehydrocholesterol, leads to the induction of an NPC-like cellular phenotype. Aspects of the NPC cellular phenotype that can be induced in SLOS fibroblasts include lysosomal storage of unesterified cholesterol, sphingosine, and glycosphingolipids. Also, similar to what is observed in NPC, dysregulation of acidic calcium stores is present in SLOS. Further research indicates that this cellular phenotype extends into both the mouse models of SLOS and the patients. The dysregulation of cholesterol trafficking in SLOS cells likely decreases cellular cholesterol bioavailabilty and thus potentially limits the therapeutic efficacy of dietary cholesterol supplementation in SLOS patients. I also show that treatment of SLOS cells with miglustat, an established therapy for NPC, ameliorates the NPC-like cellular phenotype and thus may have therapeutic benefit in SLOS. The incidence of both SLOS and NPC has been the subject of debate. Thus, using data generated from massively parallel sequencing of the human exome, I demonstrate that the previously predicted incidence of SLOS of 1:40,000 births is likely correct, but call into question the predicted NPC rate of 1:120,000 . In fact, NPC maybe closer to a rate of 1:40,000. The role of oxysterols in the teratogenicity of SLOS and the underlying secondary storage of lipids in the phenotypic presentation of SLOS has been investigated.
14
Shie, Feng-Shiun. "Cholesterol and Alzheimer's disease /." Thesis, Connect to this title online; UW restricted, 2000. http://hdl.handle.net/1773/6604.
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15
Misner, Scottie, Carol Curtis, and Evelyn Whitmer. "Fat and Cholesterol Update." College of Agriculture and Life Sciences, University of Arizona (Tucson, AZ), 2006. http://hdl.handle.net/10150/146439.
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2 pp.<br>Of all the nutrients in the food supply, fat and cholesterol probably receive the most attention from health professionals and the public alike. The scientific evidence is clear that a high-fat diet relates to chronic health problems such as heart disease, some types of cancer, diabetes, and obesity. But both fat and cholesterol are natural components of the body that are vital to good health, and too little fat in your diet is just as unhealthy as too much. This article reviews dietary fats and provides guidelines for choosing foods to balance the type and amount of fat in your diet.
16
Wang, Li Ph D. Massachusetts Institute of Technology. "Cholesterol and egg activation." Thesis, Massachusetts Institute of Technology, 2019. https://hdl.handle.net/1721.1/122709.
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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, 2019<br>Cataloged from PDF version of thesis. Page 236 blank.<br>Includes bibliographical references.<br>The high-density lipoprotein (HDL) receptor SR-BI controls the structure and fate of plasma HDL. The SR-BI knockout (KO) females are infertile, apparently due to their abnormal, cholesterol-enriched HDL particles. In this thesis, my colleagues and I examined the growth and meiotic progression of SR-BI KO oocytes and found that they underwent normal germinal vesicle breakdown; however, SR-BI KO eggs, which had accumulated excess cholesterol in vivo, spontaneously activated; they escaped metaphase II (MII) arrest and progressed to pronuclear, metaphase III and anaphase/telophase III stages. Eggs from fertile, wild-type mice were activated when loaded in vitro with excess cholesterol using a cholesterol/methyl-[beta]-cyclodextrin complex, phenocopying SR-BI KO oocytes.<br>In vitro cholesterol loading of eggs induced elevation of intracellular calcium (the [Ca²⁺]i spike), reduction in MPF and MAPK activities, extrusion of a second polar body and progression to meiotic stages beyond MI. These results suggest the infertility of SR-BI KO females is due, at least in part, to excess cholesterol in eggs inducing premature activation, and that cholesterol can activate wild-type mouse eggs to escape from MII arrest. In the Chapter 3, I studied the detailed mechanism of egg activation induced by excess cholesterol. I showed that the [Ca²⁺]i spike induced by excess cholesterol was necessary for egg activation and also sufficient for further development of the egg to the blastocysts stage. Excess cholesterol, in calcium free medium, did not induce changes in [Ca²⁺]i, indicating that extracellular calcium was required for the [Ca²⁺]i spike and also suggesting the entry of extracellular calcium via plasma membrane channel(s).<br>After screening of calcium channel inhibitors, single cell mRNA-sequencing and activation experiments using eggs from mutant females, I was able to show that co-inhibition of both the L-type calcium channel Ca[subscript v]1.3 and the transient receptor potential channel TRPC5, but not inhibition of either one alone, blocked the excess-cholesterol induced [Ca²⁺]i spike and egg activation. This result suggests that excess cholesterol activates the MII eggs by opening of Ca[subscript v]1.3 or TPRC5. Our results raise the possibility that excess cholesterol might also activate the same channels in other systems, and thus contribute to pathophysiology.<br>by Li Wang.<br>Ph. D.<br>Ph.D. Massachusetts Institute of Technology, Department of Biology
17
Ridgen, Julie Elizabeth. "The effect of exercise and dietary cholesterol on cholesterol synthesis in the hamster." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/27627.
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Physical inactivity and elevated plasma cholesterol are well characterized risk factors for the development of coronary heart disease (CHD). Consequently, manipulation of exercise intensity and dietary cholesterol may favourably alter lipid metabolism to reduce this risk. The present study examined both independent and interactive effects of exercise and dietary cholesterol on in vivo hepatic and intestinal cholesterol synthesis as well as plasma total and high density lipoprotein (HDL) cholesterol levels in hamsters. Male Syrian hamsters were randomized into one of i) low dietary cholesterol (0.03% w/w) sedentary (LC-S), ii) low cholesterol exercise (LC-E), iii) high cholesterol (0.12% w/w) sedentary (HC-S) or iv) high cholesterol exercise (HC-E) groups. Exercised hamsters were trained to run at increasing speeds on a motorized treadmill for 90 minutes daily over a two week period. Animals were subsequently run for 1 week at 70% of VO₂ max for 90 minutes each day. Cholesterol synthesis was determined by measuring the rate of incorporation of into digitonin precipitable sterols in liver and small intestine over 2 hours following IP injection of ³H₂O. Plasma total cholesterol was significantly increased by dietary cholesterol in HC versus LC groups independent of an exercise lowering effect in HC-E animals. HDL cholesterol was also elevated in response to dietary cholesterol in HC groups, however LC-E hamsters had lower plasma HDL cholesterol than any other group through an interaction between exercise and diet. Incorporation of ³H into liver cholesterol was increased in HC-S versus LC animals, whereas exercise lowered hepatic sterol synthesis in HC-E by an exercise and diet interaction. Although exercise did not affect intestinal cholesterol synthesis, dietary cholesterol significantly decreased intestinal cholesterol synthesis in HC when compared with LC groups. Thus both plasma total cholesterol and small intestine responded characteristically to changes in dietary cholesterol levels, in opposition to liver cholesterol synthesis, which showed a compensatory increase to the attenuation of intestinal sterol synthesis. The exercise induced decrease evident in plasma cholesterol levels and hepatic cholesterol synthesis was not, however, observed in the small intestine. Therefore the independent response of liver and small intestine to exercise and dietary cholesterol level in this study indicate important differences in the manner through which these organs regulate whole body cholesterol balance.<br>Land and Food Systems, Faculty of<br>Graduate
18
Bayley, Timothy M. "The longer term effect of early dietary cholesterol on cholesterol metabolism in infants." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0016/MQ44125.pdf.
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19
Demmers, Thea. "Longer-term effects of early cholesterol intake on cholesterol biosynthesis and plasma lipids." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=18193.
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Endogenous cholesterol (Ch) fractional synthesis rate (FSR) is inversely related to infant dietary Ch at 4 months (mo) of age. The objective of the present study was to determine whether level of infant dietary Ch induced changes in FSR that persisted at 18 mo. Forty-seven infants received, human milk (HM) from birth until weaned (n=15), or were randomized to receive modified cow-milk formula (MCF) with added Ch (n=15), or cow-milk formula (CF, n=17), for 12 mo. Ch contents of HM, MCF, and CF were 120, 80, and 40 mg/L, respectively. At 4 mo, FSR in the HM group was lower than in CF, but at 18 mo, there were no differences between groups. Therefore, while Ch intake prior to weaning affects FSR, the differences do not persist after weaning to unrestricted diet. These data provide further evidence that there is no imprinting of FSR in infancy by differing dietary levels of Ch.<br>Le taux de synthèse fractionée (TSF) du cholestérol (Ch) endogène est inversement proportionnel à la prise alimentaire du Ch à 4 mois (mo). L’objectif de cette étude était de verifier si ces différences du TSF persistent à 18 mo. Quarante-sept enfants ont reçu, dès la naissance, soit lait maternel (HM), jusqu’au sevrage (n=15), ou ont reçu de façon aléatoire soit du lait maternisé (CF), à base lait de vache (n=17), ou une formule modifiée par l’addition de Ch (MCF, n=15) durant 12 mo. Les HM, CF, et MCF contenaient respectivement 120, 80, 40 mg/L de Ch. À 4 mois, le TSF dans HM était plus faible que chez CF, mais cette différence avait disparue à 18 mois avec le sevrage au régime sans restriction. Ces données confirment que le Ch alimentaire chez le nourrisson n’affecte pas le TSF de façon permanente. fr
20
Bayley, Timothy M. "The longer term effect of early dietary cholesterol on cholesterol metabolism in infants /." Thesis, McGill University, 1998. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=37522.
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La synthese endogene du cholesterol (CH) a ete etudie chez 81 nouveau-nes, ages de 4 mois (BRAS 1) ou de 11 a 12 mois (BRAS2), afin d'evaluer les effets a long terme d'un supplement de CH sur l'homeostasie du CH. BRAS 1 etait compose de 32 nouveau-nes recevant soit du lait humain (HUM) (6M, 7F), une formule a base de lait de vache (VAC) (6M, 3F) contenant 3.5 mg CH/dl, ou une formule a base de lait de vache modifiee (VACM) (6M, 7F) contenant 13.5 mg CH/dl, afin d'evaluer l'effet du supplement sur les taux de synthese du CH. BRAS2 etait compose de 49 autres enfants recevant soit HUM (11M, 6F), VAC (7M, 12F) ou VACM (6M, 7F) jusqu'a l'age de 6 mois dans le but d'evaluer une hypothese d'impression genetique. Ceci a ete realise en utilisant un design "cross-over" et en montant un defi journalier de 250 g de CH a l'age de 11 mois. Le taux d'incorporation de deuterium, provenant des reserves d'eau corporelle, dans la structure du CH a servi comme indice du taux de synthese fractionnel (TSF) de ce dernier sur une periode de 48 heures. Les niveaux de CH total et LDL etaient considerablement eleves dans HUM en comparaison avec VAC et VACM a l'age de 4 mois. La concentration sanguine du CH etait semblable a 11 et 12 mois. Le TSF etait 4 fois plus eleve dans VAC et VACM relatif a HUM, mais il n'y avait pas de difference entre VAC et VACM a 11 et 12 mois. Cependant, les TSF de 4 a 12 mois ont augmente dans HUM et baisse dans VAC et VACM. Nos resultats indiquent qu'independamment du contenu des dietes, le defi journalier de CH n'as pas eu d'effet considerable ni sur les taux de synthese, ni sur les niveaux de CH sanguin. Ces resultats appuient l'idee que le CH alimentaire n'a que des effets minimes sur le metabolisme a long terme du CH.
21
Guérin, Maryse. "Transport inverse du cholesterol : roles de la lecithine cholesterol acyltransferase (lcat) et de la proteine de transfert des esters de cholesterol (cetp)." Paris 6, 1994. http://www.theses.fr/1994PA066136.
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Dans le compartiment plasmatique les lipoproteines de basse densite assurent l'approvisionnement en cholesterol des tissus extra hepatiques. Les tissus peripheriques sont cependant incapables de degrader le cholesterol ainsi accumule. Dans ces conditions, l'homeostasie du cholesterol ne peut etre maintenue que grace a un systeme d'epuration et de transport vers le foie. Cette voie de retour du cholesterol, des tissus peripheriques vers le foie, est nommee transport reverse du cholesterol. Ce systeme peut etre divise en plusieurs etapes. La premiere constitue l'efflux du cholesterol cellulaire. Par la suite le cholesterol libre nouvellement acquis est esterifie au sein des particules hdl sous l'action de la lcat. Enfin, dans une derniere etape, le cholesterol retourne au foie, soit directement par captation des particules hdl, soit via le transfert aux autres lipoproteines de basse densite, les vldl, idl et ldl, sous l'action de la proteine de transfert des esters de cholesterol, la cetp. Depuis qu'il a ete etablie une correlation inverse entre le taux de hdl plasmatiques et le risque cardio-vasculaire, l'interet pour les mecanismes regulant le taux des hdl dans le plasma ainsi que l'elimination du cholesterol, n'a cesse d'augmenter. Cependant, a l'heure actuelle, les relations existant entre l'effet protecteur des hdl contre les maladies cardio-vasculaires et le processus du systeme du transport du cholesterol ne sont pas clairement etablies. Pour aller plus loin dans la connaissance du mecanisme complexe que represente le transport reverse du cholesterol, il apparaissait necessaire de mieux comprendre les roles des deux proteines cles de ce systeme: la lcat et la cetp. Afin de definir la responsabilite de la lcat et de la cetp dans l'etablissement du profil lipoproteique, nous avons, d'une part, analyse plusieurs individus presentant une deficience familiale en lcat. Ces etudes ont permis de mettre en evidence la presence, dans le plasma de certains malades, de plusieurs particules lp-x et de type hdl. Ces complexes lipoproteiques semblent etre un facteur determinant dans l'accumulation de lipides au sein du tissu renal et du developpement de l'insuffisance renale frequemment observee chez ces malades. D'autre part, nous avons etudie l'activite de la cetp chez des patients presentant une dyslipoproteinemie. Nous avons pour cela, mis au point une nouvelle methodologie permettant a la fois l'evaluation des activites de transfert et d'echange de la cetp. Dans ces conditions, nous avons identifie les particules ldl riches en esters de cholesterol et dans l'etablissement d'un profil lipoproteique particulierement atherogene
22
Mahammad, Saleemulla. "Cholesterol in T cells homeostasis, plasma membrane organization and signaling /." Doctoral thesis, Stockholm : The Wenner-Gren Institute, Stockholm University, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-38357.
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Diss. (sammanfattning) Stockholm : Stockholms universitet, 2010.<br>At the time of the doctoral defense, the following paper was unpublished and had a status as follows: Paper 2: Manuscript. Paper 3: In press.
23
Marijanovic, Zrinka. "Cellular requirements for cholesterol and identification of genes involved in cholesterol biosynthesis and homeostasis." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=966109104.
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Grebe, Alena [Verfasser]. "Targeting cholesterol crystals in atherosclerosis with cholesterol solubilizing 2-hydroxypropyl-beta-cyclodextrin / Alena Grebe." Bonn : Universitäts- und Landesbibliothek Bonn, 2016. http://d-nb.info/1124540296/34.
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Shen, Haiqing. "New candidate gene involved in reverse cholesterol transport (RCT) : the case for phospholipid transfer protein (PLTP): interactions with dietary factors /." Thesis, Connect to Dissertations & Theses @ Tufts University, 2004.
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Thesis (Ph.D.)--Tufts University, 2004.<br>Adviser: Jose Ordovas. Submitted to the School of Nutrition Science and Policy. Includes bibliographical references (leaves 136-137). Access restricted to members of the Tufts University community. Also available via the World Wide Web;
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Al-Seeni, Madeha N. "Control of hepatic cholesterol esterification." Thesis, University of Nottingham, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293154.
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Kacher, Radhia. "Role of the cholesterol hydroxylase enzyme CYP46A1 in cholesterol metabolism and neuroprotection in Huntington's disease." Thesis, Sorbonne université, 2019. http://www.theses.fr/2019SORUS154.
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La maladie de Huntington (MH) est une maladie génétique autosomique dominante, causée par une augmentation du nombre de CAG sur le gène de la huntingtin. L’homéostasie du cholestérol cérébral est altérée dans la MH. L’expression de CYP46A1, enzyme neuronale catabolisant le cholestérol dans le cerveau, est diminuée dans le putamen des patients et dans le striatum de souris modèles de la MH. Après restauration de l’expression de CYP46A1 dans le striatum des souris Knock-In zQ175, les capacités locomotrices sont améliorées, l’agrégation de la huntingtine mutée est diminuée, l’atrophie neuronale est limitée et le métabolisme du cholestérol est stimulé. Une nouvelle signature transcriptionnelle est induite par CYP46A1, avec une restauration des voies impliquées dans l'autophagie, le protéasome, la communication synaptique et le transport axonal, connues pour leur dysfonctionnement dans la MH. CYP46A1 améliore la transmission synaptique et augmente la densité en épines synaptiques. L'élimination des agrégats par autophagie et par le protéasome est augmentée avec CYP46A1. Enfin, le transport de BDNF et de TrkB est amélioré par CYP46A1 dans un modèle in vitro de la MH. Ces résultats révèlent l'effet pléiotrope et bénéfique de la régulation du métabolisme du cholestérol dans la MH. Pour approfondir cette étude, une technique de tri cellulaire a été mise au point, afin de séparer les neurones et les astrocytes à partir de striatum de souris, pour étudier les régulations transcriptomique et lipidomique de ces deux populations. Cette étude permettra d’identifier de nouvelles cibles impliquées dans la neuroprotection par CYP46A1 et présentant un intérêt thérapeutique dans la MH<br>Huntington’s disease (HD) is an autosomal dominant neurodegenerative disease caused by abnormal CAG expansion on huntingtin’s gene. Recently, altered brain cholesterol homeostasis has been implicated in HD. Particularly, the expression of CYP46A1, the rate-limiting enzyme for cholesterol degradation in the brain, is decreased in patients’ putamen and in the striatum of HD mouse models. We restored CYP46A1 expression into the striatum of the zQ175 mice. Behavioral, neuropathological and molecular tests were performed and showed an improvement of locomotor activity and histological landmarks. Cholesterol homeostasis was restored with an increase of cholesterol degradation and synthesis. CYP46A1 induced a new transcriptional signature, with restoration of pathways involved in autophagy, proteasome, synaptic communication and axonal transport, which are known to be dysfunctional in HD. CYP46A1 improved synaptic transmission and spine density in the striatum of the zQ175 mice. Aggregate clearance mediated by autophagy and proteasome was increased after CYP46A1 expression. Finally, BDNF and TrkB transport were enhanced by CY46A1 in HD in vitro models. Overall, CYP46A1 restoration alleviates the zQ175 pathological phenotype through a global compensation. To gain further insights into CYP46A1 neuroprotection, a cell sorting strategy was set up to study the transcriptomic and lipidomic signature in purified neurons and astrocytes. This method will lead to a greater understanding of cell-type-specific regulations and cell communication. Altogether, this project gave new insights into the potential application of CYP46A1 restoration as a therapeutic strategy in HD
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Devadoss, Anando. "Cholesterol Oxidase Modified Microelectrodes for Detection of Cholesterol in the Plasma Membrane of Single Cells." Case Western Reserve University School of Graduate Studies / OhioLINK, 2006. http://rave.ohiolink.edu/etdc/view?acc_num=case1126199194.
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Paredes-Aramburú, Jacqueline, and Antonio Bernabe-Ortiz. "Asociación entre la participación en programas de asistencia alimentaria y patrones del perfil lipídico en Perú." Sociedad Chilena de Nutricion Bromatologia y Toxilogica, 2018. http://hdl.handle.net/10757/624651.
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Purpose: To assess whether the participation in food assistance programs (Community Kitchens and Glass of Milk) was associated with lipid profile patterns in the Peruvian population. We conducted a secondary data analysis using data from the National Survey of Nutritional, Biochemical, Socioeconomic, and Cultural Indicators related to Chronic Degenerative Diseases. The sample included individuals aged ≥20 years, selected from five geographic strata in Peru. From each stratum a random sample of clusters was chosen. Different Poisson regression models with robust variance were built to determine the association between food assistance programs and participant lipid profile (total cholesterol (TC), HDL-cholesterol (HDL-c), LDL-cholesterol and triglycerides (TG)). Data from 4028 participants was analyzed, 123 (3.1%) reported being beneficiaries of the Community Kitchens program and 827 (20.5%) were beneficiaries of the Glass of Milk program. An association between being a beneficiary of Community Kitchens and increased LDL-c (Prevalence ratio (PR)= 2.33; 95% CI: 1.18–4.59) was found. Being a beneficiary of the Glass of Milk program increased the probability of having low HDL-c levels (PR= 1.08; 95% CI: 1.02–1.14), but reduced the probability of hypertriglyceridemia (PR= 0.70; 95% CI: 0.56–0.88). Being a beneficiary of the Community Kitchen program was associated with increased LDL-c levels; while, being a beneficiary of the Glass of Milk increased the probability of low HDL-c, but reduced the probability of developing hypertriglyceridemia.<br>Revisión por pares
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Macklin, Diana C. "A comparison of cholesterol measurements via various blood sample types." Virtual Press, 1991. http://liblink.bsu.edu/uhtbin/catkey/774768.
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There has been inconsistencies in the performance of dry-chemistry analyzers using different blood sample types. Therefore, the purpose of this study was to determine precision and accuracy of both capillary and venous whole blood analyzed by the Reflotron (Boehringer Mannheim Diagnostics, Indianapolis, Indiana) and capillary plasma analyzed by the Ektachem DT60 (Eastman Kodak Company, Rochester, New York). Fifty subjects were recruited to provide a representative sample of cholesterol concentrations. One technician performed two fingerstick punctures and one venipuncture on each subject and analyzed the blood sample types in duplicate using each of the dry-chemistry analyzers. The methods and sample types utilized for comparison of total cholesterol are summarized below.ReflotronEktachem DT60Sigma2-Fingerstick whole2-Fingerstick plasma2-Venipuncture plasmablood2-Venipuncture whole2-Venipuncture plasmablood2-Veni uncture lasmaThe mean percent variation of the duplicate samples analyzed revealed all sample types, with the exception of fingerstick whole blood analyzed by theReflotron, met the LSP ideal goal for precision of 5 3% CV. Fingerstick wholeblood CV was 3.1%, meeting the current LSP standard of _5 5% CV for precision. The Sigma wet-chemistry assay for determination of total cholesterol was used as the reference for assessment of bias of each of the sample types. Fingerstick whole blood, via the Reflotron method, produced a positive 5.5% bias when compared to the reference, failing to meet the current LSP goal for acceptable accuracy (±5% bias). Venous whole blood analyzed using the Reflotron met this goal with a bias of +3.3%. Fingerstick plasma, via the Ektachem DT60 method, produced a bias of +2.1%, meeting the ideal LSP goal of ±3% bias. Venous plasma as measured by both the Reflotron and Ektachem DT60 also met this ideal goal (+2.0% and +1.8% bias, respectively). Overall, precision and accuracy of all sample types, with the exception of fingerstick whole blood, when analyzed by their respective dry-chemistry analyzer was acceptable.<br>School of Physical Education
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McMullen, Todd Patrick William. "Physical studies of cholesterol-phospholipid and cholesterol-glycolipid interactions in model and Acholeplasma laidlawii B membranes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/nq21603.pdf.
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Sabeva, Nadezhda Steliyanova. "REGULATION OF ABCG5 AND ABCG8 STEROL TRANSPORTERS IN BILIARY CHOLESTEROL ELIMINATION, REVERSE CHOLESTEROL TRANSPORT AND DYSLIPIDEMIA." UKnowledge, 2011. http://uknowledge.uky.edu/gradschool_diss/193.
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ATP-binding cassette transporters ABCA1 and ABCG1 initiate reverse cholesterol transport generating HDL particles, whereas ABCG5/G8 promote biliary cholesterol secretion thereby facilitating the last step of reverse cholesterol transport. Mutations in the leptin axis result in obesity and dyslipidemia in ob/ob and db/db mice. These mice have defective HDL clearance, increased plasma cholesterol and decreased biliary cholesterol elimination. My studies demonstrate that ABCG5/G8 protein is low in these animals and can be restored with caloric restriction or leptin replacement. To directly test whether ABCG5/G8 alone is able to correct reverse cholesterol transport defect, liver specific ABCG5/G8 expression was achieved in db/db mice by administration of adenoviral ABCG5 and ABCG8. Restoration of biliary cholesterol is able partially to correct dyslipidemia in obese mice, but only in the presence of ezetimibe, an inhibitor of cholesterol absorption.
ABCG5/G8 is the body’s primary defense against toxic effects of plant sterols. Plant sterols are used as cholesterol lowering food supplements. However, increased plasma plant sterol concentrations are associated with vascular lesions in dyslipidemic patients and animals. My in vitro studies demonstrate that individual plant sterol alter ABCA1 and ABCG1 abundance, cholesterol efflux and inflammatory cytokine secretion in macrophage foam cells at levels found in humans that consume plant sterol supplements.
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Volk, Catherine B. "Role of inhibition of protein prenylation in the cholesterol-dependent and cholesterol-independent effects of simvastatin." Virtual Press, 2006. http://liblink.bsu.edu/uhtbin/catkey/1339597.
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Statins are widely used to treat hypercholesterolemia. Statins inhibit cholesterol biosynthesis, thereby activating genes involved in cholesterol homeostasis, which are under the control of the Sterol Regulatory Element (SRE). Statins also have cholesterol-independent beneficial cardiovascular effects mediated through the phosphoinositide 3-kinase (PI3-K) / Akt signaling pathway and by inhibition of protein prenylation. Because statins inhibit the synthesis of isoprenoids, they can act by inhibiting the small signaling GTPases Ras and Rho, which require post-translational prenylation to become membrane-anchored and functional. We showed that simvastatin-mediated inhibition of protein prenylation does not appear to play a role in activation of SRE transcriptional activity in HepG2 cells. We also found that when isoprenoids were replenished, basal phospho-Akt decreased, suggesting that inhibition of prenylation by simvastatin mediates Akt phosphorylation. Future studies will be needed to investigate the role that inhibition of protein prenylation plays in the activation of the PI3-K/Akt pathway by simvastatin.<br>Department of Biology
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Blanco, Carlos. "Theoretical effects of decreasing saturated fat and cholesterol intake on total serum and LDL Cholesterol Levels /." The Ohio State University, 1996. http://rave.ohiolink.edu/etdc/view?acc_num=osu148793324553977.
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LEVASSEUR, DANIELLE. "Etude de la regulation de la biosynthese du cholesterol par des derives endogenes oxydes du cholesterol." Université Louis Pasteur (Strasbourg) (1971-2008), 1996. http://www.theses.fr/1996STR13251.
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Les maladies coronariennes sont la principale cause de mortalite dans les pays industrialises. L'hypercholesterolemie constitue l'un des facteurs de risques majeurs de ces pathologies. L'une des solutions adoptees en therapie consiste a reduire le taux de cholesterol circulant. Parmi les substances hypocholesterolemiantes, les inhibiteurs de la 3-hydroxy-3-methylglutaryl-coa reductase (hmgcoa reductase), enzyme regulatrice principale de la voie de biosynthese du cholesterol, sont les plus employes a ce jour. Cependant l'inhibition de la biosynthese a un stade plus tardif peut etre envisagee. Au laboratoire nous nous sommes interesses a la (3s)-2,3-epoxyde de squalene-lanosterol cyclase (e. C. 4. 5. 99. 7). Dans les cellules hepg2, des inhibiteurs de cette enzyme affectent tres efficacement la biosynthese du cholesterol par un double mecanisme. En effet, on a constate que cette inhibition entraine l'accumulation de (3s)-2,3-epoxyde de squalene et de (3s,22s)-2,3 ;22,23-diepoxyde de squalene. Ce dernier, qui est preferentiellement cyclise en (24s)-24,25-epoxyde de lanosterol, mene de facon ultime a la formation de (24s)-24,25-epoxycholesterol (chlo). Grace a un dosage du taux d'arn messager, nous avons montre que ce compose reprimait la transcription du gene de la reductase. Par la mise en evidence du role de cet oxysterol, nous pouvons affirmer que des inhibiteurs de la cyclase peuvent agir de facon synergique sur la voie de biosynthese: par la diminution de lanosterol forme (produit reactionnel de la cyclase) et par la repression de l'enzyme regulatrice, l'hmgcoa reductase. D'autre part, nous nous sommes interesses a l'influence d'un autre oxysterol sur la biosynthese du cholesterol, le (24s)-24,25-epoxyde de lanosterol, precurseur du chlo. Notre approche nous a amenes a comparer l'action de ces deux oxysterols. Dans le cadre de ce travail, nous avons egalement ete impliques dans l'etude de nouveaux inhibiteurs organofluores de la biosynthese du cholesterol, en collaboration avec le laboratoire reactivite des molecules fluorees dirige par le dr. J. P. Begue
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Mitter, Diana. "Cholesterol und der Synaptophysin-Synaptobrevin-Komplex." Doctoral thesis, [S.l.] : [s.n.], 2003. http://deposit.ddb.de/cgi-bin/dokserv?idn=966236181.
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Tan, Qiulin. "Inhibition of cholesterol biosynthesis under hypoxia." Texas A&M University, 2005. http://hdl.handle.net/1969.1/3101.
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Oxygen balance is very important and tightly regulated in mammals. Under
hypoxia, hypoxia inducible factor 1(HIF-1) dimerizes with hypoxia inducible
factor 1± (HIF-) and activates expression of several genes. Using a
mammalian two hybrid assay, we found that HIF-1 interacted with sterol
response element binding protein 1a (SREBP1a). SREBP1a regulates
transcription of HMG-CoA reductase via binding to the sterol response element
(SRE) in the promoter region. HMG-CoA reductase is the rate-limiting enzyme in
cholesterol biosynthesis. The interaction between SREBP1a and HIF-1suggests that HIF-1 may play an important role in regulation of cholesterol
biosynthesis. We tested the effects of hypoxia on the HMG-CoA reductase. We
found that hypoxia caused suppression of SRE-driven luciferase reporter gene
expression. HMG-CoA reductase mRNA levels decreased under hypoxia in both
hepatoma cells and mouse primary hepatocytes. Electrophoretic mobility shift
assay showed that HIF-1 blocked binding of SREBP1a to the SRE sequence in
vitro. Ectopic expression of HIF-1 suppressed the SRE- driven luciferase
reporter gene expression in BPR cells (HIF-1). Our results suggest that
hypoxia inhibits cholesterol biosynthesis by suppressing SREBP1a-regulated gene expression and this suppression is caused by the blockage of SREBP1a
binding to SRE sequence by HIF-1.
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Patel, Dilipkumar. "Cholesterol metabolism in monocyte-derived macrophages." Thesis, Imperial College London, 1990. http://hdl.handle.net/10044/1/46492.
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Cowan, Graeme James Macfarlane. "Studies of the cholesterol-dependent cytolysins." Thesis, University of Glasgow, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.486876.
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The cholesterol-dependent cytoiysins (COGs) are a group of toxins produced by several genera of Gram-positive bacteria, that bind to and form large oligomeric pores in target cell membranes that contain cholesterol. In addition to cell lysis, a great number of other biological functions have been described for many members of the group, including induction of cytokine release and complement activation. Some of the COGs have been shown to be critical virulence factors of their producing organisms and immunisation with a number of the COCs has been shown to be protective against disease caused by those producing organisms. The COCs are also being used in a diverse array of applications that utilise their pore-forming and toxic properties, including anti-cancer therapy, anti-viral therapy and celi biology. Pneumolysin (PLY) is a member of the CDCs produced by S. pneumoniae and is an important virulence factor and vaccine candidate. A deletion mutant of PLY, il6PLY, has been described (Kirkham et al., 2006b), and this mutant is capable of cell binding but incapable of pore formation. Enhanced green fluorescent protein (eGFP) tagged forms of PLY and il6PLY were produced and the tagged toxins had similar haemolytic and cytotoxic effects to the parent toxins. Toxin binding to host cells was visualised by epifluorescence microscopy and laser scanning confocal fluorescence microscopy. Binding of the tagged toxins to erythrocytes could also be measured by flow cytometry and an increase in the quantity of bound toxin could be detected in a dose-dependent manner over a large range of toxin concentrations. Rod-like structures were observed on membranes treated with Ll6eGFPPlY and these were further studied by SEM. These rod-like structures may be responsible for the strong aggregation effect observed upon ~6PlY treatment of erythrocytes. lntermedilysin (IlY) is a member of the CDes produced by S. intermedius. It is unique within the group in that it exhibits human-specific cytolysis and initial studies suggested that this is due to binding of a different ceilular receptor to other toxins of the family and that this receptor was a protein (Nagamune et ai, 1996). eGFP-tagged forms of IlY and Ll61lY were produced to allow tracking of the localisation of IlY and for use in development of a quantitative binding assay. It was confirmed that these proteins could be easily visualised by fluorescence microscopy and that binding could be detected by flow cytometry. A two-hybrid screen was also used to screen for proteins from a human brain eDNA library that were capable of interaction with IlY in order to identify candidate protein receptors for !LY, however no likely receptor candidates were identified. In order to determine which region is responsible for the human specificity of intermedilysin, a bank of chimeras between IIY and PLY was created. The chimeric toxins were expressed and purified and the specificity of the mutants was determined by haemolytic assay on human and rabbit erythrocytes. The specificity of the chimeric toxin was determined by the origin of the C-terminal 53/56 residues, indicating that the latter part of domain 4 is responsible for the human specificity of intermedilysin. To further resolve the region involved in human specificity or cholesterol-binding, a series of small substitution mutants was created. These revealed that the promiscuous cell binding activity of the other COCs was conferred by residues in the undecapeptide loop as this property could be transferred to by introduction of the typical undecapeptide sequence. Surface-plasmon resonance analysis of substitutions of PLY was used to detect any mutants possessing reduced binding affinity. However, problems with aggregation of purified proteins prevented quantitative data from being collected. Anthrolysin a (ALa) is a toxin produced by Bacillus anthracis, the causative agent of anthrax. It is a member of the cholesterol-dependent cytolysin (CDC) group of toxins, many of which are potential vaccine candidates that protect against their producing organisms. Pore formation by ALa was studied by transmission electron microscopy and pores were found to be consistent with those formed by other members of this toxin family. A novel genetic toxoid of anthrolysin 0, t.6mALO, was constructed and characterised and was able to bind to cells but was incapable of poreformation or haemolysis. The capacity of the haemolytic and non-haemolytic forms of ALa to protect against challenge with the toxin or B. anthracis was determined. Immunisation with both active and non-haemolytic forms of ALO elicited protection against lethal Lv. challenge with ALa but neither was protective against B. anthracis a murine Lp. challenge model. Immunisation with another CDC, pneumoiysin, did not confer cross-protection against challenge with ALO. To further resolve the region involved in human specificity or cholesterol-binding, a series of small substitution mutants was created. These revealed that the promiscuous cell binding activity of the other COCs was conferred by residues in the undecapeptide loop as this property could be transferred to by introduction of the typical undecapeptide sequence. Surface-plasmon resonance analysis of substitutions of PLY was used to detect any mutants possessing reduced binding affinity. However, problems with aggregation of purified proteins prevented quantitative data from being collected. Anthrolysin a (ALa) is a toxin produced by Bacillus anthracis, the causative agent of anthrax. It is a member of the cholesterol-dependent cytolysin (CDC) group of toxins, many of which are potential vaccine candidates that protect against their producing organisms. Pore formation by ALa was studied by transmission electron microscopy and pores were found to be consistent with those formed by other members of this toxin family. A novel genetic toxoid of anthrolysin 0, t.6mALO, was constructed and characterised and was able to bind to cells but was incapable of poreformation or haemolysis. The capacity of the haemolytic and non-haemolytic forms of ALa to protect against challenge with the toxin or B. anthracis was determined. Immunisation with both active and non-haemolytic forms of ALO elicited protection against lethal Lv. challenge with ALa but neither was protective against B. anthracis a murine Lp. challenge model. Immunisation with another CDC, pneumoiysin, did not confer cross-protection against challenge with ALa. Histopathological investigation following lethal Lv. challenge with ALO revealed acute pathology in the lungs with occlusion of alveolar vessels by fibrin deposits.
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Sather, Paula Joan. "Synthesis of cholesterol based model glycolipids." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/29876.
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The synthesis of glycolipids containing a variable length polyethylene glycol spacer group between a glucuronic acid (glu) headgroup and a cholesterol (chol) tail
glu-0CH₂(CH₂OCH₂ )nCH₂O-chol
is described. The homologs (n=2,3,5) were prepared by reaction of an excess of commercially available tri, tetra and hexaethylene glycols with cholesteryl-p-toluene sulfonate. 3-O-(8-hydroxy-3,6-dioxaoctyl) cholest-5-ene (2), 3-O-(ll-hydroxy-3,6,9-trioxaundecyl)cholest-5-ene (3) and 3-O-(17-hydroxy-3,6,9,12,15-pentaoxaheptadecyl)cholest-5-ene (4) were produced, and yields were dependent on the amount of excess used. The headgroup was prepared by esterification and acetylation of glucuronolactone to produce methyl (1, 2, 3, 4-tetra-O-acetyl-β-D-glucopyran)uronate which was then brominated at the anomeric carbon to produce methyl (2, 3, 4-tri-O-acetyl-α-D-glucopyranosyl bromide)uronate (1). The headgroup was coupled to the cholesteroxy oligoethylene glycols by a Koenig Knorr type reaction using freshly prepared silver carbonate as the catalyst. Methyl[3-O-(3,6-dioxaoctyl)cholest-5-en-3β-y1-2,3,4-tri-O-acetyl-β-D-glucopyranosid] uronate (5), Methyl[3-O-(3,6,9-trioxaundecyl) cholest-5-en-3β-yl-2,3,4-tri-0-acetyl-β-D-glucopyranosid] uronate (6), and Methyl[3-O-(3,6,9,12,15-pentaoxaheptadecyl)cholest-5-en-3β-yl-2, 3, 4-tri-O -acetyl-β-D-glucopyranosid] uronate (7) were produced with yields of up to 30%. The removal of the methyl ester and acetate protecting groups on the headgroup was accomplished using NaOH in a mixture of solvents followed by acidification with HCl to produce 3-O-(3,6-dioxaoctyl)cholest-5-en-3β-yl-β-D-glucopyranosiduronic acid (8) and 3-O-(3,6,9-trioxaundecyl)cholest-5-en-3β-yl-β-D-glucopyranosiduronic acid (9).
Octaethylene glycol and dodecaethylene glycol were prepared using a solid supported synthesis. The solid polymer used was a trityl chloride functionalized polystyrene 1% divinyl benzene. Mono protected tetraethylene glycol was prepared and attached to the polymer. The protecting group was removed, and the hydroxy terminal was converted to a mesylate leaving group by reaction with methane sulfonyl chloride. To elongate the chain, the anion of tetraethylene glycol was prepared using sodium hydride in DMF. The tetraethylene glycol bound resin was added, and reaction continued at 120 °C for 24 hours. Cleavage of the resultant product from the polymer support yielded octaethylene glycol. Repetition of the mesylation and elongation steps followed by cleavage yielded dodecaethylene glycol. The oligoethylene glycols were purified by passage through a Fractogel 40S gel permeation column.
Two different protecting groups for the tetraethylene glycol were tried. Trialkyl silyl groups were first attempted, but were abandoned due to reduced reactivity and monitoring difficulties during the deprotection. An acetate protecting group was finally used and deprotection was monitored with infrared spectroscopy.<br>Science, Faculty of<br>Chemistry, Department of<br>Graduate
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Garofalo, Flavio A. (Flavio Alberto). "Removal of cholesterol by Pseudomonas pictorum." Thesis, McGill University, 1987. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=63857.
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Corvera, Poiré Eugenia. "Permeability of lipid bilayers containing cholesterol." Thesis, McGill University, 1990. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=60030.
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Lipid-cholesterol bilayers are studied by means of a microscopic multi-state lattice model and Monte Carlo computer simulations. The model used is a direct extension of the Pink model for the main transition of pure lipid bilayers. Cholesterol is introduced as a bulky, rigid molecule with no internal degrees of freedom. The model is able to account for the chain melting of lipid molecules, and is expected to be valid at low cholesterol concentrations.<br>A minimal model for the transport of ions across membranes is used to predict the changes in the passive permeability of lipid-cholesterol bilayers for different cholesterol concentrations and different lipid chain lengths. The model assigns different probabilities of transfer to bulk, clusters and interfaces. The main assumption is that, defects due to bad packing at interfacial regions, cause the membrane to be leaky and allow the ions to permeate it. Therefore the model assigns a high probability of transfer to the interfacial regions.<br>A peak in the permeability is observed near the transition temperature, which is in accord with experimental data. The results show an increase in the passive ion permeability for increasing cholesterol concentration for the three systems under consideration. Also, an increase in the membrane permeability is predicted for decreasing chain length for all the cholesterol concentrations studied.
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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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Banerjee, Subhashis. "INHIBITION OF CHOLESTEROL SYNTHESIS BY POLICOSANOL." UKnowledge, 2010. http://uknowledge.uky.edu/gradschool_diss/4.
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Cholesterol is an essential component of the cell, but excessive blood levels are a major risk factor for the development of atherosclerotic plaques that can lead to heart disease and stroke, the foremost cause of premature death in Western societies. Policosanol, a mixture of very long chain alcohols derived from sugarcane, has gained considerable attention among the public as safe and effective means to reduce blood cholesterol levels, a belief based on some early clinical studies. My research investigates one possible mechanism by which policosanol might decrease blood cholesterol levels: the inhibition of cholesterol synthesis in the liver. Previous studies with cultured hepatoma cells have indicated that policosanol suppresses HMG-CoA reductase activity, the regulatory step in cholesterol synthesis, by activation of AMP-kinase, which then inactivates HMG-CoA reductase by phosphorylation. My studies have confirmed this activation of AMP-kinase both in hepatoma cells and in whole animals after intragastric administration of policosanol. The present studies were also undertaken to identify the upstream signaling mechanism by which policosanol activates AMP-kinase. Treatment of rat hepatoma cells with policosanol increased the amount of phosphorylated CaMKK, which can directly activate AMP-kinase, but had only a small effect on LKB1, the principal activator of AMP-kinase. Intragastric administration to mice similarly activated CaMKK, but not LKB1, in the liver. To determine if metabolism of policosanol was necessary for activation of AMP-kinase, siRNA-mediated suppression of fatty aldehyde dehydrogenase, fatty acyl CoA synthase-4, or β-ketothiolase in hepatoma cells prevented the phosphorylation of AMP-kinase and HMG-CoA reductase by policosanol, indicating that metabolism of these very long chain alcohols to fatty acids and subsequent peroxisomal β-oxidation is necessary for the suppression of cholesterol synthesis. As the principal product of fatty acid -oxidation is acetyl-CoA, further studies demonstrated that addition of acetate to cells similarly activated AMP-kinase and inactivated HMG-CoA reductase. This finding argues that the activation of AMP-kinase by policosanol results from the generation of excess acetyl-CoA via peroxisomal metabolism. Finally, although the intestine is a significant source of circulating cholesterol, policosanol was unable to activate AMP-kinase in the small intestine. These findings open new perspectives for the control of cholesterol synthesis by activators of AMP-kinase.
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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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Donckers-Roseveare, Kathryn. "Periodic feedback to reduce cholesterol levels." Thesis, Virginia Tech, 1990. http://hdl.handle.net/10919/41912.
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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.