| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Absence of atherosclerosis evolution in the coronary arterial segment covered by myocardial tissue in cholesterol-fed rabbits Ishikawa, Y., T. Ishii, et al. (1997), Virchows Arch 430(2): 163-71. Abstract: The evolution of atherosclerotic lesions is suppressed in the intima of the human coronary artery, beneath myocardial bridges. To elucidate the mechanism of the protective effect, we investigated morphological changes using the rabbit coronary artery as a model. Rabbit fed a 1%-cholesterol diet were killed at intervals up to 20 weeks. Two short segments of the left coronary arteries running in the epicardial adipose tissue (EpiLAD) and subsequently running in the myocardium (MyoLAD) were compared morphologically. The intima of the EpiLAD had flat endothelial cells with a polygonal shape, and demonstrated raised atherosclerotic lesions with increase in serum cholesterol level. In contrast, the intima of the MyoLAD was free of atherosclerotic lesions throughout the study, and the endothelial cells were spindle-shaped and engorged. While ferritin particles reached only the surroundings of the internal elastic lamina in the MyoLAD, they permeated into the media of the EpiLAD. We suggest that myocardial bridges suppress coronary atherosclerosis by an alteration of endothelial permeability, which may be due to changes in haemodynamic force tending towards a higher shear stress. The data provide an insight into the relationship between haemodynamics and the development of coronary atherosclerosis. |
| Absence of functional peroxisomes does not lead to deficiency of enzymes involved in cholesterol biosynthesis Hogenboom, S., G. J. Romeijn, et al. (2002), J Lipid Res 43(1): 90-8. Abstract: To unravel the conflicting data concerning the dependence of human cholesterol biosynthesis on functional peroxisomes, we determined activities and levels of selected enzymes involved in cholesterol biosynthesis in livers of PEX5 knockout mice, a well-characterized model for human Zellweger syndrome. We found that all enzymes measured, including putative peroxisomal enzymes, are at least as active in the peroxisome-deficient Zellweger mice as in control mice, indicating that mislocalization of enzymes to the cytosol does not lead to decreased activity or degradation. Prompted by these results, we re-examined this aspect in human subjects by specific enzyme activity measurements and immunoblotting with highly specific antisera. Our results show that the previously reported deficiencies of mevalonate kinase and phosphomevalonate kinase activity in livers from human Zellweger patients reflect the bad condition of the livers, rather than mislocalization to the cytosol.Our data provide an explanation for the conflicting findings in the literature and show that great care should be taken in the interpretation of data obtained in postmortem material. |
| Absolute benefit from cholesterol lowering in diabetic patients with coronary heart disease Strandberg, T. E. (1997), Diabetes Care 20(9): 1495-6. |
| Absorption and fluorescence spectra of polyene antibiotics in the presence of cholesterol Castanho, M. A., A. Coutinho, et al. (1992), J Biol Chem 267(1): 204-9. Abstract: The alterations in the absorption and fluorescence spectra observed for the polyene antibiotics filipin and nystatin in the presence of cholesterol are due to an exciton interaction (polyene aggregates) and cannot be attributed to a specific sterol-antibiotic complex. Filipin and nystatin molecules partition into the sterol aggregates, these structures being very efficient to induce exciton interaction; the observed splitting profile indicates that the chromophores are in a stacked arrangement (parallel transition dipoles). For filipin incorporated in lipid bilayers, the sterol is able to induce the same type of aggregate, at variance with nystatin. |
| Absorption and synthesis of cholesterol in patients with type 1 and type2 diabetes mellitus Miettinen, T. A., H. Gylling, et al. (2004), Duodecim 120(6): 721-3. |
| Absorption and tissue distribution of cholesterol in Manduca sexta Jouni, Z. E., J. Zamora, et al. (2002), Arch Insect Biochem Physiol 49(3): 167-75. Abstract: In Manduca sexta larvae, radioactive free cholesterol is absorbed directly from the midgut into mucosal cells where it is stored both in the free form (87% in males and 93% in females) and esterified form (13% in males and 7% in females). Subsequently, cholesterol is transported to fat body via lipophorin in the hemolymph exclusively in the free form. In fat body, the distribution of cholesterol between the free and esterified form varied significantly between genders and developmental stages. Except for the larval stage, males and females were able to store cholesterol in both free and esterified forms in the fat body and in the adult stage cholesterol ester accounted for more than 75% of the stored cholesterol. Placement of radioactive cholesterol at different locations in the gut-foregut, midgut, and hindgut-demonstrated that the midgut is the site where cholesterol is absorbed and released into the hemolymph. Cholesterol-labeled lipophorin injected into larval hemolymph was cleared from the hemolymph with a half-life of 10.2 h. After 17 h, most of the cleared radioactivity was recovered in the fat body (38%). Arch. |
| Absorption of cholesterol oxidation products from ordinary foodstuff in humans Linseisen, J. and G. Wolfram (1998), Ann Nutr Metab 42(4): 221-30. Abstract: BACKGROUND: Information on the absorption of cholesterol oxidation products (COP) from ordinary foodstuff in humans is scarce. METHODS: Five healthy young men were offered a salami- and Parmesan-containing meal naturally rich in COP. Plasma and lipoprotein COP concentrations were measured over the following 9 h. RESULTS: The mean plasma free (nonesterified) COP concentration showed its maximal increase 3 and 5 h after meal consumption. In contrast, the raise in plasma total COP concentration began 6 h after the meal with a maximum at 8 h and was statistically significant for 7alpha- and 7beta-hydroxycholesterol and 7-ketocholesterol. The increase in plasma total cholesterol concentration was comparable to that of total COP. Comparing the COP composition of the chylomicrons and the test meal, cholestanetriol, 7-ketocholesterol, and to a lesser extent cholesterol-alpha-epoxide were underrepresented in the chylomicrons as was the opposite for 7beta-hydroxycholesterol. In very-low-density lipoprotein, a steady increase in the COP:cholesterol ratio was observed from 6 h on. CONCLUSION: COP from ordinary foodstuff were absorbed in the human intestinal tract but differences in the bioavailability of the single COP compounds were found. |
| Absorption of dietary cholesterol oxidation products and incorporation into rat lymph chylomicrons Vine, D. F., K. D. Croft, et al. (1997), Lipids 32(8): 887-93. Abstract: Cholesterol oxidation products (oxysterols) induce macrophage lipid loading and accumulate in early arterial fatty streaks. The origin of lesion oxysterols has not been elucidated. The absorption of oxysterols from the diet and transport to the arterial wall by postprandial lipoprotein remnants may be a significant source. This study aimed to investigate the extent of oxysterol absorption and the effect on chylomicron composition. Cholesterol was heat-treated, causing 30% oxidation; the major oxidation products were 7 beta-hydroxycholesterol, 7-keto-cholesterol, 5 alpha,6 alpha-epoxycholesterol, and 5 beta,6 beta-epoxycholesterol. Conscious lymph-cannulated rats were given a bolus gastric infusion of 50 mg oxidized cholesterol or 50 mg purified cholesterol in a vehicle of triglyceride. In the rats given the oxidized cholesterol, 6% of the oxysterol load was absorbed and incorporated into lymph chylomicrons. Rats given pure cholesterol had no increase in oxysterols above baseline levels. The incorporation of oxysterols into lymph chylomicrons differed over time with 7 beta-hydroxycholesterol, having peak absorption at 3 h, followed by 7-ketocholesterol at 4 h and 5 alpha,6 alpha-epoxy-cholesterol at 5 h. The absorption of oxysterols in animals given the oxidized cholesterol gastric infusate was associated with lymph chylomicron compositional changes at 2-4 h. The oxidized cholesterol-treated group had a twofold increase in the cholesterol (890 +/- 84 micrograms vs. 440 +/- 83 microgram at 3 h) and triglyceride content (19.76 +/- 3.4 micrograms vs. 8.49 +/- 3.8 micrograms at 3 h). This led to a doubling of chylomicron size over this postprandial period, with particles having a mean diameter of 294 nm in the oxidized cholesterol-treated animals, compared to 179 nm in the purified cholesterol group. In conclusion, dietary oxysterols appear to influence postprandial lipoprotein particle size and composition. These changes may have effects on the clearance of chylomicrons from plasma, arterial delivery of oxysterols, and possible deposition in arterial lesions. |
| Absorption of intestinal free cholesterol is lowered by supplementation of Areca catechu L. extract in rats Park, Y. B., S. M. Jeon, et al. (2002), Life Sci 70(16): 1849-59. Abstract: Areca extracts exhibiting a strong inhibitory activity against pancreatic cholesterol esterase (pCEase) in vitro were previously found to lower the absorption of dietary cholesteryl ester. Therefore, to determine whether a combined Areca extract also affects the absorption of intestinal free cholesterol, male rats were fed a diet containing free cholesterol (1%, w/w) either with or without an Areca nut extract supplement (0.5%, w/w). The Areca extract supplement significantly lowered the plasma cholesterol concentration by 25% without any change in the plasma triglyceride concentration, when compared to the control group. The supplement also significantly lowered the small intestinal pCEase activity by 39.1% compared to that of the control group. As regards the hepatic and intestinal ACAT activities, only the intestinal enzyme activity was significantly lowered by the supplement, when compared to the control group. The absorbed cholesterol that appeared in the blood after an oral dose of 1,2(n)-3H free cholesterol was significantly lower in the rats supplemented with the Areca nut extract, compared with the control group. These results suggest that the inhibition of intestinal ACAT and possibly pCEase may facilitate the metabolic efficiency of the Areca nut extract as regards the absorption of intestinal free cholesterol. The structure and chemical properties of the active compound in the water-soluble Areca extract remain to be elucidated. |
| Absorption of oral ethinylestradiol is delayed by its eutectic mixture with cholesterol Diaz-Sanchez, V., O. Antunez, et al. (1991), Contraception 43(1): 45-53. Abstract: A solid dispersion of ethinylestradiol-cholesterol (EE & CHOL; eutectic 1:4 W/W) was prepared by melting and rapid cooling. The fused material was then mixed with lactose as vehicle. Soft gelatin capsules were filled with 50 mg of the final mixture to give 0.050 mg of ethinylestradiol. Six female volunteers received, one capsule of the eutectic combination of EE:CHOL or one 50 micrograms tablet of ethinylestradiol (Dianor, Syntex), in a cross-over study and in fasting state. Venous blood samples were drawn at 0, 10, 20, 30, 40, 50, 60, 90, 120, 240, 360, 480, 720, 1440 minutes after dosing. Immunoreactive EE was measured by radioimmunoassay to assess the serum concentration-time course. All subjects exhibited a significant increase in EE levels after oral administration. Mean peak EE levels, 1350 pg/ml vs 91 pg/ml (p less than 0.001), were achieved 360 minutes and 90 minutes (p less than 0.01), after administration of the eutectic and reference formulation, respectively. Eutectic mixture showed a greater area under the serum concentration-time curve, longer mean residence time of the drug in the body, and four times the value of the elimination half-life of the reference formulation. It is concluded that the combination of ethinylestradiol with cholesterol forming an eutectic mixture, when administered orally to normal women, modulates the absorption and the bioavailability of the EE. This approach may be suitable for long-acting oral treatment with sex steroids. |
| Absorption, metabolism, and serum concentrations of cholesterol in vegetarians: effects of cholesterol feeding Vuoristo, M. and T. A. Miettinen (1994), Am J Clin Nutr 59(6): 1325-31. Abstract: Serum concentrations and metabolism of cholesterol were studied in vegetarians basally and during a dietary cholesterol load. Cholesterol absorption efficiency was normal and synthesis was slightly enhanced, even though serum cholesterol precursors were not increased. The serum concentrations of total and low-density-lipoprotein cholesterol were decreased proportionally to the reduced intake and absolute absorption of cholesterol. Fecal plant sterols were negatively correlated with the absorption efficiency of cholesterol and positively with fecal sterols and cholesterol synthesis, suggesting interference of high plant sterol intakes with cholesterol absorption. Cholesterol saturation and bile acid composition of the bile were not changed. The increased serum plant sterol-cholesterol ratios were positively related to the intake and negatively to the biliary secretion of plant sterols. Cholesterol feeding increased absolute cholesterol absorption and serum concentrations of total and low-density-lipoprotein cholesterol, did not change absorption efficiency or synthesis of cholesterol, but increased fecal cholestanol excretion. |
| Abstention from filtered coffee reduces the concentrations of plasma homocysteine and serum cholesterol--a randomized controlled trial Christensen, B., A. Mosdol, et al. (2001), Am J Clin Nutr 74(3): 302-7. Abstract: BACKGROUND: Elevated concentrations of plasma total homocysteine (tHcy) and serum total cholesterol are risk factors for ischemic heart disease (IHD). Previous studies showed that the consumption of very high doses of unfiltered coffee increases tHcy and total cholesterol. OBJECTIVE: A prospective intervention study was performed to assess the effects of coffee consumption on the concentrations of tHcy and total cholesterol by using doses and brewing methods common in southeastern Norway. DESIGN: The study was an unblinded, controlled trial with 191 healthy, nonsmoking, coffee-drinking volunteers aged 24-69 y randomly assigned to 3 groups who were asked to consume for 6 consecutive weeks no coffee, 1-3 cups (approximately 175-525 mL)/d, or > or =4 cups (approximately 700 mL)/d prepared in the manner to which they were accustomed. Blood samples were drawn when the subjects were randomly assigned and at 3 and 6 wk of the trial. Dietary data were collected by questionnaire. RESULTS: Ninety-seven percent of the participants reported being regular consumers of caffeinated filtered coffee. Abstention from coffee for 6 wk was associated with a decrease in the tHcy concentration of 1.08 micromol/L and a decrease in the total cholesterol concentration of 0.28 mmol/L in participants who had been drinking on average 4 cups of filtered coffee daily for the past year. Adjustments for several possible confounders did not alter the results. CONCLUSION: Abstention from filtered coffee in doses that are commonly consumed was associated with lower concentrations of tHcy and total cholesterol. |
| Acamprosate involvement in triacylglycerol hydrolysis and transacylation with cholesterol in chronically ethanol-drinking rats Piorunska-Mikolajczak, A., M. Piorunska-Stolzmann, et al. (2004), J Basic Clin Physiol Pharmacol 15(3-4): 153-73. Abstract: Acamprosate (AC) is used as a drug for treating alcoholism. We evaluated the effect of AC on serum triacylglycerol hydrolysis (GEH, glycerol ester hydrolysis), triacylglycerol transacylation with cholesterol (GECAT, glycerol ester:cholesterol acyltransferase), and acylcholesterol hydrolysis (Cease, cholesterol ester hydrolysis) in an experimental model of alcoholism. Ethanol-preferring (PRF), non-preferring (NPF), and control (CR) male Wistar rats were treated with AC (500 mg/kg, p.o.) for 21 consecutive days. The beneficial effect of AC on lipid parameters of PRF rats included decreased triacylglycerol, total cholesterol, and LDL-cholesterol, and increased HDL-cholesterol levels. Acamprosate-compensated changes associated with ethanol consumption were observed. Acamprosate treatment decreased GECAT and increased Cease control rats, but increased GECAT and decreased CEase in PRF animals. In all groups of rats, AC treatment did not influence GEH. In conclusion, our results suggest that AC can influence triacylglycerol metabolism by its action on the balance between hydrolysis and transacylation in rats. |
| ACAT inhibition decreases LDL cholesterol in rabbits fed a cholesterol-free diet. Marked changes in LDL cholesterol without changes in LDL receptor mRNA abundance Krause, B. R., M. E. Pape, et al. (1994), Arterioscler Thromb 14(4): 598-604. Abstract: Rabbits fed low-fat, cholesterol-free diets containing casein as the sole protein source develop endogenous hypercholesterolemia (EH). To test the hypothesis that lipoprotein cholesteryl esters in EH rabbits are acyl coenzyme A:cholesterol acyltransferase (ACAT) derived, we treated EH rabbits with CI-976, a potent and selective ACAT inhibitor. In addition, since cholesterol and bile acid synthesis as well as low-density lipoprotein (LDL) receptor activity are reduced in EH rabbits, we determined whether changes in gene expression for 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, 7 alpha-hydroxylase, and the LDL receptor might be associated with the efficacy due to ACAT inhibition. Compared with EH controls, CI-976-treated rabbits (50 mg/kg per day for 5 weeks) had decreased plasma total cholesterol (-43%), very-low-density lipoprotein (VLDL) cholesterol (-62%), LDL cholesterol (-43%), plasma apolipoprotein B (-23%), liver cholesteryl esters (-39%), LDL size, VLDL and LDL cholesteryl ester content (percent of total lipids), cholesteryl oleate/cholesteryl linoleate ratios in VLDL and LDL (25% to 30%), and ex vivo liver ACAT activity. The triglyceride/cholesteryl ester ratio increased twofold to fourfold in these apolipoprotein B-containing lipoproteins. Endogenous cholesterol absorption appeared to be unaffected by drug treatment. CI-976 failed to alter specific hepatic mRNAs involved in cholesterol metabolism, but comparisons among dietary control groups revealed a marked reduction in 7 alpha-hydroxylase mRNA, no change in LDL receptor mRNA, and an increase in HMG-CoA reductase mRNA in EH rabbits compared with normal chow-fed controls.(ABSTRACT TRUNCATED AT 250 WORDS) |
| ACAT inhibitors CL 283,546 and CL 283,796 reduce LDL cholesterol without affecting cholesterol absorption in African green monkeys Wrenn, S. M., Jr., J. S. Parks, et al. (1995), J Lipid Res 36(6): 1199-210. Abstract: Previous studies with a number of selective acylcoenzyme A:cholesterol acyltransferase (ACAT) inhibitors in several animal models have demonstrated significant reductions in plasma cholesterol and, in some studies, triglyceride levels. This study was conducted to examine the effects of two ACAT inhibitors, CL 283,546 and CL 283,796, in cholesterol-high fat diet fed African green monkeys, a relevant primate model of hyperlipidemia and coronary artery atherosclerosis. Treatment with CL 283,546 or CL 283,796 resulted in significant reductions (ca. 25-30%) in total plasma cholesterol at both 10 and 30 mg/kg per day doses. This reduction in plasma cholesterol was due almost entirely to reduction in low density lipoprotein (LDL) cholesterol (ca. 45%) without significantly affecting high density lipoprotein (HDL) cholesterol, very low density lipoprotein + intermediate density lipoprotein (VLDL + IDL) cholesterol, or triglyceride concentrations. There were no significant effects on plasma concentrations of apolipoproteins A-I, E, or B and, thus, the reduction seen in LDL cholesterol appears to be due to a diminished cholesterol content of LDL particles. Our studies revealed that treatment with these compounds did not reduce cholesterol absorption, which was somewhat surprising as ACAT inhibitors are generally thought to exert their hypolipidemic effects, at least in part, by inhibition of intestinal cholesterol absorption. Our data are consistent with a principal activity of these drugs on the liver to reduce cholesteryl ester secretion in VLDL, leading to a diminished LDL-cholesterol content, and, presumably, enhanced biliary cholesterol-bile acid excretion. |
| ACAT/CEH and ACEH/LAL: two key enzymes in hepatic cellular cholesterol homeostasis and their involvement in genetic disorders Schmitz, G., A. Becker, et al. (1996), Z Gastroenterol 34 Suppl 3: 68-72. |
| ACAT1 deficiency disrupts cholesterol efflux and alters cellular morphology in macrophages Dove, D. E., Y. R. Su, et al. (2005), Arterioscler Thromb Vasc Biol 25(1): 128-34. Abstract: OBJECTIVE: Acyl-coenzyme A: cholesterol acyltransferase (ACAT) converts intracellular free cholesterol (FC) into cholesteryl esters (CE) for storage in lipid droplets. Recent studies in our laboratory have shown that the deletion of the macrophage ACAT1 gene results in apoptosis and increased atherosclerotic lesion area in the aortas of hyperlipidemic mice. The objective of the current study was to elucidate the mechanism of the increased atherosclerosis. METHODS AND RESULTS: CE storage and FC efflux were studied in ACAT1(-/-) peritoneal macrophages that were treated with acetylated low-density lipoprotein (acLDL). Our results show that efflux of cellular cholesterol was reduced by 25% in ACAT1-deficient cells compared with wild-type controls. This decrease occurred despite the upregulated expression of ABCA1, an important mediator of cholesterol efflux. In contrast, ACAT1 deficiency increased efflux of the cholesterol derived from acLDL by 32%. ACAT1-deficient macrophages also showed a 26% increase in the accumulation of FC derived from acLDL, which was associated with a 75% increase in the number of intracellular vesicles. CONCLUSIONS: Together, these data show that macrophage ACAT1 influences the efflux of both cellular and lipoprotein-derived cholesterol and propose a pathway for the pro-atherogenic transformation of ACAT1(-/-) macrophages. |
| ACAT2 deficiency limits cholesterol absorption in the cholesterol-fed mouse: impact on hepatic cholesterol homeostasis Repa, J. J., K. K. Buhman, et al. (2004), Hepatology 40(5): 1088-97. Abstract: Acyl CoA:cholesterol acyltransferase (ACAT) 2 is the major cholesterol-esterifying enzyme in mouse enterocytes and hepatocytes. Male ACAT2(+/+) and ACAT2(-/ -) mice were fed chow containing added cholesterol (0%-0.500% w/w) for 24 days. Over this range, fractional cholesterol absorption in the ACAT2(+/+) mice fell from 41.4% +/- 6.6% to 21.0% +/- 5.2%, and in their ACAT2(-/-) counterparts it fell from 35.1% +/- 4.5% to 7.9% +/- 0.8%. The mass of dietary cholesterol absorbed (mg/d per 100 g body weight) increased from 1.2 +/- 0.2 to 14.7 +/- 4.4 in the ACAT2(+/+) mice and from 1.0 +/- 0.2 to 5.5 +/- 0.6 in those without ACAT2. In the ACAT2(+/+) mice, hepatic cholesterol concentrations increased as a function of intake despite compensatory changes in cholesterol and bile acid synthesis and in the expression of adenosine triphosphate-binding cassette transporter G5 (ABCG5) and ABC transporter G8 (ABCG8). In contrast, in ACAT2(-/-) mice in which the amount of cholesterol absorbed at the highest intake was only 37% of that in the ACAT2(+/+) mice, suppression of synthesis was a sufficient adaptive response; there was no change in bile acid synthesis, ABCG5/G8 expression, or hepatic cholesterol concentration. The expression of adenosine triphosphate-binding cassette transporter A1 (ABCA1) in the jejunum was markedly elevated in the ACAT2(-/-) mice, irrespective of dietary cholesterol level. In conclusion, although ACAT2 deficiency limits cholesterol absorption, the extent to which it impacts hepatic cholesterol homeostasis depends on cholesterol intake. Loss of ACAT2 activity may result in unesterified cholesterol being absorbed via an ABCA1-mediated basolateral efflux pathway. |
| ACAT2 is localized to hepatocytes and is the major cholesterol-esterifying enzyme in human liver Parini, P., M. Davis, et al. (2004), Circulation 110(14): 2017-23. Abstract: BACKGROUND: Two acyl-coenzyme A:cholesterol acyltransferase (ACAT) genes, ACAT1 and ACAT2, have been identified that encode 2 proteins responsible for intracellular cholesterol esterification. METHODS AND RESULTS: In this study, immunohistology was used to establish their cellular localization in human liver biopsies. ACAT2 protein expression was confined to hepatocytes, whereas ACAT1 protein was found in Kupffer cells only. Studies with a highly specific ACAT2 inhibitor, pyripyropene A, in microsomal activity assays demonstrated that ACAT2 activity was highly variable among individual human liver samples, whereas ACAT1 activity was more similar in all specimens. ACAT2 provided the major cholesterol-esterifying activity in 3 of 4 human liver samples examined. CONCLUSIONS: The data suggest that in diseases in which dysregulation of cholesterol metabolism occurs, such as hypercholesterolemia and atherosclerosis, ACAT2 should be considered a target for prevention and treatment. |
| Acaterin, a novel inhibitor of acyl-CoA: cholesterol acyltransferase produced by Pseudomonas sp. A92 Naganuma, S., K. Sakai, et al. (1992), J Antibiot (Tokyo) 45(8): 1216-21. Abstract: Acaterin, a novel inhibitor of acyl-CoA: cholesterol acyltransferase (ACAT), was isolated from a culture broth of Pseudomonas sp. A92 by Diaion HP-20 column chromatography, solvent extraction and reverse phase HPLC. Spectroscopic analyses of the compound yielded 3-(1-hydroxyoctyl)-5-methyl-2(5H)-furanone as the proposed structure. In the presence of oxidized low density lipoprotein, acaterin inhibited the synthesis of cholesteryl ester in macrophage J774 by 50% at a concentration of 45 microM. Acaterin also inhibited ACAT activity in the rat liver microsomes by 50% at a concentration of 120 microM. Kinetic studies suggested that inhibition of ACAT by acaterin was noncompetitive with respect to oleoyl-CoA. |