| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Testing the accuracy of total cholesterol assays in an external quality-control program. Effect of adding sucrose to lyophilized control sera compared with use of fresh or frozen sera Baadenhuijsen, H., P. N. Demacker, et al. (1995), Clin Chem 41(5): 724-30. Abstract: We studied the suitability of various types of human serum preparations to test the accuracy of total cholesterol measurements in the External Quality Assessment scheme in The Netherlands, in which approximately 180 laboratories participate. Checked against the certified Abell/Kendall Reference Method, large reagent-dependent negative biases were observed with lyophilized serum that was insufficiently cryoprotected. The biases for the reagents of Du Pont, Roche, and Beckman averaged -16.7%, -9.2%, and -7.6% respectively; the least bias, -0.4%, was obtained with reagent from Boehringer Mannheim. The beneficial effect of cryoprotection with sucrose was demonstrated by the decrease in interreagent variation from 5.4% to 1.9%, the latter value being comparable with the values for fresh and once-frozen pooled serum (1.3% and 1.7%, respectively). We conclude that the detrimental effect of lyophilization on serum matrix can be minimized by suitable cryoprotection with 200 g/L sucrose. |
| Testing the role of apoA-I, HDL, and cholesterol efflux in the atheroprotective action of low-level apoE expression Thorngate, F. E., P. G. Yancey, et al. (2003), J Lipid Res 44(12): 2331-8. Abstract: Low levels of transgenic mouse apolipoprotein E (apoE) suppress atherosclerosis in apoE knockout (apoE-/-) mice without normalizing plasma cholesterol. To test whether this is due to facilitation of cholesterol efflux from the vessel wall, we produced apoA-I-/-/apoE-/- mice with or without the transgene. Even without apoA-I and HDL, apoA-I-/-/apoE-/- mice had the same amount of aorta cholesteryl ester as apoE-/- mice. Low apoE in the apoA-I-/-/apoE-/- transgenic mice reduced aortic lesions by 70% versus their apoA-I-/-/apoE-/- siblings. To define the free cholesterol (FC) efflux capacity of lipoproteins from the various genotypes, sera were assayed on macrophages expressing ATP-binding cassette transporter A1 (ABCA1). Surprisingly, ABCA1 FC efflux was twice as high to sera from the apoA-I-/-/apoE-/- or apoE-/- mice compared with wild-type mice, and this activity correlated with serum apoA-IV. Immunodepletion of apoA-IV from apoA-I-/-/apoE-/- serum abolished ABCA1 FC efflux, indicating that apoAI-V serves as a potent acceptor for FC efflux via ABCA1. With increasing apoE expression, apoA-IV and FC acceptor capacity decreased, indicating a reciprocal relationship between plasma apoE and apoA-IV. Low plasma apoE (1-3 x 10(-8) M) suppresses atherosclerosis by as yet undefined mechanisms, not dependent on the presence of apoA-I or HDL or an increased capacity of serum acceptors for FC efflux. |
| Testosterone enanthate at a dose of 200 mg/week decreases HDL-cholesterol levels in healthy men Meriggiola, M. C., S. Marcovina, et al. (1995), Int J Androl 18(5): 237-42. Abstract: The concept that androgen alone can provide an effective male contraceptive has been tested in a multicentre, multiphase trial by the World Health Organization. Results from this trial showed that an ester of testosterone, testosterone enanthate (TE), administered at a dose of 200 mg/week, has a very high contraceptive efficacy, and suggested that, at least in some populations, androgen alone might provide a viable option for the control of male fertility. It has been claimed that testosterone represents one of the gender-related risk factors for coronary artery disease (CAD) in men. Epidemiological and interventional studies have failed to establish a convincing relationship between testosterone and high density lipoprotein cholesterol (HDL-C). Therefore, there is concern about possible negative effects on lipoprotein asset of an androgen-alone male contraceptive. In this study we analysed the effects of long-term (12 months) administration of TE (200 mg/week) in normal healthy men. Blood samples (six men > 10 h fast = Group 1; 30 men > 4 h fast = Group 2) were drawn from 36 men, monthly before the beginning of the injections (control), every 3 months throughout the study period (treatment), and 1 month after stopping TE injections (recovery). Total cholesterol (chol), triglycerides, HDL-C and LDL-C levels were measured in these samples. Biochemical parameters were also monitored. TE administration induced a significant decrease (15-20%) in HDL-C levels that was of comparable magnitude in men from both groups (fasting and non-fasting) and occurred regardless of basal HDL-C levels. No statistically significant effect on other lipoproteins was detected. Considering all men together, HDL-C levels were decreased in 78% of the men by month 3, 83% by month 6, 94% by month 9 and 97% by month 12 of treatment. In all men the HDL-C decrease was reversible within 1 month of stopping TE administration. It is concluded that: (1) injection of 200 mg TE/week causes a 15-20% decrease in HDL-C in normal men with no effect on other lipoproteins, (2) the suppressive effect of TE is maintained throughout the 1-year-injection period, and a direct relationship between the duration of TE administration and the proportion of men showing decreased HDL-C levels, was observed. (3) The HDL-C decrease was reversible within 1 month of stopping TE administration. These data will be important in designing further studies on male contraception, and in interpreting the relationship between testosterone levels, HDL-C levels and potential cardiovascular risk. |
| Testosterone up-regulates scavenger receptor BI and stimulates cholesterol efflux from macrophages Langer, C., B. Gansz, et al. (2002), Biochem Biophys Res Commun 296(5): 1051-7. Abstract: By lowering high density lipoprotein (HDL) cholesterol, testosterone contributes to the gender difference in HDL cholesterol and has been accused to be pro-atherogenic. The mechanism by which testosterone influences HDL cholesterol is little understood. We therefore investigated the effect of testosterone on the gene expression of apolipoprotein A-I (apoA-I), hepatic lipase (HL), scavenger receptor B1 (SR-BI), and the ATP binding cassette transporter A1 (ABCA1), all of which are important regulators of HDL metabolism. In both cultivated HepG2 hepatocytes and primary human monocyte-derived macrophages, testosterone led to a dose-dependent up-regulation of SR-BI, which was assessed on both the mRNA and the protein levels. As a functional consequence, we observed an increased HDL(3)-induced cholesterol efflux from macrophages. At supraphysiological dosages, testosterone also increased the expression of HL in HepG2 cells. Testosterone had no effect on the expression of apoA-I in HepG2 cells and ABCA1 in either HepG2 cells or macrophages. These data suggest that testosterone, despite lowering HDL cholesterol, intensifies reverse cholesterol transport and thereby exerts an anti-atherogenic rather than a pro-atherogenic effect. |
| Tetradecylthioacetic acid incorporated into very low density lipoprotein: changes in the fatty acid composition and reduced plasma lipids in cholesterol-fed hamsters Froyland, L., D. K. Asiedu, et al. (1995), J Lipid Res 36(12): 2529-40. Abstract: The mechanism behind the hypolipidemic effect of tetradecylthioacetic acid (CMTTD, a non-beta-oxidizable 3-thia fatty acid) was studied in hamsters fed a high cholesterol diet (2%), which resulted in hyperlipidemia. Treating hyperlipidemic hamsters with CMTTD resulted in a progressive hypocholesterolemic and hypotriacylglycerolemic effect. Decreased plasma cholesterol was followed by a 39% and 30% reduction in VLDL-cholesterol and LDL-cholesterol, respectively. In contrast, the HDL-cholesterol content was not affected, thus decreasing the VLDL-cholesterol/HDL-cholesterol and LDL-cholesterol/HDL-cholesterol ratios. 3-Hydroxy-3-methylglutaryl- (HMG) CoA reductase activity and its mRNA level were unchanged after CMTTD administration. Also, the LDL receptor and LDL receptor-related protein (LRP-4) mRNAs were unchanged. The decrease in plasma triacylglycerol was accompanied by a 45% and 56% reduction in VLDL-triacylglycerol and LDL-triacylglycerol, respectively. The hypolipidemic effect of CMTTD was followed by a 1.4-fold increase in mitochondrial fatty acid oxidation and a 2.3-fold increase in peroxisomal fatty acid oxidation. CMTTD treatment led to an accumulation of dihomo-gamma-linolenic acid (20:3n-6) in liver, plasma, very low density lipoprotein, and heart. Noteworthy, CMTTD accumulated more in the heart, plasma, and VLDL particles compared to the liver, and in the VLDL particle alpha-linolenic acid (18:3n-3) decreased whereas eicosatetraenoic acid (20:4n-3) increased. In addition, linoleic acid (18:2n-6) and the total amount of polyunsaturated fatty acids decreased, the latter mainly due to a decrease in n-6 fatty acids. The present data show that CMTTD was detected in plasma and incorporated into VLDL, liver, and heart. The relative incorporation (mol%) of CMTTD was heart > VLDL > liver. In conclusion, CMTTD causes both a hypocholesterolemic and hypotriacylglycerolemic effect in hyperlipidemic hamsters. |
| Tetrahydrobiopterin attenuates cholesterol induced coronary hyperreactivity to endothelin Verma, S., A. S. Dumont, et al. (2001), Heart 86(6): 706-8. |
| Tetraspanin CD82 controls the association of cholesterol-dependent microdomains with the actin cytoskeleton in T lymphocytes: relevance to co-stimulation Delaguillaumie, A., J. Harriague, et al. (2004), J Cell Sci 117(Pt 22): 5269-82. Abstract: T-cell activation is initiated by the concerted engagement of the T-cell receptor and different co-stimulatory molecules, and requires cytoskeleton-dependent membrane dynamics. Here, we have studied the relationships between tetraspanins, cytoskeleton and raft microdomains, and their relevance in T-cell signaling. Localization studies and density-gradient flotation experiments indicate that part of tetraspanins localizes in raft microdomains linked to the actin cytoskeleton. First, partial coalescence of lipid raft is triggered by tetraspanin cross-linking and results in large caps in which F-actin also concentrates. Second, the amount of tetraspanins, which are recovered in the cholesterol-dependent insoluble fractions of low and intermediate density, and which appears to be membrane vesicles by electron microscopy, is under cytoskeletal influence. Disruption of actin filaments enhances the amount of tetraspanins recovered in typical raft fractions, whereas F-actin-stabilizing agents induce the opposite effect. Our data also reveal that CD82 constitutes a link between raft domains and the actin cytoskeleton, which is functionally relevant. First, tetraspanin signaling induces a selective translocation of CD82 from detergent-resistant membrane fractions to the cytoskeleton-associated pellet. Second, all functional effects linked to CD82 engagement, such as adhesion to culture plates, formation of actin bundles and early events of tyrosine phosphorylation, are abolished, or strongly reduced, by cholesterol depletion. We also show that dynamic relocalization of CD82 and F-actin at the periphery of the immune synapse is induced upon contact of T cells with antigen-presenting cells. This suggests that the tetraspanin web might participate in the membrane dynamics required for proper T-cell signaling. More generally, the interaction of tetraspanins with raft domains and with the actin cytoskeleton might relate with their role in many cellular functions as membrane organizers. |
| TGF-beta increases cholesterol efflux and ABC-1 expression in macrophage-derived foam cells: opposing the effects of IFN-gamma Panousis, C. G., G. Evans, et al. (2001), J Lipid Res 42(5): 856-63. Abstract: The regulation of ATP-binding cassette transporter 1 (ABC-1) expression by cytokines present within the microenvironment of the atheroma may play an important role in determining the impact of reverse cholesterol transport on the atherosclerotic lesion. We recently reported that the macrophage-activating cytokine interferon (IFN)-gamma inhibited both cholesterol efflux and ABC-1 expression. In the present study, we investigated the effects of transforming growth factor (TGF)-beta, a cytokine also apparent within the atheroma, on cholesterol efflux, ABC-1 expression, and its ability to antagonize the inhibitory effects of IFN-gamma. TGF-beta significantly increased cholesterol efflux in macrophage-derived foam cells from apolipoprotein E (apoE) knockout mice, with maximal effects apparent at 300 pg/ml. The increases in efflux occurred without any effect on the passive diffusion component of efflux mediated by beta-cyclodextrin. Furthermore, the increase in cholesterol efflux occurred without any changes in free or esterified cholesterol pools and was consistent with an increase in both ABC-1 message and protein. Finally, TGF-beta was also demonstrated to inhibit the IFN-gamma-mediated down-regulation of ABC-1. These results further demonstrate the importance of cytokine cross-talk to impact the process of reverse cholesterol transport through a multitude of processes including the regulation of ABC-1. |
| The 1.45 A resolution structure of the cryptogein-cholesterol complex: a close-up view of a sterol carrier protein (SCP) active site Lascombe, M. B., M. Ponchet, et al. (2002), Acta Crystallogr D Biol Crystallogr 58(Pt 9): 1442-7. Abstract: Cryptogein is a small 10 kDa elicitor produced by the phytoparasitic oomycete Phytophthora cryptogea. The protein also displays a sterol carrier activity. The native protein crystallizes in space group P4(1)22, with unit-cell parameters a = b = 46.51, c = 134.9 A (diffraction limit: 2.1 A). Its complex with cholesterol crystallizes in space group C222(1), with unit-cell parameters a = 30.96, b = 94.8, c = 65.3 A and a resolution enhanced to 1.45 A. The large inner non-specific hydrophobic cavity is able to accommodate a large variety of 3-beta-hydroxy sterols. Cryptogein probably acts as a sterol shuttle helping the pathogen to grow and complete its life cycle. |
| The A-204C polymorphism in the cholesterol 7alpha-hydroxylase (CYP7A1) gene determines the cholesterolemia responsiveness to a high-fat diet Kovar, J., P. Suchanek, et al. (2004), Physiol Res 53(5): 565-8. Abstract: The aim of the study was to ascertain whether the A-204C polymorphism in the cholesterol 7 -hydroxylase (CYP7A1) gene plays any role in determining LDL-cholesterol (LDL-C) concentration responsiveness to a high-fat diet. The concentrations of total cholesterol and LDL-cholesterol were measured in eleven healthy men (age: 30.9+/-3.2 years; BMI: 24.9+/-2.7 kg/m(2)) who were homozygous for either the -204A or -204C allele, after 3 weeks on a low-fat (LF) diet and 3 weeks on a high-fat (HF) diet. During both dietary regimens, the isocaloric amount of food was provided to volunteers; LF diet contained 22 % of energy as a fat and 2.2 mg of cholesterol/kg of body weight a day, HF diet 40 % of fat and 9.7 mg of cholesterol/kg of body weight a day. In six subjects homozygous for the -204C allele, the concentrations of cholesterol and LDL-cholesterol were significantly higher on HF than on LF diet (cholesterol: 4.62 vs. 4.00 mmol/l, p<0.05; LDL-C: 2.15 vs. 1.63 mmol/l, p<0.01, respectively); no significant change was observed in five subjects homozygous for the -204A allele. There were no other differences in lipid and lipoprotein-lipid concentrations. Therefore, the polymorphism in the cholesterol 7alpha-hydroxylase promotor region seems to be involved in the determination of cholesterol and LDL-C responsiveness to a dietary fat challenge. |
| The ABCs of cholesterol efflux Young, S. G. and C. J. Fielding (1999), Nat Genet 22(4): 316-8. |
| The ACAT inhibitor HL-004 inhibits cholesterol absorption and lowers serum cholesterol in rats Asami, Y., Y. Kondo, et al. (1998), Gen Pharmacol 31(4): 593-6. Abstract: 1. HL-004 decreased absorption of cholesteryl ester from the intestine into the lymph in a rat lymph-fistula model. 2. HL-004 reduced serum cholesterol level in acute cholesterol-fed rats. 3. HL-004 simultaneously decreased hepatic cholesteryl ester content and increased free cholesterol in cholesterol-fed rats. 4. These findings suggest that: (1) the hypocholesterolemic effect of HL-004 is principally due to inhibition of cholesterol absorption via inhibition of ACAT in the intestine; and (2) changes in hepatic cholesterol metabolism due to direct inhibition by HL-004 of hepatic ACAT may account in part for reduction of serum cholesterol level by HL-004. |
| The ACAT2 gene encodes a gatekeeper of intestinal cholesterol absorption that regulates cholesterolemia and gallstone disease Zanlungo, S. and F. Nervi (2001), Hepatology 33(3): 760-1. |
| The acceleration of gallstone destruction with synchronous biliary lithotripsy and contact dissolution in vitro using three cholesterol-solubilizing solvent Kannegieter, L. S., J. C. Brandon, et al. (1992), Invest Radiol 27(2): 140-4. Abstract: In the first-known application of its kind, shockwave lithotripsy and contact-solvent dissolution of large, calcified gallstone burdens were performed simultaneously with three chemical solvents, each tested separately in an in vitro model, with the combined effects on gallstone eradication examined. Two solvents, ethyl propionate and isopropyl acetate, were chosen for their solubilizing ability and potentially high level of patient safety. The third solvent, a 70%:30% mixture of methyl tert-butyl ether (MTBE) and dimethyl sulfoxide (DMSO), was chosen for its known ability to accelerate the dissolution of calcium-containing gallstones. All stones were matched for size, weight, and number. Gallstone lithotripsy performed in ethyl propionate was significantly more effective (P less than.02) in the production of fragments less than 2 mm when compared with bile; lithotripsy with isopropyl acetate and the MTBE/DMSO mixture showed no statistically significant effect. Biliary lithotripsy performed in an ethyl propionate medium may enhance gallstone dissolution and the production of small fragments (diameter less than 2 mm). |
| The accuracy of portable cholesterol analyzers in public screening programs Naughton, M. J., R. V. Luepker, et al. (1990), Jama 263(9): 1213-7. Abstract: To determine the accuracy of portable cholesterol analyzers in public settings, four screening organizations were accompanied to cholesterol screenings where consenting participants completed the finger-stick procedure and provided a blood sample by venipuncture. The finger-stick values were compared later with the participants' blood cholesterol values obtained in a reference laboratory. The results indicated that only one of the organizations produced cholesterol measurements entirely within the acceptable range (+/- 14.2%), while the accuracy of the other three organizations ranged from 76.5% to 96.4%. Those finger-stick values that did not fall within the acceptable range tended to underestimate the laboratory cholesterol values. Additionally, classification of the persons screened based on the National Cholesterol Education Program risk categories indicated that the finger-stick values primarily tended to produce false-negative results. The variability of the results across organizations was caused partially by insufficient operator training. However, inadequate quality-control procedures for field settings and dilution of capillary blood by tissue fluid also may have contributed to the inaccurate finger-stick results. |
| The Accutrend glucose-cholesterol meter in family practice compared to laboratory determinations Tersmette, K. W., G. J. Dinant, et al. (1995), Ned Tijdschr Geneeskd 139(32): 1638-42. Abstract: OBJECTIVE. To determine the similarity in clinical consequences that follow, according to the guidelines of the Dutch General Practice Standards, from measured glucose and cholesterol concentrations with the Accutrend glucose cholesterol meter in general practice on one hand and the usual measurements in a laboratory on the other. DESIGN. Comparative study. SETTING. Two general practices in the district 'Zuid-Limburg' in the Netherlands. METHOD. 66 patients with non-insulin-dependent diabetes mellitus and 34 control patients had their capillary blood glucose and cholesterol concentrations measured with the Accutrend glucose cholesterol meter. The same measurements were done with simultaneously taken venous blood samples, according to usual laboratory methods, in a laboratory. The clinical consequences of the measurements in the general practice and the laboratory, according to the Standards, were compared and if they contained different recommendations they were regarded as clinically relevant. RESULTS. In 5% of the cases a clinically relevant difference between the glucose measurements done in the general practice and the laboratory was found. For the cholesterol measurements a clinically relevant difference was found in 18%. Besides, 16% of the cholesterol measurements in the general practice were outside the range of the meter. CONCLUSION. The Accutrend glucose cholesterol meter is a qualitatively good instrument for blood glucose measurements in general practice. For blood cholesterol measurements, the quality as well as the range of the meter are still insufficient. |
| The ACE inhibitor alacepril suppresses atherogenesis independent of serum lipids in cholesterol-fed rabbits--critical analysis with new ultrasound technique Itoh, K., S. Yoshida, et al. (1994), Jpn Circ J 58(11): 844-54. Abstract: The effects of alacepril, an angiotensin converting enzyme inhibitor, on atherogenesis were examined in rabbits fed a hypercholesterol diet. The process of atherogenesis was evaluated in vitro by high-resolution transesophageal ultrasonography (TEE phi 4 mm, 7.5 MHz), by direct histological examination and by serum lipid examination. Of the 38 subjects, 18 were designated as the control hypercholesterol group (CH) and 20 received oral alacepril at 90 mg/day (ACE) for 13-22 weeks. Three rabbits in each group died due to pneumonia. TEE enabled a clear diagnosis as either normal, early stage or late stage of atherosclerosis. The intimal-medial thickness was significantly less in the ACE group than in the CH group, but only over the middle portion of the aorta. The ACE group had a smaller area of atheromatous plaque than the CH group (atheromatous index: 37 +/- 20* and 60 +/- 30% respectively, *p < 0.02). Serum cholesterol and triglycerides were similar in the CH group (1590 +/- 653, 258 +/- 224) and the ACE group (1574 +/- 824, 303 +/- 360 respectively). In conclusion, alacepril reduced both the area of atheromatous atheroma plaque and wall hypertrophy independent of serum lipids in cholesterol-fed rabbits. In vitro miniature TEE is a dependable method for evaluating atherosclerosis in rabbits with hypercholesterolemia. |
| The actin cytoskeleton is important for the stimulation of cholesterol esterification by atherogenic lipoproteins in macrophages Tabas, I., X. Zha, et al. (1994), J Biol Chem 269(36): 22547-56. Abstract: Stimulation of intracellular cholesterol esterification, which is catalyzed by the enzyme acyl-coenzyme A: cholesterol O-acyltransferase (ACAT), by atherogenic lipoproteins in macrophages is a key step in the ability of these cells to store lipoprotein-cholesterol and in the eventual development of atheroma foam cells. Herein, we provide evidence that the actin cytoskeleton plays an important role in the stimulation of cholesterol esterification by atherogenic lipoproteins in macrophages. When the actin cytoskeleton of cultured mouse peritoneal macrophages was disrupted by treatment with cytochalasin D or Clostridial C2 toxin, the ability of beta very low density lipoprotein (beta-VLDL) to stimulate cholesterol esterification was decreased 3-6-fold, even under conditions in which beta-VLDL protein degradation, cholesteryl ester hydrolysis, or net cholesterol delivery to the cells was matched. Esterification of cellular phospholipids and triglycerides was not affected by this treatment. Cytochalasin D treatment of macrophages also inhibited the ability of acetyl-low density lipoprotein, another foam cell-forming lipoprotein, to stimulate cholesterol esterification, but stimulation of cholesterol esterification by 25-hydroxycholesterol was not inhibited by cytochalasin D. Cytochalasin D was found to inhibit neither the exit of beta-VLDL-derived cholesterol from lysosomes nor the ability of beta-VLDL to down-regulate endogenous cholesterol synthesis. From these data we conclude that an intact actin cytoskeleton is necessary for efficient stimulation of cholesterol esterification by atherogenic lipoproteins in macrophages. Although the exact function of actin in the cholesterol esterification pathway remains to be determined, our data rule out a general role for actin in intracellular cholesterol trafficking or maintenance of ACAT enzyme activity. Rather, we speculate that actin filaments play a role in specific cellular entry processes of atherogenic lipoproteins and/or in establishing transport or contact between the plasma membrane cholesterol substrate pool and the ACAT enzyme in macrophages. |
| The activity of HMG-CoA reductase and acetyl-CoA carboxylase in human apocrine sweat glands, sebaceous glands, and hair follicles is regulated by phosphorylation and by exogenous cholesterol Smythe, C. D., M. Greenall, et al. (1998), J Invest Dermatol 111(1): 139-48. Abstract: Human apocrine and sebaceous glands function to secrete lipids, predominantly triglycerides, fatty acids, cholesterol and its esters, and, in the sebaceous gland, squalene. The enzymes that catalyze the important regulatory steps in cholesterol and fatty acid biosyntheses, 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase and acetyl-CoA carboxylase, respectively, were therefore studied in isolated human skin appendages, and their relevant kinetic parameters determined. The enzyme activities that were observed can account for previously described rates of incorporation of radiolabeled substrates into the appropriate lipids by glands in vitro. Reduced enzyme activities following homogenization in the presence of fluoride indicated that both of these enzymes in skin appendages are inactivated by phosphorylation. The activity of the enzyme known to catalyze this phosphorylation, the AMP-activated protein kinase, was also measured. Compactin was shown to inhibit HMG-CoA reductase in homogenates of these appendages. Conversely, incubation of whole sebaceous glands with compactin resulted in the stimulation of enzyme activity, which suggests that these appendages can respond to diminishing cholesterol levels. The effect of exogenous low density lipoprotein and 25-hydroxycholesterol on HMG-CoA reductase activity from skin appendages was investigated. HMG-CoA reductase activity in both apocrine and sebaceous glands was reduced following incubation with either low density lipoprotein or 25-hydroxycholesterol. Low density lipoprotein receptor and lipoprotein lipase mRNA expression was also detected in skin appendages. These results indicate that apocrine and sebaceous glands have the capacity to sequester dietary cholesterol and fatty acids that may have important implications for the understanding of both acne and axillary odor. |
| The activity of lecithin:cholesterol acyltransferase in the serum of cows at parturition or with fatty liver Uchida, E., N. Katoh, et al. (1995), Vet Res Commun 19(5): 343-51. Abstract: The activity of lecithin:cholesterol acyltransferase (LCAT), which is responsible for esterification of plasma cholesterol, was evaluated in bovine serum. It was associated with the high-density lipoprotein fraction that contains apolipoprotein A-I, an activator of LCAT. In lactating cows, the activity was around 1000 U (decrease in nmol of free cholesterol per h per ml of serum), slightly higher than in 1-month-old calves. LCAT activity decreased around parturition, at which the time the serum concentrations of cholesteryl esters and free cholesterol were concomitantly decreased. A reduced LCAT activity was also found in cows with fatty livers induced by the administration of ethionine. In the cows with fatty livers, the serum concentration of cholesteryl esters was markedly decreased, whereas that of free cholesterol was only slightly decreased, thereby increasing the free- to esterified-cholesterol ratio. These results suggest that the decrease in LCAT activity may be involved in the reduction in fertility associated with fatty liver because esterification of cholesterol by LCAT is essential for its transport from the liver to peripheral tissues, such as the corpus luteum, and because cholesterol serves as the source of progesterone synthesis in the latter organ. |