| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Increased LDL cholesterol and atherosclerosis in LDL receptor-deficient mice with attenuated expression of scavenger receptor B1 Huszar, D., M. L. Varban, et al. (2000), Arterioscler Thromb Vasc Biol 20(4): 1068-73. Abstract: Scavenger receptor BI (SR-BI) is a multiligand cell-surface receptor that plays a central role in high density lipoprotein homeostasis in rodents. To investigate a role for SR-BI in atherosclerosis, mice with attenuated SR-BI expression were crossed with low density lipoprotein (LDL) receptor-deficient mice. Compound-homozygous mutants showed increased plasma cholesterol, surprisingly due primarily to increased LDL cholesterol and apolipoprotein B levels. LDL turnover studies showed that this resulted from increased LDL cholesterol production rather than decreased LDL catabolism. Atherosclerotic lesion size was significantly increased in male compound-mutant mice relative to LDL receptor-deficient controls (93 427+/-16 079 versus 34 448+/-5 331 microm(2), respectively; P=0.003). The proatherogenic effect of attenuated SR-BI expression may in part be due to increased LDL cholesterol levels. These findings suggest that upregulation of the receptor could have therapeutic potential for the treatment of atherosclerosis. |
| Increased LDL receptor mRNA expression in colon cancer is correlated with a rise in plasma cholesterol levels after curative surgery Niendorf, A., H. Nagele, et al. (1995), Int J Cancer 61(4): 461-4. Abstract: It is currently under debate whether the low serum cholesterol levels that are frequently observed in cancer patients represent a risk factor for/or, rather, are a consequence of the tumour. We postulate that malignant tumours are directly involved in an increased catabolism of cholesterol-rich low-density lipoprotein (LDL) particles. In a prospective study of 25 patients with colorectal carcinoma, we measured intraindividual shifts in serum cholesterol levels after surgery, and the expression of LDL-receptor mRNA in surgically removed specimens. A significant rise in plasma cholesterol levels was observed in patients 3 and 12 months after curative surgery, but not after non-curative surgery. In human colon carcinoma tissues LDL receptor mRNA expression, as determined by competitive reverse-transcriptase-polymerase-chain reaction, was found to be significantly increased when compared to tissues from the tumour-free margin (median values, 1.2 x 10(6) vs. 2.0 x 10(5) molecules/micrograms total cellular RNA, respectively, n = 17). The extent of LDL-receptor mRNA expression positively correlated to the percentage rise of plasma cholesterol levels 3 months (n = 7, r = 0.8763) and 12 months (n = 6, r = 0.9181) after curative surgery. This finding provides in vivo evidence that the tumour tissue itself contributes to decreased plasma cholesterol levels in patients suffering from colorectal carcinomas. It supports the hypothesis that low cholesterol levels in cancer patients are a consequence, and not the cause, of the malignancy. |
| Increased levels of anti-oxidized low-density lipoprotein antibodies are associated with reduced levels of cholesterol in the general population Tinahones, F. J., J. M. Gomez-Zumaquero, et al. (2002), Metabolism 51(4): 429-31. Abstract: Autoantibodies against epitopes of oxidized low-density lipoprotein (LDL), initially shown in human sera, were later related with the atherosclerotic process, although recent studies have questioned this association. Moreover, their association with total cholesterol and plasma LDL, or with the other lipoproteins, is not clear. We studied the relation between the levels of autoantibodies to oxidized LDL and lipoproteins in a population of 400 subjects from the lower Guadalhorce area in Malaga, Spain. Anti-oxidized LDL antibodies were measured by enzyme-linked immunosorbent assay (ELISA), and total cholesterol, triglycerides, high-density lipoprotein (HDL) cholesterol, and lipoprotein(a) Lp(a) were measured with commercial kits. Subjects who were positive for anti-oxidized LDL antibodies had significantly lower levels of total cholesterol (P <.01) and LDL cholesterol (P <.01). There was a negative correlation between titers of anti-oxidized LDL antibodies and levels of total cholesterol (P =.007) and LDL cholesterol (P =.024). This inverse relation between the levels of anti-oxidized LDL antibodies and the levels of total cholesterol and LDL cholesterol in a large population study, together with the discordances already published, suggests that the relation between anti-oxidized LDL antibodies, arteriosclerosis, and lipids is more complex than initially thought. |
| Increased levels of cholesterol esters in glioma tissue and surrounding areas of human brain Nygren, C., H. von Holst, et al. (1997), Br J Neurosurg 11(3): 216-20. Abstract: The proliferation of glioma cells requires cholesterol, which could be provided by synthesis within the cells or by uptake of cholesterol esters in particles of Low Density Lipoprotein (LDL). Cholesterol esters and cholesterol were therefore analysed in human glioma tissue, its surrounding areas and serum from 40 patients. The analyses revealed an increased concentration of cholesterol esters up to 100 times (0.1-10 mumol/g) in both tumour-tissue and surrounding areas compared with control material (< 0.1 mumol/g). The analyses also demonstrated that cholesterol esters in tumour tissue eminated mainly from serum. The cholesterol concentrations were significantly lower in tumour tissue compared with surrounding areas as expected. These results indicate that tumour cell proliferation utilises serum derived cholesterol esters presumably carried by LDL particles. |
| Increased levels of high-density lipoprotein cholesterol are ineffective in inhibiting the development of immune responses to oxidized low-density lipoprotein and atherosclerosis in transgenic rabbits expressing human apolipoprotein (apo) A-I with severe hypercholesterolaemia Boullier, A., N. Hennuyer, et al. (2001), Clin Sci (Lond) 100(3): 343-55. Abstract: High levels of high-density lipoprotein (HDL) cholesterol have been reported to protect against the development of atherosclerosis in humans by increasing reverse cholesterol transport and inhibiting the oxidation of low-density lipoprotein (LDL) due to the paraoxonase content of HDL. The purpose of the present study was to assess if there are any relationships between in vivo increases in serum levels of immunological LDL oxidation markers autoantibodies against oxidized LDL, autoantibodies against malondialdehyde-modified LDL, LDL immune complexes and anti-cardiolipin autoantibodies, paraoxonase activity and the development of atherosclerosis in control rabbits and in transgenic rabbits expressing human apolipoprotein (apo) A-I. A total of 13 apo A-I transgenic rabbits and 18 non-transgenic littermates were fed on a cholesterol-rich diet (0.4%, w/w) for 14 weeks, and were monitored at weeks 0, 2, 6, 10 and 14. Aortic atherosclerotic lesions were measured at the end of this period. Human apo A-I transgenic rabbits with high HDL cholesterol levels were not protected against the development of atherosclerosis when they were fed on a cholesterol-rich diet which induced dramatic hypercholesterolaemia. Immunological markers of LDL oxidation increased and serum paraoxonase activity decreased similarly in control and transgenic rabbits. In conclusion, the present study demonstrates that high HDL cholesterol levels are ineffective in inhibiting increases in immunological markers of LDL oxidation and the development of atherosclerosis in a mammal with severe hypercholesterolaemia. |
| Increased macrophages, high serum M-CSF and low serum cholesterol in myelodysplasia and Kawasaki disease Shetty, V., K. Allampallam, et al. (1999), Br J Haematol 106(4): 1068. |
| Increased meal frequency associated with decreased cholesterol concentrations; Rancho Bernardo, CA, 1984-1987 Edelstein, S. L., E. L. Barrett-Connor, et al. (1992), Am J Clin Nutr 55(3): 664-9. Abstract: The hypothesis that meal frequency is associated with plasma cholesterol was tested in a population-based sample of 2034 white men and women aged 50-89 y. Total, low-density-lipoprotein (LDL) and high-density-lipoprotein (HDL) cholesterol and triglycerides were measured after a 12-h fast in a Lipid Research Clinic laboratory and meal frequency was obtained by questionnaire. The age-adjusted total cholesterol concentrations for men and women reporting greater than or equal to 4 meals/d averaged 0.23 mmol/L lower than for those who reported 1-2 meals/d (P = 0.01). Similarly, LDL concentrations were lower in those reporting higher meal frequency (0.16 mmol/L, P = 0.06). These associations persisted after adjustment for smoking, alcohol, waist-to-hip ratio, systolic blood pressure, body mass index, and dietary nutrients. These results suggest that cholesterol reductions might be achieved by modest increases in meal frequency without an increase in caloric intake. |
| Increased membrane cholesterol reduces the potentiation of GABA(A) currents by neurosteroids in dissociated hippocampal neurones Sooksawate, T. and M. A. Simmonds (1998), Neuropharmacology 37(9): 1103-10. Abstract: The effects of increased membrane cholesterol on the potentiation of GABA(A) currents by pregnanolone (5beta-pregnan-3alpha-ol-20-one), allopregnanolone (5alpha-pregnan-3alpha-ol-20-one), alphaxalone (5alpha-pregnan-3alpha-ol-11,20-dione) and propofol were investigated in acutely dissociated rat hippocampal neurones using the whole-cell patch clamp technique. Cholesterol enrichment of the neurones, isolated from 10 to 16-day-old Wistar rat brains, was achieved by incubation with cholesterol + phosphatidylcholine liposomes. Cholesterol enrichment (25.8+/-3.4%) reduced the potentiation of GABA(A) currents by pregnanolone (0.3 and 1 microM), allopregnanolone (1 microM) and alphaxalone (1 microM) but the potentiation of GABA(A) currents by propofol (5 microM) was not affected. Acute application of cholesterol (1 microM) did not significantly change the potentiation of GABA(A) currents by pregnanolone (1 microM). These results suggest that cholesterol within the neuronal membrane may compete with neurosteroids for their sites of action on the GABA(A) receptor or modulate the potentiating effect of the neurosteroids in some other ways. |
| Increased Na+,K(+)-pump activity in erythrocytes of rabbits fed cholesterol Makarov, V. L. and S. R. Kuznetsov (1995), Int J Exp Pathol 76(2): 93-6. Abstract: Na+,L(+)-pump activity, intracellular sodium, potassium and magnesium concentrations and membrane cholesterol content were studied in erythrocytes of rabbits fed cholesterol. The average activity of the Na+,K(+)-pump in erythrocytes of rabbits with high plasma cholesterol was twice that in erythrocytes of control animals. Analysis showed a positive correlation between the pump activity and plasma cholesterol. The sodium content in erythrocytes correlated negatively with plasma cholesterol, as well as with the Na+,K(+)-pump activity. No significant differences in potassium and magnesium concentrations or in the membrane cholesterol content were observed between the two groups. The results indicate that modulation of the pump activity by cholesterol is not necessarily mediated by changes in the membrane viscosity. |
| Increased nitric oxide accounts for decreased basal vascular tone and responsiveness in the resistance vessels of high-cholesterol-fed rabbits Fitch, R., V. Da Cunha, et al. (2001), Pharmacology 63(4): 220-7. Abstract: The objective of this study was to determine the effects of hypercholesterolemia on basal vascular tone and vascular responses to pharmacologic agents in hindquarter resistance vessels. Blood pressure and hindquarter blood flow were measured in conscious rabbits fed a high cholesterol diet (1%) for 17 weeks (HC) compared to age-matched rabbits fed a normal diet (control). Basal hindquarter blood flow and vascular conductance were significantly higher in HC than in control rabbits. Administration of a non-selective nitric oxide synthase (NOS) inhibitor, L-NAME (100 mg/kg) decreased basal hindquarter blood flow and vascular conductance in a greater magnitude in HC than in control rabbits, thus, abolished the differences in both the flow and conductance between 2 groups, indicating that increased NO was responsible for reduced basal vascular tone in the HC rabbits. L-NIL (30 mg/kg), a selective inducible NOS (iNOS) inhibitor had no effects on either flow or conductance. This result does not support the involvement of iNOS. In separate experiments, animals were anesthetized and instrumented with an extracorporeal circuit to measure perfusion pressure under constant blood flow to the hindquarter vascular bed. In the HC group, vascular responses to acetylcholine, S-nitroso-N-acetyl-penicillamine and phenylephrine were all attenuated when compared to the responses in the control rabbits. These results indicate that local overproduction of NO due to hypercholesteremia could desensitize smooth muscle reactivity, thus causing general vascular hyporesponsiveness to vasoactive agents. |
| Increased number of high sensitive platelets in hypercholesterolemia, cardiovascular diseases, and after incubation with cholesterol Opper, C., C. Clement, et al. (1995), Atherosclerosis 113(2): 211-7. Abstract: The number of low density platelets was found to be increased in patients with hypercholesterolemia, as compared with the number in controls. The percentage increase of the low density platelet subpopulation was even more pronounced in patients with hypercholesterolemia when compared with that in patients suffering from myocardial infarction or angina. In vitro studies with control platelets incubated with cholesterol rich liposomes showed also an increase in the subpopulation of low density platelets. After incubation of control platelets with cholesterol rich liposomes, a higher membrane anisotropy and a higher cholesterol to phospholipid (C/P) molar ratio of the plasma membrane were found. Furthermore, cholesterol-enriched platelets were more sensitive upon thrombin stimulation. The results suggest that a shift of platelet subpopulations to a higher number of low density platelets could be caused by either the level of plasma cholesterol or an in-vitro incubation with cholesterol rich liposomes. |
| Increased plasma and renal clearance of an exchangeable pool of apolipoprotein A-I in subjects with low levels of high density lipoprotein cholesterol Horowitz, B. S., I. J. Goldberg, et al. (1993), J Clin Invest 91(4): 1743-52. Abstract: Plasma levels of HDL apo A-I are reduced in individuals with low HDL cholesterol (HDL-C) concentrations as a result of increased fractional catabolic rates (FCRs). To determine the basis for the high apo A-I FCRs, seven subjects with low HDL-C levels (31.0 +/- 4.3 mg/dl) were compared with three subjects with high HDL-C levels (72.0 +/- 4.5 mg/dl). Each subject received autologous HDL that was labeled directly by the iodine-monochloride method (whole-labeled) and autologous HDL that was labeled by exchange with homologous radiolabeled apo A-I (exchange-labeled). Blood was obtained for 2 wk, specific activities determined, and FCRs (d-1 +/- SD) estimated. In every subject, whether in the low or high HDL-C group, the exchange-labeled FCR was greater than the whole-labeled FCR. The exchange-labeled FCR was higher in the low HDL-C group (0.339 +/- 0.043) versus the high HDL-C group (0.234 +/- 0.047; P < 0.009). The whole-labeled FCR was also greater in the low HDL-C group (0.239 +/- 0.023) versus the high HDL-C group (0.161 +/- 0.064; P < 0.02). In addition, in both low and high HDL groups ultracentrifugation resulted in more radioactivity in d > 1.210 (as percentage of total plasma counts per minute) with the exchange-labeled tracer than with the whole-labeled tracer (12.55 +/- 4.95% vs. 1.02 +/- 0.38%; P < 0.003). With both HDL tracers, more radioactivity was found in d > 1.210 in the low versus the high HDL-C groups. When apo A-I catabolism was studied by perfusing isolated rabbit kidneys with whole-labeled HDL, there was twice as much accumulation (cpm/g cortex) of HDL apo A-I isolated from subjects with low HDL-C than from subjects with high HDL-C (P < 0.0025). Finally, HDL that had been isolated from subjects with high levels of HDL-C was triglyceride enriched and exposed to partially purified lipases before perfusion through kidneys. Threefold more apo A-I from modified HDL accumulated in the cortex compared with the unmodified preparation (P < 0.007). The results of these in vivo and ex vivo studies indicate that individuals with low HDL-C levels have more loosely bound, easily exchanged apo A-I and that this exchangeable apo A-I is more readily cleared by the kidney. |
| Increased plasma apolipoprotein E-rich high-density lipoprotein and its effect on serum high-density lipoprotein cholesterol determination in patients with familial hyperalphalipoproteinemia due to cholesteryl ester transfer activity deficiency Chiba, H., M. Eto, et al. (1993), Biochem Med Metab Biol 49(1): 79-89. Abstract: Plasma apo E-rich HDL was studied in regard to its quantity and chemical composition in the members of a family with cholesteryl ester transfer activity deficiency, exhibiting familial hyperalphalipoproteinemia. The approach involved a simple precipitation method established in our laboratory. Serum apo E-rich HDL concentrations for two homozygous members were elevated up to 66 and 60 mg/dl in terms of cholesterol (normal, 6.7 +/- 2.3 mg/dl, n = 38), and to 9.4 and 10.8 mg/dl in terms of apo E (normal, 2.6 +/- 1.5 mg/dl, n = 38). The cholesterol/apo E ratio (mole/mole) of apo E-rich HDL was higher in two homozygotes (669 and 531) than in two cholestatic patients with elevated apo E-rich HDL (268 and 149) and in normal subjects (242 +/- 115, n = 38). Chromatographic studies of the serum from a homozygote showed enlargement of all HDL subclasses and apo E in the larger HDL subclass. These facts indicate that the increase of apo E-rich HDL in this disease occurs secondarily to the enlargement of HDL particles, which require substances to cover their cores, having expanded due to the accumulation of cholesteryl ester. The sera from the homozygotes gave HDL cholesterol concentrations which were remarkably discrepant among commercial precipitating reagents, because of the difference in recovery of apo E-rich HDL with these reagents. |
| Increased plasma cholesteryl ester transfer protein in obese subjects. A possible mechanism for the reduction of serum HDL cholesterol levels in obesity Arai, T., S. Yamashita, et al. (1994), Arterioscler Thromb 14(7): 1129-36. Abstract: It is well known that obesity is frequently associated with low levels of serum high-density lipoprotein (HDL) cholesterol. However, the mechanism for this reduction has not been fully clarified. Cholesteryl ester transfer protein (CETP) transfers cholesteryl ester from HDL to apolipoprotein B-containing lipoproteins and plays an important role in regulating the concentration and composition of HDL. To elucidate the mechanism for the reduction of serum HDL cholesterol in obesity, we analyzed serum lipoproteins, CETP, and postheparin lipoprotein lipase (LPL) and hepatic triglyceride lipase (HTGL) activities in 30 obese subjects (17 women and 13 men, age 44 +/- 14 years, mean +/- SD). We also investigated the relationship between these variables, total adiposity, and indices of body fat distribution. The average body mass index of the obese subjects was 33.1 +/- 4.8 kg/m2 (range, 26.4 to 43.8 kg/m2). The obese subjects showed significantly lower serum HDL cholesterol levels than control subjects (1.04 +/- 0.28 versus 1.50 +/- 0.34 mmol/L, P <.01). In the obese subjects, both activities and protein mass of CETP and postheparin HTGL activities were significantly increased, whereas postheparin LPL activities were significantly decreased. CETP activities, independent of postheparin HTGL and LPL activities, were correlated negatively with HDL cholesterol (r = -.39, P <.05) and the cholesteryl ester to triglyceride ratio of HDL2 and HDL3 (r = -.36, P <.05; r = -.46, P <.05, respectively).(ABSTRACT TRUNCATED AT 250 WORDS) |
| Increased plasma concentration of endothelin-1 in cholesterol-fed rats Miyauchi, T., Y. Sugishita, et al. (1992), Atherosclerosis 93(3): 257-9. |
| Increased plasma HDL cholesterol levels and biliary cholesterol excretion in hamster by LCAT overexpression Zhang, A. H., S. Gao, et al. (2004), FEBS Lett 570(1-3): 25-9. Abstract: Lecithin cholesterol acyltransferase (LCAT) is a key enzyme in the metabolism of high density lipoprotein (HDL), which has been found inversely correlated with atherosclerosis. Adenovirus mediated overexpression of human LCAT (hLCAT) in hamsters resulted in increased levels of plasma total cholesterol, HDL cholesterol, phospholipids and enlarged particle size of HDL. It also increased cholesterol and total bile acid concentrations in bile. Hepatic mRNA level of cholesterol 7alpha-hydroxylase increased 2.7-fold in hamsters. However, such effects were not observed in mice in a parallel experiment. This study suggests that overexpression of hLCAT in hamsters facilitated reverse cholesterol transport. Similar metabolic changes in humans might modify atherogenic risk. |
| Increased plasma HDL-cholesterol and apo A-I in breast cancer patients undergoing adjuvant tamoxifen therapy Mastroianni, A., C. Bellati, et al. (2000), Clin Biochem 33(6): 513-6. |
| Increased plasma level of cholesterol-5 beta,6 beta-epoxide in endometrial cancer patients Kucuk, O., M. Churley, et al. (1994), Cancer Epidemiol Biomarkers Prev 3(7): 571-4. Abstract: Plasma levels of alpha- and beta-isomers of cholesterol-5, 6-epoxides were quantitated in a pilot study of 9 women with endometrial cancer and 9 race- and age-matched control women by isotope dilution gas chromatography/mass spectrometry. Endometrial cancer cases had significantly higher cholesterol-5 beta,6 beta-epoxide levels than the controls (P = 0.01). The mean plasma beta-epoxide level was 0.71 +/- 0.46 ng/ml for the cases and 0.35 +/- 0.25 ng/ml for the controls. No significant differences were found between the plasma alpha-epoxide levels of the cases and the controls. Plasma levels of various carotenoids, tocopherols, and ascorbic acid were also quantitated by high performance liquid chromatography. An inverse correlation was present between the plasma levels of cholesterol-5 beta,6 beta-epoxide and cis-lutein/zeaxanthin (P = 0.01). These data suggest a possible role for cholesterol-5 beta,6 beta-epoxide as a biomarker of endometrial cancer risk. Further studies are warranted to investigate the possible association between the oxidation products of cholesterol and endometrial cancer and to determine the interactive role of antioxidants. |
| Increased plasma, biliary, and hepatic cholesterol precursors in pigs with ileal autotransplantation-induced malabsorption of cholesterol and bile acids Pakarinen, M. P., J. Halttunen, et al. (1998), Scand J Gastroenterol 33(3): 319-26. Abstract: BACKGROUND: Small-bowel transplantation impairs intestinal absorptive function for unknown reasons. METHODS: The proportions of plasma, biliary, and hepatic cholesterol precursors to cholesterol were determined by gas-liquid chromatography after resection of the proximal 75% of the porcine jejunoileum (n = 15) and autotransplantation of the remaining ileum (n = 15) and were related to in vivo absorption and fecal excretion of cholesterol. RESULTS: Ileal autotransplantation significantly decreased serum (18%; P < 0.05) and liver (7.6%; P < 0.05) cholesterol content, the esterification percentage of serum cholesterol (5.1%; P < 0.0001), and the total amount of cholesterol absorbed (48%; P < 0.05) and increased fecal excretion of bile acids (108%; P < 0.0001), net cholesterol elimination (53%; P < 0.001), and the proportions of plasma (207%; P < 0.0001), biliary (183%; P < 0.0001), and hepatic (114%; P < 0.0001) cholesterol precursors. The increases were most striking for the side-chain-saturated demethylated sterols, cholesterol and lathosterol, and monomethyl sterols, whose bile/liver and plasma/liver ratios were increased in the autotransplantation group. Plasma, biliary, and hepatic precursor proportions were positively related to each other and similarly correlated with fecal bile acids and the net elimination of cholesterol in feces. CONCLUSIONS: These findings suggest that ileal autotransplantation in pigs with proximal gut resection increased the levels of cholesterol precursor sterols in plasma, bile, and liver mainly due to a bile-acid-malabsorption-induced increase in hepatic synthesis of cholesterol. Enhanced secretion of cholesterol precursors from the liver into the plasma and bile may have contributed to their increased values during the increased rate of cholesterogenesis. |
| Increased prebeta-HDL levels, cholesterol efflux, and LCAT-mediated esterification in mice expressing the human cholesteryl ester transfer protein (CETP) and human apolipoprotein A-I (apoA-I) transgenes Francone, O. L., L. Royer, et al. (1996), J Lipid Res 37(6): 1268-77. Abstract: The effects of cholesteryl ester transfer protein (CETP) on the distribution of apolipoprotein (apo) A-I between high density lipoprotein (HDL) subspecies and its impact on efflux and esterification of cell-derived cholesterol was studied in transgenic mice expressing either the human apoA-I (HuAITg) or both the human apoA-I and CETP (HuAICETPTg) transgenes. The simultaneous expression of the human CETP and apoA-I transgenes induced a 2-fold increase in the proportion of human apoA-I in the prebeta-HDL fraction and 1.4- and 2.2-fold increases in the HDL3a and HDL3c fractions, respectively, at the expense of the larger HDL2b population. HuAICETPTg mouse plasma has a greater ability to cause efflux of cholesterol from 3H-labeled fibroblasts than plasma from HuAITg mice. Furthermore, the LCAT-mediated esterification of cell-derived cholesterol is increased 1.7-fold in mice expressing the human apoA-I and CETP transgenes compared to HuAITg mouse plasma. LCAT activity (measured with an exogenous substrate) was increased 1.4-fold and LCAT mRNA levels were increased 1.3-fold as a result of CETP expression. Taken together, these data indicate that in vivo, the expression of CETP resulted in an increase in the proportion of apoA-I in the prebeta-HDL fraction and a stimulation of the efflux and esterification of cell-derived cholesterol. |