Cholesterol Journal Articles

Record 5901 to 5920

Essential role for cholesterol in synaptic plasticity and neuronal degeneration
Koudinov, A. R. and N. V. Koudinova (2001), Faseb J 15(10): 1858-60.

Essential role for the (hepatic) LDL receptor in macrophage apolipoprotein E-induced reduction in serum cholesterol levels and atherosclerosis
Van Eck, M., K. W. Van Dijk, et al. (2001), Atherosclerosis 154(1): 103-12.
Abstract: Apolipoprotein E (apoE) is a high affinity ligand for several receptor systems in the liver, including the low-density lipoprotein (LDL) receptor, and non-LDL receptor sites, like the LDL receptor-related protein (LRP), the putative remnant receptor and/or proteoglycans. Although the liver is the major source of apoE synthesis, apoE is also produced by a wide variety of other cell types, including macrophages. In the present study, the role of the LDL receptor in the removal of lipoprotein remnants, enriched with macrophage-derived apoE from the circulation, was determined using the technique of bone marrow transplantation (BMT). Reconstitution of macrophage apoE production in apoE-deficient mice resulted in a serum apoE concentration of only 2% of the concentration in wild-type C57Bl/6 mice. This low level of apoE nevertheless reduced VLDL and LDL cholesterol 12-fold (P<0.001) and fourfold (P<0.001), respectively, thereby reducing serum cholesterol levels and the susceptibility to atherosclerosis. In contrast, reconstitution of macrophage apoE synthesis in mice lacking both apoE and the LDL receptor induced only a twofold (P<0.001) reduction in VLDL cholesterol and had no significant effect on atherosclerotic lesion development, although serum apoE levels were 93% of the concentration in normal C57Bl/6 mice. In conclusion, a functional (hepatic) LDL receptor is essential for the efficient removal of macrophage apoE-enriched lipoprotein remnants from the circulation and thus for normalization of serum cholesterol levels and protection against atherosclerotic lesion development in apoE-deficient mice.

Establishing reference total serum cholesterol values for Saudi children
Rafii, Z. S., A. A. al Nasser, et al. (1994), Ann Clin Biochem 31 (Pt 4): 347-50.
Abstract: Total serum cholesterol was measured in 1320 normal Saudi children aged 0-14 years. The result was 3.88 (0.83) mmol/L mean (SD) and there was no statistical difference between girls and boys. Results were lowest in the 0-4 year age group and highest in the 5-9 year age group. Percentile values were established for three age groups and compared with those published for American children; no statistical differences were observed. Unlike other developing countries Saudi children do not have lower serum cholesterol than their western counterparts. We believe that these findings reflect changing dietary habits and increasing affluence in Saudi Arabia.

Establishment of two morphologically distinct PC12 cell lines resistant to 25-OH-cholesterol toxicity
Chang, J. Y., K. D. Phelan, et al. (1997), Biochem Biophys Res Commun 239(2): 429-34.
Abstract: Two novel populations of spontaneous PC12 cell mutants resistant to a toxic concentration of 25-OH-cholesterol (5 microg/ml, 12.5 microM) were isolated and designated as R25R and F25R based on cell morphology. R25R consisted of round cells that were morphologically similar to the parent PC12 cells, and responded to nerve growth factor by extending neurites. F25R was a group of process-bearing flat cells that did not assume a neuronal morphology in the presence of nerve growth factor. These two cell lines also acquired some cross-resistance toward other cholesterol oxides. Nerve growth factor induced prominent voltage-dependent calcium currents in parent PC12 cells and in R25R, but not in F25R. Further experiments indicated that the parent PC12 cells, R25R and F25R exhibited different properties when challenged with a variety of toxic insults, including amphotericin B, serum withdrawal and beta-amyloid protein treatment.

Esterification of cholesterol oxidation products and their effect on the rate of cholesterol esterification in macrophages
Dushkin, M. I., E. V. Mandrikova, et al. (1991), Vopr Med Khim 37(3): 2-5.
Abstract: Effects of cholesterol (CH) autooxidation products on incorporation of 14C-oleate into cholesteryl esters (CE) and their possible esterification were studied in cultivated mice peritoneal macrophages (MPM). 25 Mg/ml of purified CH and 25 Mg/ml of autooxidized CH stimulated (4- and 17-fold, respectively) the cholesterol esterification in MPM. In presence of 4 Mg/ml 25-hydroxy CH or the mixture of 4 Mg/ml 7 alpha-, 7 beta-hydroxy CH and 7-keto CH incorporation of oleate into cellular CE was increased 20- and 4-fold, respectively. 4 Mg/ml concentration of cholestane-3 beta, 5 alpha, 6 beta-friol caused no effects. Mono- and diesters of 14C-hydroxy CH were found after 8 hrs incubation of the steroid with MPM. Incorporation of 14C-25 hydroxy CH into its esters occurred at the rate, which exceeded 6-7-fold the 14C-CH incorporation into CE. Esterification of 7 alpha-, 7 beta-hydroxyCH and 7-ketoCH was studied, 0.52% label of the total cell sterols radioactivity was detected in the fraction of nonpolar steroids. 14C-cholestane-3 beta,5 alpha,6 beta-triol was not esterified in MPM. The stimulating effects of 25-hydroxyCH on oleate incorporation into CE and its esterification in MPM were inhibited in presence of 10 Mg/ml progesterone, an inhibitor of acyl-CoA:cholesterol acyltransferase activity. Induction of CE formation in MPM by means of choltransferase activity. Induction of CE formation in MPM by means of cholesterol oxidation products may be responsible for development of foam cells, while esterification of polar steroids in cells appears to be of importance in decrease of their toxic and metabolic effects.

Esterification of oxysterols by human plasma lecithin-cholesterol acyltransferase
Szedlacsek, S. E., E. Wasowicz, et al. (1995), J Biol Chem 270(20): 11812-9.
Abstract: In the present study, lecithin-cholesterol acyltransferase (LCAT) catalyzed esterification of oxysterols was investigated by using discoidal bilayer particles (DBP) containing various oxysterols, phosphatidylcholines, and apolipoprotein A-I. The esterified oxysterols were analyzed by high pressure liquid chromatography, gas chromatography, and mass spectrometry. LCAT esterified all oxysterols tested that are known to be present in human plasma. The esterification yields in almost all cases were relatively high, often as high as the yield of cholesterol esterification. When DBP preparations containing 27-hydroxycholesterol and various phosphatidylcholines were used for the LCAT reaction, both monoesters and diesters were produced. The mass spectrometry analysis showed that the monoester was produced by the esterification of the 3 beta-hydroxyl group and not the 27-hydroxyl group. The diesters were apparently produced by the esterification of the 27-hydroxyl group only after the esterification of the 3 beta-hydroxyl group. Phosphatidylcholine containing a saturated acyl group at sn-1 position and an unsaturated acyl group at sn-2 position gave generally high esterification yield. The esterification of various oxysterols was compared by using DBP containing dioleoyl-phosphatidylcholine and individual oxysterols. All oxysterols produced 3 beta-oleoyl monoesters. Unlike 27-hydroxycholesterol, 25-hydroxycholesterol, 7 alpha-hydroxycholesterol, 7 beta-hydroxycholesterol, or cholestanetriol did not produce diesters. Various factors influencing the formation of the monoesters and diesters from 27-hydroxycholesterol were investigated. When dioleoyl-phosphatidylcholine was used as the acyl donor, prolonged dialysis of DBP preparations and increase in the ratio of the enzyme concentration to substrate particle concentration increased the diester formation. Significant amounts of diesters were also produced by using 1-palmitoyl-2-oleoyl-phosphatidylcholine and other phosphatidylcholines as the acyl donors. By analyzing the conditions of monoester and diester formation, a scheme for the LCAT reaction pathway was proposed.

Esterification of plasma membrane cholesterol and triacylglycerol-rich lipoprotein secretion in CaCo-2 cells: possible role of p-glycoprotein
Field, F. J., E. Born, et al. (1995), J Lipid Res 36(7): 1533-43.
Abstract: Acylcoenzyme A:cholesterol acyltransferase (ACAT) and/or cholesteryl esters have been implicated as important factors in the normal assembly of apolipoprotein (apoB)-containing lipoproteins. The predominant substrate for ACAT is believed to originate from cholesterol contained within the plasma membrane. To investigate a possible role of intestinal plasma membrane cholesterol in triacylglycerol-rich lipoprotein synthesis and secretion, CaCo-2 cells were incubated with agents that are known to interfere with cholesterol transport from the plasma membrane to the ER. Progesterone, verapamil, and trifluoperazine significantly decreased the movement of cholesterol from plasma membrane to endoplasmic reticulum (ER) in CaCo-2 cells. Without altering the synthesis of apoB and independent of their effects on cellular cholesterol esterification, progesterone, verapamil, and trifluoperazine decreased the basolateral secretion of triacylglycerols, cholesteryl esters, and immunoreactive and newly synthesized apoB. The three agents also interfered with the esterification of cholesterol absorbed from taurocholate micelles. As progesterone, verapamil, and trifluoperazine are recognized inhibitors of p-glycoprotein, a variety of agents that have been shown to interfere with p-glycoprotein function were tested to investigate their effects on cholesterol transport and apoB secretion. All the agents significantly decreased in parallel both cholesterol transport and apoB secretion. In contrast, methotrexate, an antimetabolite that does not interact with p-glycoprotein, had no effect. Nigericin, a potassium ionophore, which causes alkalinization of intracellular vesicles, also caused a profound inhibition of cholesterol transport and apoB secretion. Preventing plasma membrane cholesterol from arriving at the ER, or inhibiting the esterification of plasma membrane cholesterol, does not alter apoB secretion. However, the results suggest a possible role for p-glycoprotein in normal cholesterol trafficking and triacylglycerol-rich lipoprotein secretion in CaCo-2 cells. It is postulated that p-glycoprotein might function to maintain the acidic environment of transport vesicles, and therefore, could play a role in the transport of lipids by the intestine.

Esterified cholesterol accumulation induced by aggregated LDL uptake in human vascular smooth muscle cells is reduced by HMG-CoA reductase inhibitors
Llorente-Cortes, V., J. Martinez-Gonzalez, et al. (1998), Arterioscler Thromb Vasc Biol 18(5): 738-46.
Abstract: Vascular smooth muscle cell (VSMC) proliferation is a key event in the development of atherosclerotic lesions. VSMCs synthesize extracellular matrix, where low density lipoproteins (LDLs) are trapped and become aggregated (agLDL). The objective of this study was to investigate the cholesterol uptake and accumulation triggered by agLDL in comparison with native LDL (nLDL) on unstimulated and platelet-derived growth factor-stimulated human aortic VSMCs and the role of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors on these processes. Esterified cholesterol (EC) accumulation induced by agLDL in VSMCs was correlated with the degree of aggregation and concentration. The EC content of VSMCs treated with 100 microg/mL of agLDL (80% aggregated) increased approximately 70-fold over that in VSMCs incubated with the same concentration of nLDL. Whereas nLDL-derived EC was increased approximately twofold in platelet-derived growth factor-stimulated VSMCs, there was no effect of platelet-derived growth factor (10(-9) mol/L) on the uptake of agLDL. The 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor simvastatin (5 micromol/L) reduced EC accumulation derived from agLDL uptake by 58% and 35% in platelet-derived growth factor-stimulated and unstimulated VSMCs, respectively. This inhibition was overcome by geranylgeraniol (10 micromol/L) and partially by farnesol (10 micromol/L). Fluorescence microscopy of the cellular internalization of agLDL labeled with the fluorochrome 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine demonstrated that simvastatin reduces EC accumulation derived from agLDL by inhibiting its endocytosis and that the effect is completely reversed by geranygeraniol. These results indicate that agLDLs are rapidly internalized by human VSMCs and that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors modulate EC accumulation. These data suggest a possible mechanism by which statins could contribute to the passivation and stabilization of actively growing atherosclerotic lesions.

Esterified cholesterol and triglyceride are present in plasma membranes of Chinese hamster ovary cells
Mackinnon, W. B., G. L. May, et al. (1992), Eur J Biochem 205(2): 827-39.
Abstract: The chemical composition of highly purified plasma membrane preparations from a series of malignant Chinese hamster ovary (CHO) cell lines were undertaken to ascertain if neutral lipid, including cholesteryl ester and triacylglycerol, were present. Triacylglycerols (33-41 nmol/mg total lipid) and cholesteryl ester (226-271 nmol/mg) were measured in the plasma membranes and differences in the chemical composition of these membranes recorded. The most significant difference was a gradual decrease in the level of free cholesterol from wild type (312 +/- 7 nmol/mg total plasma membrane lipid), Pod RII-6 (268 +/- 64 nmol/mg total plasma membrane lipid), Col R-22 (243 +/- 39 nmol/mg total plasma membrane lipid) to EOT (204 +/- 20 nmol/mg total plasma membrane lipid), with a concomitant increase in the degree of saturation of the cholesteryl ester fatty acids, particularly palmitic acid. No statistically significant differences were apparent in the chemical composition of the whole cells in this series. The one-dimensional (1D) 1H-NMR spectra of the four malignant cell lines showed a gradation in intensity of lipid resonances, in the order of wild type, Pod RII-6, Col R-22 and EOT, with EOT having the strongest lipid spectrum. Interestingly, the increase in acyl-chain signal intensities in the 1H-NMR spectra of this series of CHO cells and emergence of signals from cholesterol and/or cholesteryl ester, coincide with alterations in the amount of free cholesterol and the degree of saturation of the fatty-acyl chain of the esterified cholesterol in the plasma membranes. It is our hypothesis that, together, cholesteryl ester and triacylglycerol form domains in the plasma membrane and that when the cholesteryl ester has a largely saturated fatty acid content, the lipids are in isotropic liquid phase and hence visible by NMR.

Estimating an individual's true cholesterol level and response to intervention
Irwig, L., P. Glasziou, et al. (1991), Jama 266(12): 1678-85.
Abstract: An individual's blood cholesterol measurement may differ from the true level because of short-term biological and technical measurement variability. Using data on the within-individual and population variance of serum cholesterol, we addressed the following clinical concerns: Given a cholesterol measurement, what is the individual's likely true level? The confidence interval for the true level is wide and asymmetrical around extreme measurements because of regression to the mean. Of particular concern is the misclassification of people with a screening measurement below 5.2 mmol/L who may be advised that their cholesterol level is "desirable" when their true level warrants further action To what extent does blood cholesterol change in response to an intervention? In general, confidence intervals are too wide to allow decision making and patient feedback about an individual's cholesterol response to a dietary intervention, even with multiple measurements. If no change is observed in an individual's cholesterol value based on three measurements before and three after dietary intervention, the 80% confidence interval ranges from a true increase of 4% to a true decrease of 9%.

Estimating cholesterol treatment rates among individuals with multiple risk factors and without coronary heart disease
Nag, S. S., T. A. Pearson, et al. (2005), Am J Cardiol 95(7): 862-4.
Abstract: This retrospective study examined lipid-lowering therapy treatment rates from 2000 to 2001 using the Ingenix LabRx Database. Patients with multiple risk factors without coronary heart disease were identified based on the presence of >/=2 of the following: men >/=45 years, women >/=55 years, hypertension, high-density lipoprotein cholesterol <40 mg/dl, total cholesterol >/=200 mg/dl, or obesity. Lipid treatment rates were estimated among those needing therapy (defined as low-density lipoprotein cholesterol >/=130 mg/dl or currently receiving lipid-lowering therapy). The overall lipid-lowering therapy treatment rate was 38% and the estimated lipid treatment gap (percent needing treatment who were not receiving it) was 62%.

Estimating low-density lipoprotein cholesterol by the Friedewald equation is adequate for classifying patients on the basis of nationally recommended cutpoints
Warnick, G. R., R. H. Knopp, et al. (1990), Clin Chem 36(1): 15-9.
Abstract: We compared low-density lipoprotein cholesterol (LDL) values obtained by the Friedewald formula--i.e., total cholesterol minus high-density lipoprotein (HDL) cholesterol minus very-low-density lipoprotein (VLDL) cholesterol (estimated as triglyceride divided by 5)--with those obtained by lipoprotein fractionation, using 4736 specimens. When triglycerides were less than 2.0 g/L, greater than 90% of estimated LDL cholesterol values were acceptable, within +/- 10% of measured values. At triglyceride concentrations of 2.0-4.0 g/L and 4.0-6.0 g/L, only 72% and 39%, respectively, of the estimates were acceptable. LDL values derived from an alternative formula, estimating VLDL as triglycerides divided by 6, were even less accurate. Nevertheless, the use of estimated LDL for risk classification based on the National Cholesterol Education Program Adult Treatment Panel cutpoints of 1.30 and 1.60 g/L was considered acceptable. At triglyceride concentrations less than or equal to 5.0 g/L, 88% of classifications based on estimated LDL (using triglycerides divided by 5) were concordant with those by measured LDL. Eleven percent of classifications were shifted across one cutpoint, evenly distributed between high and low. Fewer than 1% of classifications, all with Type III hyperlipoproteinemia, were misclassified two cutpoints high. Refinements in the estimation model did not substantially improve LDL estimation or concordance of risk classification.

Estimating the benefits of cholesterol lowering: are risk factors for coronary heart disease multiplicative?
Coughlin, S. S. (1992), J Clin Epidemiol 45(12): 1451.

Estimating the long-term effects of storage at -70 degrees C on cholesterol, triglyceride, and HDL-cholesterol measurements in stored sera
Shih, W. J., P. S. Bachorik, et al. (2000), Clin Chem 46(3): 351-64.
Abstract: We estimated the effects of long-term storage at -70 degrees C on serum total cholesterol, HDL-cholesterol, and triglycerides in specimens that had been stored for up to 7 years. These estimates were made using measurements in serial specimens collected from the placebo control group of the Air Force/Texas Coronary Atherosclerosis Prevention Study over a period of approximately 5 years. We compared the group means for pairs of serial specimens taken at 6- and 12-month intervals, assuming that (a) a negligible placebo effect occurred between the serial specimen pairs; (b) in the absence of storage effects, the variation in the group means would reflect only normal biological variation and would not materially affect the group means for the serial specimens; (c) any systematic changes in these group means would reflect storage-related changes; and (d) storage-related changes are cumulative, i.e., the overall changes for a given storage period are the sum of the changes during previous storage periods. We observed average decreases of 2.0% per year for total cholesterol over 7 years and 2.8% per year in triglycerides for the first 5 years. HDL-cholesterol decreased by 1.3% per year, but this change was not statistically significant. This approach may be useful for estimating storage-related changes for studies in specimens stored for a period of years and for which stability data may not be available.

Estimation of cardiovascular risk: total cholesterol versus lipoprotein profile
Branchi, A., A. Rovellini, et al. (1994), Int J Clin Lab Res 24(2): 106-12.
Abstract: The complete lipoprotein profile is thought to give more information about the individual risk of coronary heart disease than total cholesterol alone. Although total cholesterol has a low sensitivity in the correct assessment of the risk of coronary heart disease, it may be of value in screening programs because of its low cost. In this study of 5,335 subjects, total cholesterol gave a different assessment of coronary heart disease risk (United States National Cholesterol Education Program guidelines) in 25% of subjects than the complete lipoprotein profile. Differences in risk assignment were mainly accounted for by high- and low-density lipoprotein-cholesterol (Friedewald equation). The calculated low-density lipoprotein-cholesterol was highly correlated with the value measured with a mixed ultracentrifugation and precipitation procedure. However, calculated values gave estimates of coronary heart disease risk which were 20% different from those from measure values. In 200 subjects in whom the lipoprotein profile was assessed three times in 1 year, the total cholesterol low-density lipoprotein-cholesterol varied by more than 30 mg/dl (0.78 mmol/l) in 52% and 50%, respectively, triglycerides by more than 30 mg/dl (0.34 mmol/l) in 75%, and high-density lipoprotein-cholesterol by more than 15 mg/dl (0.39 mmol/l) in 34%. Compared with the mean of the measurements, the single measurement of total cholesterol misclassified 48% of subjects, low-density lipoprotein-cholesterol 60%, high-density lipoprotein-cholesterol 12%, and 28%. We conclude that total cholesterol alone may be misleading in the assignment of coronary heart disease risk. Calculation of low-density lipoprotein-cholesterol, although less accurate than desirable, is the only way of evaluating this in clinical practice.(ABSTRACT TRUNCATED AT 250 WORDS)

Estimation of cholesterol sulphate in blood plasma and in erythrocyte membranes from individuals with Down's syndrome or diabetes mellitus type I
Przybylska, M., M. Bryszewska, et al. (1995), Clin Biochem 28(6): 593-7.
Abstract: OBJECTIVES: Plasma and erythrocyte membrane cholesterol sulphate (CS) were measured in patients suffering from diabetes and Down's syndrome. DESIGN AND METHODS: The procedure for separation and determination of CS comprised HPTLC (high-performance thin-layer chromatography) and densitometry. RESULTS: The mean plasma and RBC membranes CS concentrations (+/- SD) of the control group (n = 16) was 188 +/- 47 micrograms/dL and 343 +/- 57 micrograms/10(12) RBC, respectively. In 15 patients with diabetes and 12 Down's syndrome patients substantially higher CS levels were found (diabetes: plasma-348 +/- 60 micrograms/dL; RBC membranes-646 +/- 113 micrograms/10(12) RBC; Down's syndrome: plasma-245 +/- 54 micrograms/dL; RBC membranes 427 +/- 74 micrograms/10(12) RBC). Analysis of variance and multiple comparison (Newman-Keuls test) show statistically significant differences between all samples both for erythrocytes, F(2.41) = 52.24, p < 0.05, and plasma, F(2.41) = 34.92, p < 0.05. CONCLUSIONS: It is postulated that differences in CS levels may contribute to changes of erythrocyte properties in these pathological states.

Estimation of dolichol and cholesterol synthesis in microsomes and peroxisomes isolated from rat liver
Grunler, J., J. M. Olsson, et al. (1995), FEBS Lett 358(3): 230-2.
Abstract: The participation of peroxisomal and microsomal fractions from rat liver in dolichol and cholesterol synthesis was investigated using marker enzymes. Recovery was 8% for peroxisomes and 33% for microsomes, with virtually no cross-contamination between these fractions. Using these data, it was calculated that the peroxisomal branch-point enzyme activities for dolichol and cholesterol biosynthesis, i.e. cis-prenyltransferase and squalene synthase, were 25% and 12%, respectively, of the total homogenate activity. Treatment with mevinolin increased the peroxisomal contribution in the case of both enzymes, to levels almost equal to that of their microsomal counterparts. These results indicate that peroxisomes play a role in the biosynthesis of isoprenoid lipids and that the extent of this participation is increased extensively when peroxisomes are induced by various treatments.

Estimation of LDL cholesterol based on the Friedewald formula and on apo B levels
Bairaktari, E., K. Hatzidimou, et al. (2000), Clin Biochem 33(7): 549-55.
Abstract: OBJECTIVES: The plasma apolipoprotein B (apo B) concentrations have been considered to be a more accurate representation of atherogenic particles and it has been proposed that the formula LDL-C (mmol/L) = 0.41TC - 0.32TG + 1.70apo B - 0.27 is reliable for the estimation of LDL-C (Clin Chem 1997; 43: 808-15). We undertook the present study to investigate the reliability of this formula in a large number of hyperlipidemic patients. DESIGN AND METHODS: 1) The Friedewald formula (LDL-F) and the apo B-based formula (LDL-B) were compared with the beta-quantification reference procedure in 130 individuals with a wide range of total cholesterol (TC) and triglyceride (TG) levels, and 2) the LDL-C levels obtained by the Friedewald formula were compared with those calculated by the apo B-based formula in 1010 individuals attending our outpatient lipid clinic. RESULTS: The LDL-F and the LDL-B formulae for LDL-C estimation were found to be in good agreement with the beta-quantification (r = 0.96 and 0.97, respectively). The bias of each method plotted as a function of TG (up to 4.52 mmol/L) was found positive for the LDL-F, whereas the LDL-B was independent of the concentrations of TG. When a large number of individuals were examined, a good correlation between the two equations was found (n = 1010, r = 0.98). The difference between the two methods was not correlated with serum TG levels. However, it was correlated to serum TC, and apo B levels. CONCLUSIONS: The LDL-B formula is a more reliable and accurate method than the LDL-F formula, especially at TG levels >2.26 mmol/L, although it underestimates LDL-C concentrations. Furthermore, this equation can be used in hypertriglyceridemic patients (TG >4.52 mmol/L) in whom the Friedewald equation is inaccurate.

Estimation of low density lipoprotein cholesterol concentration: regression analysis versus Friedewald's formula
Eblen-Zajjur, A. and M. Eblen-Zajjur (2001), Rev Med Chil 129(11): 1263-70.
Abstract: BACKGROUND: The Friedewald formula is used to estimate cholesterol of low density lipoprotein (LDL) from total cholesterol (CT), cholesterol of high density lipoprotein (HDL) and triglycerides (TG), but there are doubts about its precision. AIM: To compare Friedewald formula and regression analysis for the calculation of LDL cholesterol. MATERIAL AND METHODS: One hundred and fifty plasma samples from asymptomatic adults (aged 47.7 +/- 13 years, 50.6% male) were analyzed. CT, HDL, LDL and TG were determined by enzymatic methods. Friedewald formula (LDLc = CT-HDL-(TG/5)) and multiple regression analysis were applied to estimate LDL concentration. RESULTS: Mean total cholesterol was 175.3 +/- 39.7 mg/dl, HDL cholesterol was 35.57 +/- 0.8 mg/dl and TG was 128.4 +/- 65.4 mg/dl. Mean values for LDL cholesterol were significantly higher than those estimated by the Friedewald formula (136.4 +/- 37.9 mg/dl and 114.1 +/- 37.4 mg/dl respectively, p < 0.001) with a mean underestimation of 16.4 +/- 11.7%. LDL cholesterol values were directly proportional to TG concentration. Multiple regression analysis (LDLr = -14.376 + (age x 0.198) + (CT x 0.949) + (HDL x -0.474) + (TG x -0.064) showed no statistical differences with those obtained by the enzymatic method. CONCLUSIONS: These results confirm the underestimation of LDL concentration by the Friedewald formula despite normal range of TG concentration. A multiple regression analysis should be used to estimate LDL concentration with precision.

Estimation of plant sterol and cholesterol intake in Finland: quality of new values and their effect on intake
Valsta, L. M., A. Lemstrom, et al. (2004), Br J Nutr 92(4): 671-8.
Abstract: The Finnish national food composition database Fineli was updated with recent analytical values for plant sterols (PS) (sitosterol, campesterol, stigmasterol, avenasterol, brassicasterols and stanols) and cholesterol. The quality of the new analytical data was assessed. The aims of the present study were: (1) to compare the effect of old and new database values on PS and cholesterol intakes based on average per capita food consumption data; (2) to estimate the current intake and major sources of these compounds in various population groups according to the national FINDIET 1997 survey data. The intake of total PS was 305 mg/d for men and 237 mg/d for women. The respective intakes for cholesterol were 284 mg/d and 201 mg/d. Women had a higher density of PS in their diets than men, whereas the cholesterol density in the diets did not differ between genders. Cereals, margarine, vegetables and vegetable oils were the main food sources of PS. Meat, meat products and eggs were the main sources of cholesterol. A 9 % greater PS intake estimate was obtained with the new PS database compared with the old PS database, probably due to minor methodological differences between the new and old analyses. Notable changes in analytical methods suggest a lower value (-19 %) for cholesterol intake calculated from the new database compared with the old one. We conclude that researchers can have confidence in the new values for PS and cholesterol, because systematic evaluation of the new analytical values showed them to be of high quality.

Cholesterol Articles and Abstracts

Cholesterol Journal Articles