Cholesterol Journal Articles

Record 8901 to 8920

Mesenteric and hepatic vascular reactivity in Donryu rats with and without a cholesterol-supplemented diet
Ralevic, V., G. Aliev, et al. (1996), Eur J Pharmacol 313(3): 221-7.
Abstract: Vascular function of Donryu rats fed on a normal or cholesterol-supplemented diet was examined in the isolated perfused mesenteric arterial bed and portally perfused liver. In mesenteric preparations, frequency-dependent vasoconstriction to electrical field stimulation (4-32 Hz, 1 ms, 90 V, 30 s) and dose-dependent vasoconstriction to noradrenaline (0.15-1500 nmol) was similar in both groups. Dose-dependent vasoconstriction to alpha, beta-methylene ATP (0.05-500 nmol) via P2x purinoceptors was significantly impaired in Donryu rats fed on a cholesterol-supplemented diet. In preparations with raised tone (methoxamine 5-35 microM), there was no significant difference in endothelium-dependent relaxation to acetylcholine and ATP, or endothelium-independent relaxation to sodium nitroprusside. In liver preparations, there was no difference in frequency-dependent vasoconstriction to electrical field stimulation (2-32 Hz, 1 ms, 90 V, 30 s), or dose-dependent vasoconstriction to noradrenaline (0.05-500 nmol) and alpha, beta-methylene ATP (0.05-500 nmol) between the groups. In conclusion, in mesenteric arteries, but not in the hepatic portal vasculature of Donryu rats fed on cholesterol P2x purinoceptor function is impaired, but sympathetic neurotransmission is unaffected. Mesenteric endothelial and smooth muscle function is unimpaired.

Mesophase formation by ceramides and cholesterol: a model for stratum corneum lipid packing?
Parrott, D. T. and J. E. Turner (1993), Biochim Biophys Acta 1147(2): 273-6.
Abstract: Previous X-ray diffraction and electron microscopy experiments have suggested that there is an unusual double bilayer structure formed by stratum corneum lipids, with a lamellar spacing of about 131 A (White, S.H., Mirejovsky, D. and King, G.I. (1988) Biochemistry 27, 3725-3732; Hou, S.Y.E., Mitra, A.K., White, S.H., Menon, G.K., Ghadially, R. and Elias, P.M. (1991) J. Invest. Dermatol. 96, 215-223; Bouwstra, J.A., De Vries, M.A., Gouris, G.S., Bras, W., Brussee, J. and Ponec, M. (1991) J. Controlled Release 15, 209-220). Two contradictory models have been proposed for this structure. In the Downing model, used to explain electron microscopy observations, acylceramides are vital, acting as a 'lynch-pin' and holding the lipid layers together (Swartzendruber, W.C., Kitko, D.J., Madison, K.C. and Downing, D.T. (1989) J. Invest. Dermatol. 92, 251-257). Alternatively, to explain X-ray diffraction results from intact corneum, protein intercallation into the lipid bilayers is suggested, since an electron dense region wider than can be accounted for by lipid headgroups alone, is required (Bouwstra, J.A., De Vries, M.A., Gouris, G.S., Bras, W., Brussee, J. and Ponec, M. (1991) J. Controlled Release 15, 209-220). Thus, existing models require the presence of either acylceramides or protein. We describe how a similar structure can be prepared in vitro using mixtures of cholesterol and ceramides. Cholesterol induces a novel double-bilayer structure in ceramides II, and IV. This result is in conflict with the existing literature which cites acylceramides, or protein as instrumental in maintaining the in vivo structure of the phase. Characterisation has been carried out using optical microscopy and synchrotron X-ray diffraction.

Meta-analysis of the cholesterol-lowering effects of dietary fiber
Truswell, A. S. (1999), Am J Clin Nutr 70(5): 942-3.

Meta-analysis, clinical trials, and transferability of research results into practice. The case of cholesterol-lowering interventions in the secondary prevention of coronary heart disease
Marchioli, R., R. M. Marfisi, et al. (1996), Arch Intern Med 156(11): 1158-72.
Abstract: OBJECTIVE: To evaluate, in the comprehensive scenario of "evidence-based" medicine, the transferability of the results of published randomized clinical trials and meta-analyses on cholesterol-lowering interventions to clinical practice. METHOD: Overview of randomized clinical trials on cholesterol-lowering interventions in the secondary prevention of coronary heart disease. RESULTS: The present overview on secondary prevention of coronary heart disease included 34 trials with cholesterol-lowering interventions in 24968 individuals. There was a 12.5% mortality in the group that was allocated active intervention and a 17.2% mortality in the control group (risk reduction, 13%; 95% confidence interval, -19% to -6%). Coronary and cardiovascular odds of deaths were significantly reduced. No clear association was found between noncoronary mortality and cholesterol-lowering interventions. Baseline total cholesterol levels had no clear influence on total mortality. Intermediate (10%-20%) and high (> 20%) total cholesterol reductions were associated with similar reductions in the odds of death (-23% and -30%, respectively). No conclusion could be reached for patients who were less represented in the studies (ie, women and elderly persons). Patients with more complicated baseline clinical conditions (eg, congestive heart failure) had little nonsignificant benefit from cholesterol-lowering interventions. CONCLUSIONS: The effect of cholesterol-lowering interventions at least in the secondary prevention of coronary heart disease can be considered as established, but the transferability of such results to real-life patients remains the critical, unanswered question.

Meta-analysis: its role in medical research and in assessment of the association between low levels of cholesterol and excess mortality
O'Brien, P. C. (1993), Mayo Clin Proc 68(1): 91-3.

Metabolic and behavioral covariates of high-density lipoprotein cholesterol and triglyceride concentrations in postmenopausal women
Laws, A., A. C. King, et al. (1993), J Am Geriatr Soc 41(12): 1289-94.
Abstract: OBJECTIVE: To determine predictors of high-density lipoprotein cholesterol (HDL) and triglyceride (TG) concentrations in postmenopausal women. DESIGN: Cross-sectional study. SETTING: Clinical research facility. PARTICIPANTS: One hundred twenty-seven healthy, relatively sedentary, postmenopausal women not on estrogen replacement, mean age 57 years. MEASUREMENTS: Alcohol intake, cigarette smoking, aerobic fitness (VO2max), body mass index (BMI), percent body fat, waist-hip ratio, lipids and lipoproteins, fasting plasma glucose (FPG), and insulin (FPI) concentrations. RESULTS: In univariate analyses, HDL was significantly (P < 0.05) inversely related to BMI, waist-hip ratio, smoking, FPG, and FPI, and directly related to VO2max and alcohol intake. Triglycerides were related directly to BMI, waist-hip ratio, percent body fat, FPG, and FPI, and inversely to VO2max. In stepwise multiple regressions, BMI, waist-hip ratio, alcohol, smoking, and FPG were significantly associated with HDL (R2 for the model = 0.43). Addition of TG to these models reduced relations of BMI and waist-hip ratio, but not the other variables, to insignificance. For triglycerides, waist-hip ratio, alcohol, smoking, FPG, and FPI were significant predictors (R2 = 0.33). VO2max and percent body fat did not contribute to any model. CONCLUSIONS: Obesity, abdominal obesity, smoking, alcohol intake, and measures of carbohydrate metabolism predict HDL and triglyceride concentrations in postmenopausal women.

Metabolic and functional properties of cholesterol-poor platelets
Del Principe, D., A. Menichelli, et al. (1991), Ann N Y Acad Sci 623: 437-40.

Metabolic and genetic control of HDL cholesterol levels
Tall, A. R. (1992), J Intern Med 231(6): 661-8.
Abstract: Variation of HDL cholesterol levels in man shows a strong inverse relationship to the incidence of atherosclerotic vascular disease. Thus the regulation of HDL cholesterol levels has been the subject of intense investigation. Human genetic differences in cholesteryl ester transfer protein and hepatic lipase illustrate the importance of these factors in the normal catabolism of HDL, while metabolic and population studies show that lipoprotein lipase activity plays a central role in the transfer of lipids and apoproteins into HDL. Metabolic turnover studies in humans suggest that variations in the fractional catabolism of the HDL structural proteins, apoA-I and apoA-II, account for much of the variation of HDL levels in human populations. Although the catabolism of these apolipoproteins is poorly understood, changes in the core lipid composition of HDL may lead to changes in catabolism of the HDL proteins. The core lipid composition of HDL appears to be determined by lipid transfer processes, and the activities of lipoprotein and hepatic lipase. Thus many genetic and environmental factors that influence HDL levels appear to operate by changing the activities of the lipases or the lipid transfer process.

Metabolic and hormonal profiles: HDL cholesterol as a plausible biomarker of breast cancer risk. The Norwegian EBBA Study
Furberg, A. S., G. Jasienska, et al. (2005), Cancer Epidemiol Biomarkers Prev 14(1): 33-40.
Abstract: Low serum high-density lipoprotein cholesterol (HDL-C) is an important component of the metabolic syndrome and has recently been related to increased breast cancer risk in overweight and obese women. We therefore questioned whether serum HDL-C might be a biologically sound marker of breast cancer risk. We obtained cross-sectional data among 206 healthy women ages 25 to 35 years who participated in the Norwegian EBBA study. We included salivary ovarian steroid concentrations assessed by daily samples throughout one entire menstrual cycle, metabolic profile with measures of adiposity body mass index (BMI) and truncal fat percentage, serum concentrations of lipids and hormones (insulin, leptin, testosterone, dehydroepiandrostendione sulfate, insulin-like growth factor-I, and its principal binding protein), and mammographic parenchymal pattern. We examined how components of the metabolic syndrome, including low serum HDL-C, were related to levels of hormones, and free estradiol concentration in particular, and studied predictors of mammographic parenchymal patterns in regression models. In women with BMI > or = 23.6 kg/m(2) (median), overall average salivary estradiol concentration dropped by 2.4 pmol/L (0.7 pg/mL; 13.2% change in mean for the total population) by each 0.33 mmol/L (12.8 mg/dl; 1SD) increase in serum HDL-C (P = 0.03; P(interaction) = 0.03). A subgroup of women characterized by both relatively high BMI (> or =23.6 kg/m(2)) and high serum LDL-C/HDL-C ratio (> or = 2.08; 75 percentile) had substantially higher levels of salivary estradiol by cycle day than other women (P = 0.001). BMI was the strongest predictor of overall average estradiol with a direct relationship (P< 0.001). Serum HDL-C was inversely related to serum leptin, insulin, and dehydroepiandrostendione sulfate (P < 0.001, P < 0.01, and P < 0.05, respectively). There was a direct relationship between breast density and healthy metabolic profiles (low BMI, high serum HDL-C; P < 0.001) and salivary progesterone concentrations (P < 0.05). Our findings support the hypothesis that low serum HDL-C might reflect an unfavorable hormonal profile with, in particular, increased levels of estrogens and gives further clues to biomarkers of breast cancer risk especially in overweight and obese women.

Metabolic basis of cholesterol gallstone disease
Cooper, A. D. (1991), Gastroenterol Clin North Am 20(1): 21-46.
Abstract: Our understanding of the fundamental processes that control cholesterol and bile salt homeostasis is expanding rapidly; however, there are still large gaps in our knowledge, particularly regarding the mechanism of bile formation and the control of biliary lipid secretion. Defects in bile salt secretion, differences in the relative proportion of various bile salts, and an increased rate of cholesterol secretion have all been found to lead to the formation of lithogenic bile. As our understanding of these processes increases, better strategies for the prevention and treatment of gallstones will emerge.

Metabolic cholesterol depletion hinders cell-surface trafficking of the nicotinic acetylcholine receptor
Pediconi, M. F., C. E. Gallegos, et al. (2004), Neuroscience 128(2): 239-49.
Abstract: The effects of metabolic inhibition of cholesterol biosynthesis on the trafficking of the nicotinic acetylcholine receptor (AChR) to the cell membrane were studied in living CHO-K1/A5, a Chinese hamster ovary clonal line that heterologously expresses adult alpha2betadeltaepsilon mouse AChR. To this end, we submitted CHO-K1/A5 cells to long-term cholesterol deprivation, elicited by Mevinolin, a potent inhibitor of 3-hydroxy-3-methyl-glutaryl-CoA reductase and applied a combination of biochemical, pharmacological and fluorescence microscopy techniques to follow the fate of the AChR. When CHO-K1/A5 cells were grown for 48 h in lipid-deficient medium supplemented with 0.5 microM Mevinolin, total cholesterol was significantly reduced (40%). Concomitantly, the maximum number of binding sites (Bmax) of the cell-surface AChR for the competitive antagonist alpha-bungarotoxin was reduced from 647+/-30 to 352+/-34 fmol/mg protein, i.e. by 46%. The apparent dissociation constant (Kdapp) for alpha-bungarotoxin of the AChRs remaining at the cell surface was not modified by cholesterol depletion. Similarly, the half-concentration inhibiting the specific binding of the radioligand (IC50) for another competitive antagonist, d-tubocurarine, did not differ from that in control cells. The decrease in cell-surface AChR was paralleled by an increase in intracellular AChR levels, which rose from 44+/-2.1% in control cells to 74+/-3.3% in Mevinolin-treated cells. When analyzed by wide-field fluorescence microscopy, the fluorescence signal arising from alpha-bungarotoxin labeled cell-surface AChRs was reduced by approximately 70% in Mevinolin-treated cells. The distribution of intracellular AChR also changed: Alexa594-alpha-bungarotoxin-labeled AChR exhibited a highly compartmentalized pattern, concentrating at the perinuclear and Golgi-like regions. Temperature-arrest of protein trafficking magnified this effect, emphasizing the Golgi localization of the AChR. Colocalization studies using the transiently expressed fluorescent trans-Golgi/trans-Golgi network marker pEYFP/human beta1,4-galactosyltransferase and the trans-Golgi network marker syntaxin 6 provided additional support for the Golgi localization of intracellular AChRs. The low AChR cell-surface expression and the increase in intracellular AChR pools in cholesterol-depleted cells raise the possibility that cholesterol participates in the trafficking of the receptor protein to the plasmalemma and its stability at this surface location.

Metabolic effects of converting enzyme inhibitors: focus on the reduction of cholesterol and lipoprotein(a) by fosinopril
Schlueter, W., T. Keilani, et al. (1993), Am J Cardiol 72(20): 37H-44H.
Abstract: It is generally believed that the use of angiotensin-converting enzyme (ACE) inhibitors has no effect on the lipid profile. Our recent data show that in patients with proteinuric renal disease, serum levels of total cholesterol and lipoprotein(a) Lp(a) may be lowered during treatment with an ACE inhibitor, fosinopril sodium. During a 12-week randomized, placebo-controlled, double-blind study involving 26 patients with mild-to-moderate renal impairment, fosinopril administration was associated with significant decreases in both urinary protein excretion and serum total cholesterol levels, whereas placebo was not. During a 6-week washout phase, both parameters returned to baseline in fosinopril-treated patients and remained unchanged in placebo recipients. In addition, fosinopril-treated patients had a decrease in plasma levels of Lp(a), whereas this was not seen in placebo-treated patients. When data from a subset of 13 patients with proteinuric renal disease and hypertension were examined, a significant decrease in serum total cholesterol levels was observed; this decrease reversed after discontinuation of fosinopril. Analysis of the effect of fosinopril on plasma Lp(a) levels in a subset of patients who had type II diabetes mellitus and overt proteinuria revealed a significant decrease in plasma Lp(a) after administration of fosinopril. Moreover, fosinopril lowered plasma Lp(a) levels in blacks, whose pretreatment levels were higher than those of whites with comparable degrees of proteinuria and levels of serum total cholesterol. Thus, the reduction in serum Lp(a) levels may be related not only to amelioration of proteinuria, but also to another direct action of fosinopril on the metabolism of Lp(a).

Metabolic factors clustering, lipoprotein cholesterol, apolipoprotein B, lipoprotein (a) and apolipoprotein E phenotypes in premature coronary artery disease in French Canadians
Weber, M., S. McNicoll, et al. (1997), Can J Cardiol 13(3): 253-60.
Abstract: Plasma lipoprotein cholesterol abnormalities, diabetes, hypertension and smoking have all been identified as independent predictors of cardiovascular events. Clustering of multiple risk factors suggests a common metabolic link among high blood pressure, insulin resistance, plasma lipoprotein abnormalities and obesity. New guidelines for the management of dyslipidemias target patients with established coronary artery disease (CAD), and high risk patients with multiple risk factors and severe genetic lipoprotein disorders, such as familial hypercholesterolemia. To determine the prevalence of lipoprotein, apolipoprotein and metabolic disorders in premature CAD, 243 men and 61 women with premature CAD (occurring before age 60 years) and 203 age- and sex-matched controls (152 men, 61 women) were studied. After correcting for beta-blocker use (40% of men and 54% of women), hypertension and diabetes were seen more frequently in CAD patients than in controls. In men and women, cholesterol, triglycerides, low density lipoprotein (LDL) cholesterol, apolipoprotein B and lipoprotein (a) were significantly higher, and high density lipoprotein (HDL) cholesterol was lower, in CAD patients than in controls. By stratifying patients according to LDL cholesterol: HDL cholesterol ratio (5 or less, or greater than 5) and by triglyceride levels (less than 2.3 mmol/L, or 2.3 mmol/L or greater), significantly more men and women with CAD were found to have an elevated LDL cholesterol:HDL cholesterol ratio and elevated triglycerides (13.8% versus 1.9%, men and women combined, CAD versus controls, P < 0.0001). A metabolic factor index was devised, assigning a score of 1 each for presence of hypertension, lipoprotein abnormalities, diabetes or fasting blood glucose above 7.0 mmol/L, and a body mass index of 27 or greater. The prevalence of a metabolic factor index of 3 or more was 29.2% in CAD men versus 6.7% in controls (P < 0.0001) and 38.3% in CAD women versus 11.7% in controls (P < 0.01). Familial hypercholesterolemia was seen in fewer than 5% of patients with premature CAD and type III dyslipoproteinemia in one of 343 CAD patients. The distribution of apolipoprotein E phenotypes was the same in CAD patients and controls. Multivariate analysis revealed that in men, HDL cholesterol, lipoprotein (a) levels and smoking were the best predictors of risk. In men, plasma levels of LDL cholesterol, triglycerides or body mass index did not enter the model at the P < 0.05 level. In women, low HDL cholesterol, lipoprotein (a), the presence of diabetes, smoking and apolipoprotein B levels were all predictors of risk (P < 0.05). However, the clustering of risk factors may be the best predictor of risk. In this selected population, HDL and lipoprotein (a) are the best metabolic markers of premature CAD; metabolic factor clustering is common in patients with premature CAD.

Metabolic fate of pancreas-derived cholesterol esterase in intestine: an in vitro study using Caco-2 cells
Huang, Y. and D. Y. Hui (1990), J Lipid Res 31(11): 2029-37.
Abstract: Bile salt-stimulated cholesterol esterase is synthesized in the pancreatic acinar cells and is released into the intestinal lumen where it catalyzes cholesterol absorption. In the current study, Caco-2 cells were used as an in vitro model to study the interaction between the pancreatic cholesterol esterase with intestinal cells. Results showed that addition of increasing concentrations of cholesterol esterase in the incubation medium increased the uptake of micellar cholesteryl oleate by Caco-2 cells. The cholesterol esterase also increased the cellular uptake of the nonhydrolyzable cholesteryl linoleoyl ether. However, maximum uptake of the cholesteryl ether analog was 50% of that for cholesteryl oleate. The initial interaction of cholesterol esterase with Caco-2 cells was mediated by binding of the protein to a low affinity and high capacity binding site on the cell surface. Cholesterol esterase bound to the cell surface could be internalized via a monensin-sensitive mechanism. The cholesterol esterase taken up by the cells had a short residence time and was either degraded or was rapidly re-secreted from the cells. Chloroquine had no effect on the degradation or re-secretion of cholesterol esterase by Caco-2 cells, indicating that lysosomes were not involved with these processes. The cholesterol esterase taken up by the cells was not available to mediate further cholesterol uptake. These results indicated that the bile salt-stimulated cholesterol esterase secreted from pancreas could facilitate intestinal lipid absorption only transiently. The data suggest that the regulation of cholesterol esterase synthesis and secretion by the pancreas may be important for regulation of cholesterol absorption.

Metabolic heterogeneity associated with high plasma triglyceride or low HDL cholesterol levels in men
Lamarche, B., J. P. Despres, et al. (1993), Arterioscler Thromb 13(1): 33-40.
Abstract: To further understand the factors involved in the regulation of high plasma triglyceride (TG) or low plasma high density lipoprotein cholesterol (HDL-C) levels, three groups of male subjects (normal TG with low HDL-C levels, high TG with normal HDL-C levels, and high TG with low HDL-C levels) were compared with a sample of normolipemic men with normal TG and HDL-C plasma levels. Mean age was 34 years (range, 20-42 years), and none of the subjects had plasma TG levels > 4.0 mmol/l or familial hypercholesterolemia. Both groups of subjects with high TG levels had a higher body mass index, waist circumference, waist-to-hip circumferences ratio, and a higher ratio of abdominal to femoral adipose tissue areas as measured by computed tomography when compared with normolipemic control subjects. However, during an oral glucose tolerance test only high TG-low HDL-C men had fasting hyperinsulinemia and higher plasma insulin levels compared with normolipemic subjects. In addition, the high TG-low HDL-C group showed reduced HDL apoprotein (apo) A-I levels and a low HDL2-C/HDL3-C ratio. These changes were observed along with a nonsignificant trend for a lower plasma postheparin lipoprotein lipase activity. However, among subjects with high TG and normal HDL-C levels, no evidence of insulin resistance or of a reduction in postheparin lipoprotein lipase activity was observed, suggesting that the high plasma TG levels could be attributed to an increased production of apo B-containing lipoproteins, as high plasma apo B and low density lipoprotein (LDL)-apo B levels were observed in this group.(ABSTRACT TRUNCATED AT 250 WORDS)

Metabolic heterogeneity underlying postprandial lipemia among men with low fasting high density lipoprotein cholesterol concentrations
Couillard, C., N. Bergeron, et al. (2000), J Clin Endocrinol Metab 85(12): 4575-82.
Abstract: The high triglyceride (TG) and low high density lipoprotein (HDL) cholesterol dyslipidemia has been associated with increased postprandial lipemia. Although fasting TG is a powerful predictor of postprandial hyperlipidemia, the role of hypoalphalipoproteinemia in postprandial TG metabolism is uncertain. We have studied postprandial lipemia among 63 men with low fasting plasma HDL cholesterol concentrations (<0.9 mmol/L), but with either low (<2.0 mmol/L) or high (>2.0 mmol/L) fasting plasma TG levels. A significant relationship was noted between postprandial TG response and fasting HDL cholesterol concentration (r = -0.43; P: < 0.0005). We also found that men with high TG/low HDL dyslipidemia (high TG and low HDL cholesterol; n = 16) were characterized by abdominal obesity as well as increased visceral adipose tissue accumulation, whereas normolipidemic controls (low TG and high HDL cholesterol; n = 26) and men with isolated low HDL cholesterol concentrations (low TG and low HDL cholesterol; n = 17) were not characterized by features of the insulin resistance syndrome (visceral obesity, hyperinsulinemia, and hypertriglyceridemia). Although controls and men with isolated low HDL cholesterol levels had similar postprandial lipemic responses, men with the high TG/low HDL dyslipidemia had a marked increase in their postprandial TG responses to the fat load compared with the other subgroups (P: < 0. 001). Men with the high TG/low HDL dyslipidemia were also characterized by higher concentrations of apolipoprotein (apo) B-48 and B-100 particles (chylomicron remnants and very low density lipoproteins, respectively) before and during the postprandial period compared with the other subjects. These results suggest that low HDL cholesterol concentration is a heterogeneous metabolic phenotype that it is not associated with postprandial hyperlipidemia unless accompanied by other features of the insulin resistance syndrome.

Metabolic inhibition of cardiomyocytes causes an increase in sarcolemmal fluidity which may be due to loss of cellular cholesterol
Bastiaanse, E. M., D. E. Atsma, et al. (1995), Arch Biochem Biophys 319(2): 350-4.
Abstract: We examined whether metabolic inhibition (5 mM NaCN + 10 mM 2-deoxyglucose) affects sarcolemmal fluidity in cultured neonatal cardiomyocytes. As a measure of sarcolemmal fluidity we determined the fluorescence steady-state anisotropy (rss, which is reciprocally related to membrane fluidity) of cardiomyocytes labeled with 1-(4-trimethylammoniumphenyl)-6-phenyl-1,3,5-hexatriene, p-toluenesulfonate. During metabolic inhibition, membrane fluidity increased progressively: after 30 min rss had fallen by 6.7 +/- 1.2% (mean +/- SE; n = 9; P < 0.05) compared to baseline values, and after 90 min by 14.5 +/- 3.5% (P < 0.05; n = 5). Beyond 90 min rss did not decrease any further. During control incubations (without metabolic inhibition), no significant changes in rss were observed. During metabolic inhibition cellular free cholesterol content declined: after 30 min free cholesterol content had decreased by 12.2 +/- 3.1% (P < 0.02; n = 4), compared to baseline values, and after 90 min by 31.1 +/- 8.3% (P < 0.02; n = 4). We conclude that metabolic inhibition induces an increase in sarcolemmal fluidity, which may be caused by a decrease in sarcolemmal free cholesterol content.

Metabolic mechanisms for responses to dietary cholesterol and fat in high and low LDL responding baboons (Papio sp.)
Kushwaha, R. S., C. A. Reardon, et al. (1994), J Lipid Res 35(4): 633-43.
Abstract: These studies were conducted to determine how plasma low density lipoprotein (LDL) cholesterol levels respond to dietary cholesterol, fed in increasing amounts with either corn oil or coconut oil diets, in high as compared to low LDL responding baboons; and to determine how apolipoprotein (apo) B transcription levels are modulated in response to dietary lipids. Eight high and eight low LDL responding pedigreed adult baboons, balanced for sire, age, sex, and weight, were challenged for successive 7-week periods with increasing levels of dietary cholesterol combined with either coconut oil or corn oil. At the end of each dietary period, plasma and lipoprotein lipids, apoB, apoA-I, and hepatic mRNA levels for apolipoproteins were measured. As dietary cholesterol increased, plasma cholesterol concentrations (mostly LDL cholesterol) increased in both phenotypes and with both types of fat, but phenotypic differences were greater with coconut oil. There was not a consistent dose-response relationship of plasma or LDL cholesterol levels to increasing intakes of dietary cholesterol. Neither dietary cholesterol, type of dietary fat, nor LDL phenotype affected hepatic apoB or apoE mRNA levels. In a second experiment to resolve the inconsistent dose-response to dietary cholesterol, we fed the animals varying levels of dietary cholesterol combined with coconut oil, and separated the challenge periods with intervening 12-week chow periods. Plasma and LDL cholesterol and apoB concentrations rose consistently with increasing dietary cholesterol, and the slope of the increase diminished at the higher doses. The results suggest that genetic differences in the initial response of LDL cholesterol to dietary cholesterol and saturated fatty acids are not due to the differences in hepatic transcription of apoB, and that the preceding dietary intake of cholesterol and saturated fatty acids is a major determinant of the response of plasma lipids and the associated metabolic processes to a dietary challenge. The response of baboon plasma LDL cholesterol concentrations to dietary cholesterol, when fed with saturated fatty acids, is similar to that of humans.

Metabolic profile of pre-pregnancy, pregnancy and early lactation in multiple lambing Sakiz ewes. 2. Changes in plasma progesterone, estradiol-17beta and cholesterol levels
Ozpinar, A. and A. Firat (2003), Ann Nutr Metab 47(3-4): 139-43.
Abstract: Twenty synchronized Sakiz ewes (aged 3-4 years) were used in this study. Blood samples were taken once in pre-pregnancy and at the 100th day of pregnancy. At the 120th day of pregnancy and the 10th day postpartum, blood samples were collected every 2 h for 24 h from 10 ewes. Plasma progesterone and estradiol-17beta levels were estimated by radioimmunoassay. Plasma cholesterol levels were determined by colorimetric method. Plasma progesterone levels increased during pregnancy and especially late pregnancy and decreased to basal values during lactation. Plasma estradiol-17beta and cholesterol levels were not significantly different between pre-pregnancy, pregnancy and early lactation periods. The insignificant rise in plasma cholesterol during pregnancy showed that pregnancy toxemia may not occur in multiple lambing ewes when fed a balanced diet sufficient in energy and protein levels. The increased plasma progesterone level above normal observed during pregnancy and especially late pregnancy may be interpreted as a feature of multiple lambing breeds.

Metabolic syndrome: major impact on coronary risk in a population with low cholesterol levels--a prospective and cross-sectional evaluation
Onat, A., K. Ceyhan, et al. (2002), Atherosclerosis 165(2): 285-92.
Abstract: The prevalence and the excess coronary heart disease (CHD) risk of the metabolic syndrome (MS) and its components were investigated in the Turkish Adult Risk Factor Study in both a prospective and a cross-sectional manner. In a population sample, representative of Turkish adults who have low levels of high- and low-density lipoprotein-cholesterol (HDL-C and LDL-C), MS was identified in conformity with the definition used in the recent NCEP guidelines. Prospective analysis was based on 2398 men and women (mean age at baseline 49.1+/-13 years) who had a baseline examination in 1997/98 and were followed-up for a mean of 3 years. CHD was diagnosed based on clinical findings and Minnesota coding of resting electrocardiograms. Fatal and nonfatal CHD developed in 126 subjects. 27% of men and 38.6% of women were found to have MS at baseline examination. When adjusted for age, MS was an independent predictor of subsequent overall fatal and nonfatal CHD in both genders, displaying an RR of 1.71. At the final cross-sectional evaluation, coronary risk associated with MS in men was primarily accounted for by standard MS components (largely inherent in glucose intolerance, hypertension and in a surrogate of small, dense LDL particles), in addition to a minor independent contribution by C-reactive protein (CRP). In women with MS, a substantial residual coronary risk remained after controlling for five components, which was partly accounted for by levels of LDL-C and CRP. It was estimated that MS was the culprit in just over half the cases of CHD in Turkey. CONCLUSION: MS was the major determinant of CHD risk in a population having generally low levels of HDL-C and LDL-C in middle-aged and elderly adults, extending to three out of every eight adults, and imposing an overall excess CHD risk of approximately 70%. In contrast to men, a substantial residual coronary risk is retained in Turkish women after controlling for five MS components.

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