| For medical practitioners and the general public - Cholesterol Journal Article Catalog. |
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| Jejunal limb obstruction caused by a cholesterol stone 15 years after a total gastrectomy and 20 years after a cholecystectomy: report of a case Wada, N., M. Seki, et al. (2000), Surg Today 30(2): 181-4. Abstract: We present herein the rare case of a 74-year-old woman found to have jejunal limb obstruction caused by a cholesterol stone 15 years after a total gastrectomy with Roux-en-Y anastomosis, and 20 years after a cholecystectomy. The patient complained of repeated episodes of upper abdominal distress on three separate occasions over a period of 20 months, and jejunal limb obstruction was diagnosed by abdominal computed tomography scanning and (99m)Tc scintigraphy. Surgery revealed a stone incarcerated in the jejunal limb, where the anastomosis had become slightly stenotic. The removed stone was 3.5 cm in diameter and was subsequently demonstrated to be a cholesterol stone by chemical analysis. This report is thought to be the first to describe jejunal limb obstruction caused by a gallstone incarcerated in the jejunal limb after a total gastrectomy in a patient with a history of cholecystectomy. |
| Joe Goldstein and Mike Brown: from cholesterol homeostasis to new paradigms in membrane biology Anderson, R. G. (2003), Trends Cell Biol 13(10): 534-9. Abstract: Joe Goldstein and Mike Brown have worked for over 30 years on the molecular basis of cholesterol homeostasis. Through the systematic use of genetics, biochemistry, molecular biology and cell biology, they have identified a complex set of interacting molecules that work coordinately to regulate cholesterol import and synthesis. Not only did they identify the crucial proteins in this pathway but also determined their function. An unexpected outcome of their work has been a new understanding of the structure and function of cell membranes. From the low-density lipoprotein receptor to sterol regulatory element binding protein (SREBP) to SREBP cleavage-activating protein to Insig-1, each protein has provided a new and fundamentally novel insight into how membranes function as molecular sensors that respond to changes in the metabolic condition of the cell by moving molecules between cellular compartments.* |
| Joint distribution of non-HDL and LDL cholesterol and coronary heart disease risk prediction among individuals with and without diabetes Liu, J., C. Sempos, et al. (2005), Diabetes Care 28(8): 1916-21. Abstract: OBJECTIVE: To assess coronary heart disease (CHD) risk within levels of the joint distribution of non-HDL and LDL cholesterol among individuals with and without diabetes. RESEARCH DESIGN AND METHODS: We used four publicly available data sets for this pooled post hoc analysis and confined the eligible subjects to white individuals aged > or = 30 years and free of CHD at baseline (12,660 men and 6,721 women). Diabetes status was defined as either "reported by physician-diagnosed and on medication" or having a fasting glucose level > or = 126 mg/dl at the baseline examination. The primary end point was CHD death. Within diabetes categories, risk was assessed based on lipid levels (in mg/dl): non-HDL <130 and LDL <100 (group 1); non-HDL <130 and LDL > or = 100 (group 2); non-HDL > or = 130 and LDL <100 (group 3); and non-HDL > or = 130 and LDL > or = 100 (group 4). Group 1 within those without diabetes was the overall reference group. RESULTS: Of the subjects studied, approximately 6% of men and 4% of women were defined as having diabetes. A total of 773 CHD deaths occurred during the average 13 years of follow-up time. A Cox proportional hazard model was used to estimate the relative risk (RR) of CHD death. Those with diabetes had a 200% higher RR than those without diabetes. In a multivariate model, CHD risk in those with diabetes did not increase with increasing LDL, whereas it did increase with increasing non-HDL: RR (95% confidence interval) for group 1: 5.7 (2.0-16.8); group 2: 5.7 (1.6-20.7); group 3: 7.2 (2.6-19.8); and group 4: 7.1 (3.7-13.6). CONCLUSIONS: Non-HDL is a stronger predictor of CHD death among those with diabetes than LDL and should be given more consideration in the clinical approach to risk reduction among diabetic patients. |
| Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study. Implications for treatment Manninen, V., L. Tenkanen, et al. (1992), Circulation 85(1): 37-45. Abstract: BACKGROUND. We studied the joint effect of baseline triglyceride and lipoprotein cholesterol levels on the incidence of cardiac end points in the trial group (n = 4,081) of the Helsinki Heart Study, a 5-year randomized coronary primary prevention trial among dyslipidemic middle-aged men. The relative risks (RR) were calculated using Cox proportional hazards models with a dummy variable technique that allows simultaneous study of subgroup combinations from the placebo and treatment groups. METHODS AND RESULTS. In the placebo group (n = 2,045), the low density lipoprotein cholesterol (LDL-C)/high density lipoprotein cholesterol (HDL-C) ratio was the best single predictor of cardiac events. This ratio in combination with the serum triglyceride level revealed a high-risk subgroup: subjects with LDL-C/HDL-C ratio greater than 5 and triglycerides greater than 2.3 mmol/l had a RR of 3.8 (95% CI, 2.2-6.6) compared with those with LDL-C/HDL-C ratio less than or equal to 5 and triglyceride concentration less than or equal to 2.3 mmol/l. In subjects with triglyceride concentration greater than 2.3 mmol/l and LDL-C/HDL-C ratio less than or equal to 5, RR was close to unity (1.1), whereas in those with triglyceride level less than or equal to 2.3 mmol/l and LDL-C/HDL-C ratio greater than 5, RR was 1.2. The high-risk group with LDL-C/HDL-C ratio greater than 5 and triglyceride level greater than 2.3 mmol/l profited most from treatment with gemfibrozil, with a 71% lower incidence of coronary heart disease events than the corresponding placebo subgroup. In all other subgroups, the reduction in CHD incidence was substantially smaller. CONCLUSIONS. Serum triglyceride concentration has prognostic value, both for assessing coronary heart disease risk and in predicting the effect of gemfibrozil treatment, especially when used in combination with HDL-C and LDL-C. |
| Joint effects of serum triglycerides and LDL and HDL cholesterol Avins, A. L. and S. B. Hulley (1993), Circulation 87(1): 300-1. |
| Joint role of non-HDL cholesterol and glycated haemoglobin in predicting future coronary heart disease events among women with type 2 diabetes Schulze, M. B., I. Shai, et al. (2004), Diabetologia 47(12): 2129-36. Abstract: AIMS/HYPOTHESIS: Non-HDL cholesterol (the sum of LDL, VLDL and IDL cholesterol) is considered to be particularly valuable in the management of dyslipidaemia in type 2 diabetes. However, it remains uncertain whether the association between non-HDL cholesterol and cardiovascular risk in type 2 diabetes depends on the status of hyperglycaemia. We aimed to determine whether non-HDL cholesterol predicts CHD events among diabetic women independently of currently established risk factors and the status of glycaemic control. METHODS: We prospectively followed 921 diabetic women in the Nurses' Health Study, who were free of cardiovascular disease at the time that blood was drawn in 1989/90. During 10 years of follow-up, we identified 122 incident CHD cases. RESULTS: After adjustment for age, BMI, smoking, alcohol consumption, and other lifestyle risk factors, the multivariate relative risks (RRs) of CHD for extreme quartiles were 1.97 (95% CI: 1.14-3.43) for non-HDL cholesterol, 1.78 (1.02-3.11) for apolipoprotein B-100, and 1.93 (1.15-3.22) for LDL cholesterol. However, the association between non-HDL cholesterol and CHD risk was only apparent among women with elevated fasting triglycerides (RR for extreme quartiles: 3.80; p=0.045). HbA(1)c was strongly associated with increased CHD risk (RR for increase by 1 unit: 1.24; 95% CI: 1.13-1.35), and both non-HDL cholesterol and HbA(1)c additively predicted CHD risk (RR for the combination of high non-HDL cholesterol and high HbA(1)c tertiles: 4.59). CONCLUSIONS/INTERPRETATION: Our study suggests that non-HDL cholesterol and HbA(1)c are potent predictors of CHD risk in diabetic women. Therapies to lower CHD risk in diabetic patients should emphasise both glycaemic control and lipid lowering. |
| Justification and imperatives of the campaign against excess cholesterol and prevention of atherosclerosis de Gennes, J. L. (1993), Bull Acad Natl Med 177(4): 597-608; discussion 609-11. Abstract: Recently, violent attacks have been orchestrated, by various media and the press against medical action, via diet or drug therapy, on excess cholesterol, in order to improve primary or secondary cardiovascular prevention. The amplitude of this campaign implies a dangerous risk of a deleterious effects both on the public and on medical guidelines. The opportunity for open discussion of this question, and of a clear reply, appears to be highly desirable for all concerned. Although it is quite true that total blood cholesterol levels in excess of 200 mg/dl (5.2 mmol/l) are not automatically dangerous, they nonetheless require complete profiling of cholesterol distribution among the different fractions and, if possible, a complementary study of ApoB, ApoA1 and Lpa fractions. It must be recalled that even modest rises in total cholesterol (250 +/- 30 mgs/dl) can be atherogenic, and particularly, when present in the non-HDL fractions, and involving a low HDL Cholesterol level (< 36 mg/dl or 0.9 mmol/l). In all these cases, the associated determination of triglyceride levels is absolutely necessary. Moreover these modest rises in cholesterol have to take into account the possible association of other risk factors, such as hypertension, cigarette smoking, diabetes, obesity and. hyperfibrinogemia. The claims of the natural protection of French people against atherosclerosis and of the irrelevance of precocious cholesterol screening, then finally of non-demonstrated benefits of such prevention, with respect to other risks due to diet or drug treatment of cholesterol disorders must be precisely rediscussed and clarified. The crucial importance of the maintenance of our present efforts in cardiovascular prevention for clinicians, concerned patients, and the general public, must be especially stressed. |
| Karl Popper and the cholesterol hypothesis Ravnskov, U. (2004), Tidsskr Nor Laegeforen 124(19): 2517. |
| Kefir consumption does not alter plasma lipid levels or cholesterol fractional synthesis rates relative to milk in hyperlipidemic men: a randomized controlled trial ISRCTN10820810 St-Onge, M. P., E. R. Farnworth, et al. (2002), BMC Complement Altern Med 2: 1. Abstract: BACKGROUND: Fermented milk products have been shown to affect serum cholesterol concentrations in humans. Kefir, a fermented milk product, has been traditionally consumed for its potential health benefits but has to date not been studied for its hypocholesterolemic properties. METHODS: Thirteen healthy mildly hypercholesterolemic male subjects consumed a dairy supplement in randomized crossover trial for 2 periods of 4 wk each. Subjects were blinded to the dairy supplement consumed. Blood samples were collected at baseline and after 4 wk of supplementation for measurement of plasma total, low-density lipoprotein, and high-density lipoprotein cholesterol and triglyceride concentrations, as well as fatty acid profile and cholesterol synthesis rate. Fecal samples were collected at baseline and after 2 and 4 wk of supplementation for determination of fecal short chain fatty acid level and bacterial content. RESULTS: Kefir had no effect on total cholesterol, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol or triglyceride concentrations nor on cholesterol fractional synthesis rates after 4 wk of supplementation. No significant change on plasma fatty acid levels was observed with diet. However, both kefir and milk increased (p < 0.05) fecal isobutyric, isovaleric and propionic acids as well as the total amount of fecal short chain fatty acids. Kefir supplementation resulted in increased fecal bacterial content in the majority of the subjects. CONCLUSIONS: Since kefir consumption did not result in lowered plasma lipid concentrations, the results of this study do not support consumption of kefir as a cholesterol-lowering agent. |
| Keishi-bukuryo-gan preserves the endothelium dependent relaxation of thoracic aorta in cholesterol-fed rabbit by limiting superoxide generation Sekiya, N., H. Goto, et al. (2002), Phytother Res 16(6): 524-8. Abstract: Formerly, we have reported that keishi-bukuryo-gan prevents the progression of atherosclerosis in cholesterol-fed rabbits and inhibits the free radical-induced RBC haemolysis in rats.The present study was performed to investigate how keishi-bukuryo-gan (KBG) inhibits the early stage of atherosclerosis. Plasma lipid concentration and hydroxyl radical generation during respiratory burst in neutrophils were evaluated at the start and end of the study. The protective effect of KBG against endothelium disorder due to hypercholesterolaemia was examined. Twelve male Japanese white rabbits (2 kg body weight) were divided into two groups. Group A (n = 6) was fed standard rabbit chow containing 1% cholesterol for 4 weeks. Group B (n = 6) was fed standard rabbit chow containing 1% cholesterol and 1% KBG for 4 weeks. In the plasma lipid concentration, only the lipid peroxide concentration of group A was significantly higher than that of group B. At the end of the study, DMPO-OH, the spin-trapped adduct of hydroxyl radicals generated by neutrophils, was increased in both groups, and this increase was marked in group B. Endothelium-dependent vasodilatation by acetylcholine increased significantly in group B compared with group A. Thus, KBG protects the vascular endothelium function by its antioxidative effect and by inhibiting the release of free radicals from neutrophils in vivo. |
| Keishi-bukuryo-gan prevents the progression of atherosclerosis in cholesterol-fed rabbit Sekiya, N., N. Tanaka, et al. (1999), Phytother Res 13(3): 192-6. Abstract: In this study, we examined whether in vivo keishi-bukuryo-gan (a Kampo formulation) could prevent the progression of atherosclerosis in cholesterol-fed rabbits, an animal model for hypercholesterolaemia. Sixteen male Japanese white rabbits (2 kg body weight) were divided into two groups. Group A (n = 8) was fed standard rabbit chow containing 1% cholesterol for 8 weeks. Group B (n = 8) was fed standard rabbit chow containing 1% cholesterol and 1% keishi-bukuryo-gan for 8 weeks. At the end of the experiment, average plasma concentrations of total-cholesterol and IDL-cholesterol were 2055.9 +/- 201.8 mg/dL and 408.1 +/- 62.6 mg/dL in group A and 1950.5 +/- 126.3 mg/dL and 407.6 +/- 56.6 mg/dL in group B, respectively. The percentage of the surface area of the total thoracic aorta with visible plaque was significantly reduced by keishi-bukuryo-gan administration; group A was 33.2% +/- 5.3% and group B was 14.3% +/- 2.9%. beta-very low density lipoprotein (VLDL) and low density lipoprotein (LDL) isolated from cholesterol fed rabbits treated with keishi-bukuryo-gan (group B) were shown to be highly resistant to oxidative modification by cupric ion. Sera isolated from rabbits administered keishi-bukuryo-gan had reduced lipid peroxide formation compared with those from rabbits without keishi-bukuryo-gan. Thus, keishi-bukuryo-gan prevents the progression of atherosclerosis in cholesterol-fed rabbits in vivo by limiting oxidative LDL modification. |
| Kids, cholesterol, carotids, and coronaries Weintraub, M. I. (1991), Jama 266(17): 2373-4. |
| Kinetic analysis of high-mobility-group proteins HMG-1 and HMG-I/Y binding to cholesterol-tagged DNA on a supported lipid monolayer Webster, C. I., M. A. Cooper, et al. (2000), Nucleic Acids Res 28(7): 1618-24. Abstract: High-mobility-group proteins HMG-1 and HMG-I/Y bind to multiple sites within a 268 bp A/T-rich enhancer element of the pea plastocyanin gene (PetE). Within a 31 bp region of the enhancer, the binding site for HMG-1 overlaps with the binding site for HMG-I/Y. The kinetics of binding and the affinities of HMG-1 and HMG-I/Y for the 31 bp DNA were determined using surface plasmon resonance. Due to very high non-specific interactions of the HMG proteins with a carboxymethyl-dextran matrix, a novel method using a cholesterol tag to anchor the DNA in a supported lipid monolayer on a thin gold film was devised. The phosphatidylcholine monolayer produced a surface that reduced background interactions to a minimum and permitted the measurement of highly reproducible protein-DNA interactions. The association rate constant (k (a)) of HMG-I/Y with the 31 bp DNA was approximately 5-fold higher than the rate constant for HMG-1, whereas the dissociation constant (K (D)) for HMG-I/Y (3.1 nM) was approximately 7-fold lower than that for HMG-1 (20.1 nM). This suggests that HMG-I/Y should bind preferentially at the overlapping binding site within this region of the PetE enhancer. |
| Kinetic studies and analytical application of cholesterol oxidase and peroxidase immobilized to synthetic polymer Yotova, L. K. and I. P. Ivanov (2000), Appl Biochem Biotechnol 87(2): 141-51. Abstract: A method for individual and simultaneous covalent immobilization of cholesterol oxidase and peroxidase to copolymer of acrylonitrile with acrylamide is described. The effect of immobilization on the catalytic properties of the covalently bound enzymes was studied. The immobilized enzymes showed no change in pH optima and an increase in temperature optima, activation energy, and Km' compared to data received from experiments with soluble enzymes. A small glass column packed with immobilized multienzyme complex was used to develop a method for manual determination of cholesterol in foodstuffs (e.g., in mayonnaise "Olinease"). The method was characterized by high analytical precision (coefficient of variation = 2.67%). The results show high correlation with those obtained by the Kageyama method (r = 0.986). The method is economical (the enzyme-carrier conjugate may be used more than 300 times), precise, easy to perform, and less time-consuming than the manual methods utilizing soluble enzymes. The established manual method can be proposed for cholesterol determination in foodstuffs. |
| Kinetic studies of cholesterol oxidation as inhibited by stearylamine during heating Chien, J. T., D. Y. Huang, et al. (2004), J Agric Food Chem 52(23): 7132-8. Abstract: The formation of cholesterol oxidation products (COPs) during heating in the presence of stearylamine at 140 degrees C was analyzed by high-performance liquid chromatography (HPLC) and kinetically studied by use of nonlinear regression models. Results indicated that the COPs concentration increased with increasing heating time, and stearylamine was shown to reduce both oxidation and degradation rates of cholesterol. Without stearylamine, the highest rate constant (per hour) was observed for epoxidation (545.4), followed by free radical chain reaction (251.0), reduction (147.3), dehydration (95.8), triol dehydrogenation (4.7), degradation (0.34), triol formation (0.31), and dehydrogenation (0.13). With stearylamine, the epoxidation and free radical chain reaction rates could be reduced by about 800- and 3.4-fold, respectively, and triol formation during oxidation could be completely inhibited. In addition, the reactions for reduction, dehydration, degradation, and dehydrogenation could proceed slower in the presence of stearylamine. The kinetic model developed in this study can be used to predict the inhibition of COPs formation by stearylamine during heating of cholesterol. |
| Kinetics and size of cholesterol lateral domains in synaptosomal membranes: modification by sphingomyelinase and effects on membrane enzyme activity Rao, A. M., U. Igbavboa, et al. (1993), Neurochem Int 23(1): 45-52. Abstract: Cholesterol domains and transport have been well-studied in non-neuronal membranes in contrast to neuronal membranes. The purpose of the experiments reported in this paper was to determine: (1) exchangeable and non-exchangeable cholesterol domains or pools were present in brain synaptosomal membranes; (2) effects of hydrolysis of sphingomyelin on cholesterol pools, that has previously been shown to alter membrane cholesterol in non-neuronal membranes and; (3) sphingomyelin hydrolysis and enzyme activity. Cholesterol pools were determined using cholesterol exchange between radiolabeled small unilamellar vesicles and mouse synaptosomes. Activity of Ca(2+)+Mg(2+)-ATPase and Na(+)+K(+)-ATPase were measured in synaptosomal membranes following treatment with sphingomyelinase. The size of the exchangeable pool of synaptosomal membrane cholesterol was approx 50% of total membrane cholesterol when measured at 37 degrees C. The t1/2 of cholesterol exchange at 37 degrees C in synaptosomes was approx 10 h. Lowering the incubation temperature to 25 degrees C, significantly reduced the size of the exchangeable pool and significantly increased the t1/2 of cholesterol exchange. Sphingomyelinase treatment of synaptosomes significantly slowed cholesterol exchange but did not modify the size of the exchangeable pool of cholesterol. Ca(2+)+Mg(2+)-ATPase activity was significantly inhibited by sphingomyelinase treatment as compared to Na(+)+K(+)-ATPase activity. Cholesterol domains were described in neuronal tissue and the size and kinetics of those pools were altered by temperature-induced changes in fluidity and hydrolysis of sphingomyelin. Sphingomyelinase-induced changes in Ca(2+)+Mg(2+)-ATPase activity were not affected by hydrolysis of sphingomyelin but appeared to be associated with a reduction in cytofacial phosphatidylinositol. |
| Kinetics of biliary secretion of chylomicron remnant cholesterol (esters) in the rat van Dijk, M. C., M. Pieters, et al. (1993), Eur J Biochem 211(3): 781-7. Abstract: Chylomicrons labelled with 3Hcholesterol/3Hcholesterol esters in a ratio of 25.5: 74.5, were rapidly removed from rat serum in vivo, and taken up predominantly by the parenchymal liver cells (88.2%) of the hepatic uptake at 15 min after injection). Lactoferrin reduced the liver uptake of chylomicron remnants by 72%, at 20 min after injection. It appeared that the free cholesterol which is present in the chylomicrons is not readily exchanged within the used time period with other cholesterol pools in the animal. Between 10-60 min after injection of 3H-labelled chylomicrons, cholesterol esters are hydrolysed in the liver. Appearance of radioactivity in bile was rapid and at 3, 24 and 72 h after injection, 13.4%, 44.0% and 70.0%, respectively, of the injected dose appeared in bile, mainly as bile acids (> 90%). Lactoferrin reduced the biliary secretion of radioactivity, especially during the first hour after injection. The total amount of radioactivity recovered was 58.0% of the injected dose at 72 h after injection. After injection of beta-migrating very low-density lipoprotein labelled with 3Hcholesterol/3Hcholesterol esters in a ratio of 23.5:76.5, the maximum amount of radioactivity secreted in bile was much lower than with chylomicrons (2.6% cf. 5.2% at 1 h after injection), although the kinetics of the initial liver association and cholesterol ester hydrolysis were even more rapid. Biliary accumulation of radioactivity was also lower with 50.5% of the injected dose recovered at 72 h after injection. It can be concluded from these studies that the processing of chylomicron remnant cholesterol components in the liver and the subsequent secretion in the bile mainly as bile acids is very efficient. The efficient liver uptake of chylomicron remnants by the liver remnant receptor is thereby essential to achieve this high percentage of removal, thus protecting against extrahepatic cholesterol (ester) deposition. |
| Kinetics of HDL cholesterol and paraoxonase activity in moderate alcohol consumers Sierksma, A., M. S. van der Gaag, et al. (2002), Alcohol Clin Exp Res 26(9): 1430-5. Abstract: BACKGROUND: The inverse association between moderate drinking and coronary heart disease mortality is well established. This study was performed to investigate the kinetics of the alcohol-induced increases in apo A-1, HDL cholesterol, and paraoxonase (PON) activity, as well as to study whether the alcohol-induced increases in PON activity differ within different PON polymorphisms, and to investigate whether moderate alcohol consumption has similar effects on the outcome measures in postmenopausal women as in middle-aged men. METHODS: In a randomized, diet-controlled, crossover study, 10 middle-aged men and 9 postmenopausal women, all apparently healthy, nonsmoking, and moderate alcohol drinkers, consumed beer or no-alcohol beer (control) with evening dinner during two successive periods of 3 weeks. During the beer period, alcohol intake equaled 40 and 30 g/day for men and women, respectively. The total diet was supplied to the subjects and had essentially the same composition during these 6 weeks. Before each treatment was a 1-week washout period, in which the subjects were not allowed to drink alcoholic beverages. RESULTS: Moderate alcohol consumption significantly increased serum apo A-I level after 5 days (3.7%, p < 0.05); after 10 days, serum HDL cholesterol level was increased (6.8%, p < 0.001), and after 15 days serum PON activity was increased (3.7%, p < 0.05), all compared with no alcohol consumption. Gene polymorphisms did not modulate the alcohol effect on PON. CONCLUSIONS: Serum apo A-I, HDL cholesterol, and PON activity were significantly increased during 3 weeks of moderate alcohol consumption as compared with no alcohol consumption. Moreover, the results suggest that there is a sequence in induction of these parameters. After an increase in apo A-I, HDL cholesterol is increased followed by an increase in PON activity. Increased serum HDL cholesterol level and PON activity may be a mechanism of action not only in healthy middle-aged men but also in postmenopausal women, underlying the reduced coronary heart disease risk in moderate drinkers. |
| Kiwis, food and cholesterol: New Zealand consumers' food concerns and awareness of nutritional guidelines Worsley, A., A. Worsley, et al. (1991), Aust J Public Health 15(4): 296-300. Abstract: New Zealand food shoppers' nutrition and food concerns and attitudes to cholesterol screening were assessed during four consecutive surveys. Over 1000 shoppers were interviewed during each survey, as part of the evaluation of the Heart Food Festival in 1988-89. Over two thirds of the respondents reported that they usually read the ingredients label on food products. Over a third were concerned about the presence of additives in foods (36 per cent), along with fat (27 per cent), salt (18 per cent), sugar (14 per cent) and fibre (5 per cent). Over half indicated that reductions in fat intake would make their diets healthier. One in five reported they were aware of the New Zealand nutrition guidelines. Only one third of respondents could correctly identify the bottom row of the healthy food pyramid. Almost one in eight respondents knew their cholesterol levels and a further two thirds wished to know them. Few differences were observed between the responses of early and late school leavers. In contrast, pronounced differences were associated with gender and the respondents' age groups. The results suggest that awareness of links between nutrition and heart disease is widespread. Educational and empowerment strategies are required to translate such awareness into dietary change. |
| KLF11-mediated repression antagonizes Sp1/sterol-responsive element-binding protein-induced transcriptional activation of caveolin-1 in response to cholesterol signaling Cao, S., M. E. Fernandez-Zapico, et al. (2005), J Biol Chem 280(3): 1901-10. Abstract: Cholesterol is a potent regulator of gene expression via a canonical pathway co-regulated by SREBP and Sp1. Here we establish the caveolin-1 gene promoter as a cell type-specific model for SREBP/Sp1 regulation whereby lipoprotein cholesterol depletion activates caveolin-1 transcription in endothelial type cells, but not in fibroblasts, both in vitro and in vivo. By extending this model, we describe a novel pathway distinct from the prototypical SREBP/Sp1 regulatory loop involving the Sp1-like protein, KLF11. Through a combination of RNA interference, chromatin immunoprecipitation assays, electrophoretic mobility shift assays, and reporter assays, we demonstrate that in the presence of cholesterol, KLF11 acts as a dominant repressor of the caveolin-1 gene. Mechanistically, cholesterol depletion results in displacement of KLF11 from an Sp1 site flanking an SRE, indicating that activation by SREBP/Sp1 requires antagonism of KLF11 repression. The displacement of KLF11 results from both a down-regulation of its expression and competition by Sp1 for DNA binding. Therefore, these studies identify a novel pathway whereby KLF11 repression is coordinated with Sp1/SREBP activation of cholesterol-dependent gene expression in a cell type-specific manner and outline the mechanisms by which these functions are achieved. |