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At least 127 records · Page 7Linked to original sources
PubMed2004

Fish protein hydrolysate reduces plasma total cholesterol, increases the proportion of HDL cholesterol, and lowers acyl-CoA:cholesterol acyltransferase activity in liver of Zucker rats.

There is growing evidence that soy protein improves the blood lipid profiles of animals and humans. We compared the effects of fish protein hydrolysate (FPH), soy protein, and casein (control) on lipid metabolism in Wistar rats and genetically obese Zucker (fa/fa) rats. In Zucker rats, FPH treatment affected the fatty acid composition in liver, plasma, and triacylglycerol-rich lipoproteins. The mRNA levels of Delta 5 and Delta 6 desaturases were reduced by FPH and soy protein feeding compared with casein feeding. In Zucker rats both FPH and soy protein treatment reduced the plasma cholesterol level. Furthermore, the HDL cholesterol:total cholesterol ratio was greater in these rats and in the Wistar rats fed FPH and soy protein compared with those fed casein. Although fecal total bile acids were greater in soy protein-fed Zucker rats than in casein-fed controls, those fed FPH did not differ from the controls. However, the acyl-CoA:cholesterol acyltransferase activity was reduced in Zucker rats fed FPH and tended to be lower (P = 0.13) in those fed soy protein compared with those fed casein. Low ratios of methionine to glycine and lysine to arginine in the FPH and soy protein diets, compared with the casein diet, may be involved in lowering the plasma cholesterol concentration. Our results indicate that the effects of FPH and soy protein on fatty acid metabolism are similar in many respects, but the hypocholesterolemic effects of FPH and soy protein appear to be due to different mechanisms. FPH may have a role as a cardioprotective nutrient.

Acyl Coenzyme A↗
PubMed1997

Cholesterol efflux, lecithin-cholesterol acyltransferase activity, and pre-beta particle formation by serum from human apolipoprotein A-I and apolipoprotein A-I/apolipoprotein A-II transgenic mice consistent with the latter being less effective for reverse cholesterol transport.

Studies assessing fatty streak formation in mice have revealed that human apolipoprotein A-I (apoAI) transgenic mice (TgAI) have 15-fold less atherosclerosis susceptibility than combined human apolipoprotein A-I/human apolipoprotein A-II (apoAI:AII) transgenics (TgAI:AII) and 40-fold less than nontransgenic control mice. In order to examine the biochemical mechanisms underlying those in vivo observations, we have compared in vitro properties of serum from the different groups of animals for participation in cholesterol efflux, LCAT activation, and pre-beta particle formation. Analysis of cholesterol efflux from both Fu5AH hepatoma and Ob1771 adipose cells revealed serum from the TgAI to be the most efficient in promoting efflux. The two-dimensional electrophoresis of mouse serum shows that control mice have exclusively apoAI in alpha particles. TgAI and TgAI:AII mice have 30 and 38% of total apoAI in particles with pre-beta electrophoretic mobility, respectively. The distribution of cell-derived cholesterol between these apoAI-containing lipoprotein subspecies after 1 and 60 min of incubation with Fu5AH hepatoma cells was examined. This revealed after a 1 min incubation 66 +/- 8 and 83 +/- 9% of the counts in particles with pre-beta mobility for TgAI and TgAI:AII mice, respectively; while after 60 min of incubation, only 6 +/- 2% of counts remained in pre-beta particles from the TgAI and 30 +/- 3% for the TgAI:AII. This suggests faster movement of cholesterol from pre-beta to alpha particles in plasma from the TgAI. Consistent with this is the observation that LCAT activity with both exogenous and endogenous substrate increased in the TgAI versus the TgAI:AII mice. The previously observed decrease in fatty streak formation in the TgAI versus the TgAI:AII and control mice is consistent with the in vitro studies presented here and suggests that HDL containing human apoAI is a more effective participant in the postulated early steps in reverse cholesterol transport than HDL containing both human apoAI and human apoAII, and/or murine HDL.

Animals↗
PubMed1991

Results of a province-wide quality assurance program assessing the accuracy of cholesterol, triglycerides, and high-density lipoprotein cholesterol measurements and calculated low-density lipoprotein cholesterol in Ontario, using fresh human serum.

To evaluate laboratory performance, eight to 13 samples of fresh human serum from volunteers were sent to 250 laboratories in the Canadian province of Ontario licensed to perform lipid analysis. Fresh human specimens were used because of potential matrix effects with processed materials. We show that on all survey samples, 71% (range, 63% to 82%) of participating laboratories are within +/- 5% of the target cholesterol value and that 93% are within +/- 10%. The goal of the National Cholesterol Education Program for 1992 is total error of no more than +/- 9% for 95% of results. The unblanked triglycerides results show that on all samples 40% (14% to 59%) of participants are within +/- 5% and 68% (range, 31% to 86%) are within +/- 10% of the target value. For triglycerides results from 0.9 to 2.0 mmol/L, 80% or more are within +/- 0.2 mmol/L. Between 2.0 and 3.0 mmol/L, 90% are within +/- 0.3 mmol/L of the target values. For high-density lipoprotein cholesterol, for all samples 35% (range, 24% to 50%) of laboratories are within +/- 5% and 68% (range, 55% to 88%) are within +/- 10%. A range of 80% to 95% of participants are within +/- 0.2 mmol/L of the target values. For calculated low-density lipoprotein cholesterol, 51% and 62% of the laboratories surveyed are within +/- 5%, with 83% and 89% within +/- 10% of the target values. We conclude that the laboratory measurement of lipids is approaching the degree of accuracy and precision required for clinical purposes, and that the use of fresh human serum samples is a viable approach to their proficiency testing.

Blood Chemical Analysis↗
PubMed1982

Effects of niceritrol (pentaerythritol tetranicotinate) on plasma lipoprotein concentration: increment of high density lipoprotein(HDL) cholesterol and HDL-cholesterol/low density lipoprotein cholesterol ratio in hypo-high density lipoproteinemia.

The purpose of the present study was to investigate the effects of niceritrol on HDL metabolism. In study (A), niceritrol, 750 mg/day was given for initial period of 12 weeks and 1,500 mg/day was prescribed for an additional 12 weeks to 12 subjects. In six of them, the HDL cholesterol (Ch) levels were less than 45 mg/100 ml with normal plasma cholesterol levels and with plasma triglyceride levels of less than 250 mg/100 ml. In the remaining six subjects, HDL-Ch, plasma cholesterol and triglyceride levels were all within normal limits except in one subject having a higher triglyceride level, 213 mg/100 ml. Plasma lipoproteins were fractionated by sequential ultracentrifugation and analyzed for cholesterol, triglyceride (TG), phospholipid(PL), apolipoprotein(Apo) B and Apo A-I, every 4 weeks. Niceritrol decreased plasma-Ch, VLDL-Ch, LDL-Ch, plasma-TG, VLDL-TG, plasma-PL, VLDL-PL and LDL-PL. Niceritrol increased HDL-Ch and the HDL-Ch/LDL-Ch ratio. These effects were more significant for the dose of 1,500 mg/day than 750 mg/day and were more marked in the patients with lower pretreatment HDL-Ch levels. Apo B level at 20 weeks was significantly lower than that before treatment. Initial plasma Apo A-I levels of the patients were approximately one-half of the control plasma. After treatment with niceritrol, Apo A-I concentration tended to increase. In study (B), changes of lipids concentration in HDL2 and HDL3 fraction were investigated in 5 patients during treatment with niceritrol, 1,500 mg/day for 8 weeks. Lipoproteins were analyzed every 2 weeks. HDL2-Ch levels tended to increase without significant changes of HDL3-Ch levels and HDL2-Ch/HDL3-Ch ratio showed a tendency to increase. A significantly but weakly inverse correlation between changes of VLDL-TG and HDL-Ch was observed, suggesting that the increment of HDL might be due partly to promoted lipolysis of TG-rich lipoproteins. However, it was suggested that the effects of niceritrol on lipoprotein synthesis in the liver and HDL catabolism should be considered.

Aged↗
PubMed1992

Two different allelic mutations in the lecithin-cholesterol acyltransferase gene associated with the fish eye syndrome. Lecithin-cholesterol acyltransferase (Thr123----Ile) and lecithin-cholesterol acyltransferase (Thr347----Met).

We have elucidated the genetic defect in a 66-yr-old patient with fish eye syndrome (FES) presenting with severe corneal opacities and hypoalphalipoproteinemia. The patient's plasma concentration of high density lipoprotein (HDL) cholesterol was reduced at 7.7 mg/dl (35.1-65.3 mg/dl in controls) and the HDL cholesteryl ester content was 31% (60-80% in controls); however, total plasma cholesteryl esters were similar to normal (60% of total cholesterol vs. a mean of 66% in controls). The patient's plasma cholesterol esterification rate was slightly reduced at 51 nmol/ml per h (control subjects: 61-106 nmol/ml per h), whereas lecithin-cholesterol acyltransferase (LCAT) activity, assayed using a HDL-like exogenous proteoliposome substrate, was virtually absent (0.9 nmol/ml per h vs. 25.1-27.9 nmol/ml per h in control subjects). DNA sequence analysis of the proband's LCAT gene revealed two separate C to T transitions resulting in the substitution of Thr123 with Ile and Thr347 with Met. The mutation at codon 347 created a new restriction site for the enzyme Nla III. Analysis of the patient's polymerase chain reaction-amplified DNA containing the region of the Thr347 mutation by digestion with Nla III confirmed that the proband is a compound heterozygote for both defects. The patient's daughter, who is asymptomatic despite a 50% reduction of LCAT activity, is heterozygous for the Thr123----Ile mutation. Our data indicate that the regions adjacent to Thr123 and Thr347 of LCAT may play an important role in HDL cholesterol esterification, suggesting that these regions may contain a portion of the LCAT binding domain(s) for HDL.

Aged↗
PubMed2006

Cholesterol, cholesterol-lowering agents/statins, and urologic disease: Part III--A rapid review of FDA-approved cholesterol-lowering agents.

There are a variety of agents, dosages, and mechanisms involved in reducing cholesterol. Statins are the most well-known class and three of the six currently available agents have now lost patent protection. Thus, large reductions in price are expected in 2006-2007 across the entire class. The other classes of cholesterol-lowering agents include targeted triglyceride reducers and high-density lipoprotein boosters; two other classes include primarily cholesterol absorption inhibitors. A recent addition to the cholesterol-lowering prescriptions include prescription omega-3 products, which are highly concentrated, have excellent quality control, and are used to reduce abnormally high levels of triglycerides. All of these agents can be used in some restricted combination, or individually to significantly impact the various forms of lipids in the bloodstream. The bottom line is that practitioners have a large diversity of medications available for cholesterol lowering, and this is enormously exciting at a time when these agents have such profound effects in a variety of disciplines.

Anion Exchange Resins↗
PubMed2006

Achieving LDL cholesterol, non-HDL cholesterol, and apolipoprotein B target levels in high-risk patients: Measuring Effective Reductions in Cholesterol Using Rosuvastatin therapY (MERCURY) II.

BACKGROUND: National Cholesterol Education Program Adult Treatment Panel III guidelines for patients at a high risk of coronary heart disease set a low-density lipoprotein cholesterol (LDL-C) target of < 100 mg/dL. This target can be difficult to attain with diet and current therapy. METHODS: In a 16-week multinational trial, 1993 high-risk patients were randomized to rosuvastatin 20 mg, atorvastatin 10 mg, atorvastatin 20 mg, simvastatin 20 mg, or simvastatin 40 mg for 8 weeks. Patients either remained on starting treatment or switched to lower or milligram-equivalent doses of rosuvastatin for 8 more weeks. RESULTS: At 16 weeks, more patients achieved their LDL-C target by switching to rosuvastatin 10 mg than staying on atorvastatin 10 mg (66% vs 42%, P < .001) or simvastatin 20 mg (73% vs 32%, P < .001). Changing to rosuvastatin 20 mg brought more patients to their LDL-C target than staying on atorvastatin 20 mg (79% vs 64%, P < .001) or simvastatin 40 mg (84% vs 56%, P < .001). More very high risk patients achieved an LDL-C target of < 70 mg/dL when changed to rosuvastatin from atorvastatin or simvastatin (within-arm comparisons P < .01). More hypertriglyceridemic patients (triglycerides > or = 200 mg/dL) met LDL-C, non-high-density lipoprotein cholesterol (non-HDL-C), and apolipoprotein B targets by changing to rosuvastatin. Switching to rosuvastatin produced greater reductions in LDL-C, total cholesterol, non-HDL-C, apolipoprotein B, and lipid ratios. All treatments were well tolerated, with no differences among treatment groups in skeletal muscle, hepatic, or renal toxicity. CONCLUSION: Rosuvastatin 10 or 20 mg is an effective and safe therapeutic option for high-risk patients to achieve their lipid and apolipoprotein targets.

Aged↗
PubMed2003

An isoenergetic very low carbohydrate diet improves serum HDL cholesterol and triacylglycerol concentrations, the total cholesterol to HDL cholesterol ratio and postprandial pipemic responses compared with a low fat diet in normal weight, normolipidemic women.

Very low carbohydrate diets are popular, yet little is known about their effects on blood lipids and other cardiovascular disease risk factors. We reported previously that a very low carbohydrate diet favorably affected fasting and postprandial triacylglycerols, LDL subclasses and HDL cholesterol (HDL-C) in men but the effects in women are unclear. We compared the effects of a very low carbohydrate and a low fat diet on fasting lipids, postprandial lipemia and markers of inflammation in women. We conducted a balanced, randomized, two-period, crossover study in 10 healthy normolipidemic women who consumed both a low fat (<30% fat) and a very low carbohydrate (<10% carbohydrate) diet for 4 wk each. Two blood draws were performed on separate days at 0, 2 and 4 wk and an oral fat tolerance test was performed at baseline and after each diet period. Compared with the low fat diet, the very low carbohydrate diet increased (P <or= 0.05) fasting serum total cholesterol (16%), LDL cholesterol (LDL-C) (15%) and HDL-C (33%) and decreased serum triacylglycerols (-30%), the total cholesterol to HDL ratio (-13%) and the area under the 8-h postprandial triacylglycerol curve (-31%). There were no significant changes in LDL size or markers of inflammation (C-reactive protein, interleukin-6, tumor necrosis factor-alpha) after the very low carbohydrate diet. In normal weight, normolipidemic women, a short-term very low carbohydrate diet modestly increased LDL-C, yet there were favorable effects on cardiovascular disease risk status by virtue of a relatively larger increase in HDL-C and a decrease in fasting and postprandial triaclyglycerols.

Adult↗
PubMed2003

Improvement in Japanese clinical laboratory measurements of total cholesterol and HDL-cholesterol by the US Cholesterol Reference Method Laboratory Network.

BACKGROUND: Accurate and precise measurements of total cholesterol (TC) and HDL-cholesterol (HDL-C) are necessary for effective diagnosis and treatment of lipid disorders. We studied the impact of TC certification and HDL-C evaluation in Japanese clinical laboratories to standardize their measurements. METHODS: We selected 78 laboratories participated at least twice for TC and 46 laboratories participated twice for HDL-C in the standardization protocols developed by the Cholesterol Reference Method Laboratory Network (CRMLN). We compared the initial and subsequent results using the performance guidelines established by US National Cholesterol Education Program (NCEP). RESULTS: For TC, mean percentage bias of all participants was -0.93% and -0.49% for the initial and second rounds, respectively. Mean within-sample CV was 0.72% and 0.69% for the initial and second rounds, respectively. For HDL-C, mean percentage bias of all participants was -1.86% and -0.06% for the initial and second events, respectively. Mean among-run CV was 1.56% and 1.58% for the initial and second events, respectively. CONCLUSIONS: TC accuracy in the second round than the initial round tended to improvement although statistically not significant, however in the five years follow-up, mean absolute percentage bias was reduced over time. HDL-C accuracy was statistically improved in the second event than the initial event. The precision for both TC and HDL-C did not change. This study shows CRMLN protocols contribute effectively to improvement of TC and HDL-C performance.

Certification↗
PubMed2003

Barley beta-glucan lowers serum cholesterol based on the up-regulation of cholesterol 7alpha-hydroxylase activity and mRNA abundance in cholesterol-fed rats.

Barley, which is high in soluble dietary fiber (particularly beta-glucan), is thought to have hypocholesterolemic effects. The present study was performed to further elucidate the hypocholesterolemic actions of waxy barley, and the extent to which they can be attributed to beta-glucan. Male Sprague-Dawley rats (n=21) were fed control (fiber-free) diets, diets with the addition of 2.5%, refined beta-glucan or 30% waxy barley that provides approximately 2.5% beta-glucan in the diet for 2 wk. Body weight gain and food efficiency of rats were unaffected by diet. beta-glucan or waxy barley decreased serum levels of total cholesterol (p < 0.05) by 13.5% or 18.9%, and also decreased LDL-cholesterol 19.4% or 24.3%, respectively. Addition of refined beta-glucan or waxy barley to the diet resulted in greater bile acid excretions (p < 0.05) compared to the control group. The waxy barley diet up-regulated by 2. 3 times and the beta-glucan diet by 1.5 times the activity of cholesterol 7a-hydroxylase (CYP7A1). Hepatic CYP7A1 mRNA level paralleled the increases in enzyme activity. The results of this study suggest that the hypocholesterolemic effects of both beta-glucan and a waxy barley diet may be due to the enhancement of CYP7A1 expression resulting from increased fecal excretion of bile acids.

Animals↗
PubMed1999

Effects of NTE-122, an acyl-CoA:cholesterol acyltransferase inhibitor, on cholesterol esterification and lipid secretion from CaCo-2 cells, and cholesterol absorption in rats.

The effect of NTE-122 (trans-1,4-bis[[1-cyclohexyl-3-(4-dimethylamino phenyl)ureido]methyl]cyclohexane), an acyl-CoA:cholesterol acyltransferase (ACAT) inhibitor, on cholesterol absorption was investigated. NTE-122 inhibited whole-cell ACAT activity in CaCo-2 cells, a human intestinal cell line, with an IC50 value of 4.7 nM. In CaCo-2 cells cultured on a membrane filter, NTE-122 pronouncedly inhibited the basolateral secretion of newly synthesized cholesteryl esters, and significantly reduced the basolateral secretion of newly synthesized triglycerides without influencing the cellular triglyceride synthesis. Furthermore, NTE-122 (1 mg/kg, p.o.) inhibited [14C]cholesterol absorption in rats. These results suggest that NTE-122 is capable of exhibiting anti-hyperlipidemic effects by reducing the absorption of dietary cholesterol.

Aniline Compounds↗
PubMed1977

Amperometric determination of total cholesterol in serum, with use of immobilized cholesterol ester hydrolase and cholesterol oxidase.

We describe an electrochemical method for simple, rapid, and economical assay of total serum cholesterol with use of immobilized cholesterol esterase (EC 3.1.1.13) and cholesterol oxidase (EC 1.1.3.6). A rotating porous cell was specially designed to hold the immobilized enzymes firmly and to allow the reaction mixture to pass through the enzyme layer easily, thus catalyzing the enzymatic transformation quickly. Hydrogen peroxide resulting from a catalytic reactions was measured amperometrically at +0.60 V cs. a standard calomel electrode. The calibration curve for total serum cholesterol was linear from 0 to 5.00 g/liter. The method is specific, precise, and inexpensive. Our results correlate well with those obtained by the method of Abell et al. [Stand. Methods Clin. Chem. 2, 26 (1958)], the correlation coefficient being 0.992. Ascorbic acid or bilirubin in concentrations up to 700 mg/liter do not interfere. The immobilized enzymes are stable, and the same immobilized-enzyme stirrer can be used for at least 200 accurate, reproducible assays.

Carboxylic Ester Hydrolases↗
PubMed1976

Polarographic method for rapid microdetermination of cholesterol with cholesterol esterase and cholesterol oxidase.

Cholesterol concentrations in serum are enzymatically determined rapidly by use of a polarographic oxygen analyzer with a circuit modified to record simultaneously the amount and rate of oxygen consumption. The final assay system, assessed from the oxygen consumption value that we found to be optimum, consists of 1 ml of sodium phosphate buffer (0.6 mol/liter, pH 7.0) containing NaN3 (10 mg/liter), Triton X-100 surfactant (10 ml/liter), 0.4 U of cholesterol ester hydrolase, and 0.6 U of cholesterol oxidase. Oxygen consumption and cholesterol concentration are linearly related to 8.0 g/liter, and only 10 mul of serum is required. Replicate analyses of pooled serum by the present method demonstrated the following inter-run precision: mean = 1731 mg/liter, SD = 22.3 mg/liter, CV = 1.3%. Bilirubin and ascorbic acid were without effect on the present method, unlike the enzymatic colorimetric methods.

Carboxylic Ester Hydrolases↗
PubMed1993

Blood cholesterol screening: influence of fasting state, biological variation and the single cholesterol assay on total cholesterol level.

Postprandial changes in plasma total cholesterol (TC) are minimal and there is essentially no difference between fasting vs random TC concentrations, as reflected in the small diurnal coefficient of variation (CV) for TC of 2.5%. Similarly, a cholesterol-rich meal within the last 24 hours lacked an impact on plasma TC. Thus, random specimens are acceptable in blood cholesterol screening. The intraindividual biological CV (CVb) for plasma TC as measured over a long period was estimated from the data of several published studies to be 6.0%, which, when combined with a probable analytical CV (CVa) of 5% during screening, gave a total intraindividual CV (CVt) of about 8% for the single cholesterol assay. There is consensus that 'high TC values' acquired during screening should be confirmed under the conventional laboratory setting capable of CVa of 3% or less.

Cholesterol↗