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Plasma Lipid Levels (plasma + lipid_level)

Distribution by Scientific Domains

Life Sciences	45%
Medical Sciences	36%

Selected Abstracts

The A370T Variant (StuI Polymorphism) in the LDL Receptor Gene is not Associated with Plasma Lipid Levels or Cardiovascular Risk in UK Men

ANNALS OF HUMAN GENETICS, Issue 6 2006
José Ricardo S. Vieira
Summary Over 800 different missense mutations in the low density lipoprotein (LDL) receptor gene (LDLR) have been identified in patients with familial hypercholesterolaemia (FH). Only two of them, including the Alanine to Threonine change at position 370 (A370T), have been discovered in FH patients but do not cause FH. The frequency of the 370T allele has been reported worldwide to be between 0.022 and 0.070, with no clear association with high cholesterol levels or risk for coronary heart disease (CHD) and stroke. To explore this relationship in more detail we have determined this genotype in 2,659 healthy middle-aged (50,61 years) men participating in the prospective Second Northwick Park Heart Study, with 236 CHD and 67 stroke incident events. The genotype distribution was in Hardy-Weinberg equilibrium and in the no-event group the frequency of 370T was 0.046 (95% CI 0.040,0.052). Overall, there was no significant association of the 370T allele with any measured plasma lipid trait, and there was no difference in genotype distribution or allele frequency between the no-event and CHD (0.059; 95% CI 0.040,0.085) or stroke (0.037; 95% CI 0.012,0.085) groups ( p= 0.18 and 0.65, respectively). There was evidence for significant interaction ( p= 0.006) between body mass index (BMI) and genotype on CHD risk, with 370A homozygotes showing the expected higher CHD risk for those with higher BMI, whilst risk for 370T allele carriers was highest in men in the lowest tertile of BMI. The explanation for this association is unclear, and may simply be chance. Thus, these data confirm the absence of a significant impact of the A370T polymorphism on LDL receptor function, at least as measured by the effect on plasma lipid levels and CHD risk. [source]

Alcohol Inhibits the Progression as Well as the Initiation of Atherosclerotic Lesions in C57Bl/6 Hyperlipidemic Mice

ALCOHOLISM, Issue 9 2000
Eugene E. Emeson
Background: Evidence that a moderate consumption of alcohol is associated with a reduced incidence of and mortality due to coronary artery disease continues to accumulate. Despite recent evidence that substances in red wine confer resistance to coronary artery disease, it is clear that at least a substantial proportion of the protective effect is due to the alcohol content of the beverage. We have previously shown that the chronic ingestion of alcohol incorporated into a total liquid diet during a 24-week period inhibits the development of fatty streak lesions in hyperlipidemic C57Bl/6 mice. We have now repeated this study and demonstrated that alcohol continues to markedly inhibit atherogenesis during a 48-week period. Methods: Mice were fed a high fat atherogenic liquid diet with 0% or 6% alcohol or a high fat atherogenic pelleted diet with 0% or 15% alcohol in their drinking water. After 24 and 48 weeks on these diets, subgroups of mice were euthanized and the aortas were studied for extent of atherosclerosis. Plasma lipid levels were also measured and flow cytometry studies performed to characterize their T and B lymphocyte populations. Additional groups of mice were given the high fat atherogenic diets for 24 weeks to allow lesions to develop and were then treated with alcohol diets to determine whether they inhibit the progression of the lesions. Results: The alcohol diets suppressed the development of atherosclerotic lesions at both 24 and 48 weeks in both the liquid and pelleted diet models. The addition of the alcohol diets after allowing lesions to form for 24 weeks halted the further progression of the lesions. The alcohol treatments also decreased the plasma levels of total cholesterol and high density lipoprotein (HDL) cholesterol at almost all time intervals. Conclusions: We conclude that alcohol not only inhibits the initial development of atherosclerotic lesions but also inhibits the progression of existing atherosclerotic lesions. The alcohol-mediated decrease in HDL cholesterol in these experiments suggests that HDL plays little or no role in amelioration of atherogenesis in this model. [source]

Comparative analysis of triacylglycerols from Olea europaea L. fruits using HPLC and MALDI-TOFMS

EUROPEAN JOURNAL OF LIPID SCIENCE AND TECHNOLOGY, Issue 5 2010
Faouzi Sakouhi
Abstract MALDI-TOFMS and HPLC are two analytical methods that were used to characterize triacylglycerols (TAG) of the Meski, Sayali, and Picholine Tunisian olive varieties. The HPLC chromatograms of the oils showed the presence of 15 TAG species, among which triolein (OOO) was the most abundant (21,48%). In the Sayali cultivar, OOO was the predominant TAG species followed by POO and LOO. However, the minor TAG molecules were represented by LnLO and LnLP. MALDI mass spectra produced sodiated ([M,+,Na]+) and potassiated ([M,+,K]+) TAG molecules; only the major TAG were potassiated [OOO,+,K] ([OOO,+,K]+, [POO,+,K]+, and [LOO,+,K]+). In contrast to the HPLC chromatograms, the MALDI mass spectra showed 13 peaks of TAG. The major peak was detected at m/z,907, which corresponds to OOO with an Na+ adduct. The results from both HPLC and MALDI techniques predict the fatty acid composition and their percentages for each olive variety. Practical applications: TAG are the main components in vegetable oils. These biomolecules determine the physical, chemical, and nutritional properties of the oils. The nutritional benefits of TAG are related to DAG (moderate plasma lipid level) and esterified FA, which are intermediate biosynthetic molecules of TAG. TAG analysis is necessary to discriminate between oils of different origin, since some oils have similar FA profiles. Olive products, oils, and table olives, are the main diet sources of TAG in the Mediterranean countries. In this work, chromatographic and spectrometric methods were used for TAG analysis and characterization of Tunisian olive varieties. [source]

Modulation of plasma lipid levels affects benzo[a]pyrene-induced DNA damage in tissues of two hyperlipidemic mouse models

ENVIRONMENTAL AND MOLECULAR MUTAGENESIS, Issue 4 2003
Daniëlle M.J. Curfs
Abstract The role of plasma lipids in the uptake, transportation, and distribution of lipophilic carcinogens like benzo[a]pyrene (B[a]P) remains unclear. Therefore, we studied the effects of dietary-modulated plasma lipids on B[a]P-induced DNA damage in several organs of two hyperlipidemic mouse models. Male apolipoprotein E (ApoE)*3-Leiden (n = 22) and ApoE knockout (ApoE-KO) mice (n = 20) were fed a high-fat cholesterol (HFC) diet or low-fat cholesterol (LFC; standard mouse chow) diet for 3 weeks, after which the animals were exposed to a single oral dose of 5 mg/kg bw B[a]P or vehicle and killed 4 days later. Plasma lipids were determined and DNA adducts were measured in aorta, heart, lung, liver, brain, and stomach. Total cholesterol and low-density lipoprotein (LDL) cholesterol were increased in all animals on a HFC diet, whereas a decrease of triglycerides was seen only in the ApoE-KO mice. In ApoE-KO mice on a normal diet, DNA-adduct levels were highest in aorta (10.8 ± 1.4 adducts/108 nucleotides), followed by brain (7.8 ± 1.3), lung (3.3 ± 0.7), heart (3.1 ± 0.6), liver (1.5 ± 0.2) and stomach (1.2 ± 0.2). In the ApoE*3-Leiden mice, adduct levels were equally high in aorta, heart, and lung (4.6 ± 0.7, 5.0 ± 0.5 and 4.6 ± 0.4, respectively), followed by stomach (2.7 ± 0.4), brain (2.3 ± 0.2), and liver (1.7 ± 0.2). In the ApoE-KO mice, the HFC diet intervention resulted in lower adduct levels in lung (2.1 ± 0.2), heart (1.9 ± 0.2), and brain (2.9 ± 0.5), as compared with the LFC group. In contrast, a nonsignificant increase of adducts was found in aorta (13.1 ± 1.5). A similar but nonsignificant trend was observed in the ApoE*3-Leiden mice. Multiple regression analysis showed that in aorta, DNA adducts were inversely related to plasma triglycerides (P = 0.004) and were also modulated by the ApoE genotype (P < 0.001). The results of the present study support further investigation into the role of dietary modulation of plasma lipids, ApoE, and polycyclic aromatic hydrocarbon exposure on the formation of DNA adducts in chronic degenerative diseases. Environ. Mol. Mutagen. 42:243,249, 2003. © 2003 Wiley-Liss, Inc. [source]

High HDL-cholesterol in women with rheumatoid arthritis on low-dose glucocorticoid therapy

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 9 2008
C. García-Gómez
ABSTRACT Background, Dyslipidaemia has been described in non-treated rheumatoid arthritis (RA), and improves after therapy with disease modifying anti-rheumatic drugs or glucocorticoids; however, it has generally been perceived that glucocorticoids adversely affect lipid metabolism. The association of low dose glucocorticoid therapy with plasma lipid levels was evaluated in female RA patients. Materials and methods, A cross-sectional study was conducted in 78 female RA patients [mean age: 60 (12) years; mean disease duration: 13 (9) years]. Sixty-five (83%) were on glucocorticoid therapy [total equivalent mean prednisone dose: 5·1 (1·7) mg d,1]. Each patient was assessed through a self-reported questionnaire, structured interview and physical examination. Blood samples were obtained for routine biochemistry, lipid profile and haematological tests. Lipid profiles of RA patients who were and were not on glucocorticoid therapy were compared. Results, Clinical and laboratory features of the two groups of patients were similar, except for the Health Assessment Questionnaire and body mass index, which were significantly higher in the patients on glucocorticoid therapy. These patients had 14·7% higher serum high-density lipoprotein cholesterol (HDL-c) levels than untreated patients (P = 0·043), mainly at the expense of HDL2 subfraction, which was 24·4% higher (P < 0·039), whereas HDL3-c was only 7·4% higher (P = 0·219). Serum levels of glucose and total cholesterol, triglyceride, low-density lipoprotein cholesterol (LDL -c), very low-density lipoprotein cholesterol, apolipoproteins A-I and B were not increased in patients on glucocorticoid therapy. Conclusions, Low dose glucocorticoid therapy in RA patients is associated with an increase in HDL-c, without increasing LDL-c or triglyceride. These lipid changes may overall be considered favourable. [source]

Effect of hesperidin and naringin on the plasma lipid profile and plasma antioxidant activity in rats fed a cholesterol-containing diet

JOURNAL OF THE SCIENCE OF FOOD AND AGRICULTURE, Issue 7 2007
Shela Gorinstein
Abstract The objective of this study was to compare the influence of hesperidin and naringin, the main flavonones of orange and grapefruit, on plasma lipid profile and antioxidant activity in rats fed a cholesterol-containing diet. Sixty male Wistar rats were randomly divided into six groups of 10, named Control, Hesperidin, Naringin, Chol, Chol/Hesperidin and Chol/Naringin. The Control group was fed a basal diet (BD) and 1,2 mL of distilled water. To the BD of the other five groups were added 0.1,0.2 mg of hesperidin dissolved in 1,2 mL of distilled water (Hesperidin group), 0.46,0.92 mg of naringin in 1,2 mL of water (Naringin group), 1% of non-oxidised cholesterol (NOC) and 1,2 mL of water (Chol), 1% of NOC and 0.1,0.2 mg of hesperidin in 1,2 mL of water (Chol/Hesperidin), 1% of NOC and 0.46,0.92 mg of naringin in 1,2 mL of water (Chol/Naringin). After 30 days of the experiment it was found that the diets supplemented with hesperidin and naringin increased the plasma antioxidant activity. In conclusion, diets supplemented with hesperidin and naringin significantly hindered the increase in plasma lipid levels caused by cholesterol feeding. Hesperidin and naringin, bioactive compounds of citrus fruits, are powerful plasma lipid lowering and plasma antioxidant activity increasing flavonones. Copyright © 2007 Society of Chemical Industry [source]

Adaptive dimensions of health research among indigenous Siberians,

AMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 2 2007
J. Josh Snodgrass
Present evidence suggests that modern humans were the first hominid species to successfully colonize high-latitude environments (,55°N). Given evidence for a recent (<200,000 years) lower latitude naissance of modern humans, the global dispersal and successful settlement of arctic and subarctic regions represent an unprecedented adaptive shift. This adaptive shift, which included cultural, behavioral, and biological dimensions, allowed human populations to cope with the myriad environmental stressors encountered in circumpolar regions. Although unique morphological and physiological adaptations among contemporary northern residents have been recognized for decades, human biologists are only now beginning to consider whether biological adaptations to regional environmental conditions influence health changes associated with economic modernization and lifestyle change. Recent studies have documented basal metabolic rates (BMRs) among indigenous Siberian populations that are systematically elevated compared to lower latitude groups; this metabolic elevation apparently is a physiological adaptation to cold stress experienced in the circumpolar environment. Important health implications of metabolic adaptation are suggested by research with the Yakut (Sakha), Evenki, and Buriat of Siberia. BMR is significantly positively correlated with blood pressure, independently of body size, body composition, and various potentially confounding variables (e.g., age and smoking). Further, this research has documented a significant negative association between BMR and LDL cholesterol, which remains after controlling for potential confounders; this suggests that high metabolic turnover among indigenous Siberians has a protective effect with regard to plasma lipid levels. These results underscore the importance of incorporating an evolutionary approach into health research among northern populations. Am. J. Hum. Biol. 19:165,180, 2007. © 2007 Wiley-Liss, Inc. [source]

Panax notoginseng (Burk.) effects on fibrinogen and lipid plasma level in rats fed on a high-fat diet

PHYTOTHERAPY RESEARCH, Issue 2 2003
A. F. G. Cicero
Abstract Several studies have shown that notoginsenoides improve diastolic function in hypertensive subjects, induce the fibrinolytic system in in vitro models and act as antiproliferative agents on vessel leiomyocytes. Our aim was to evaluate their effect on fibrinogen and lipid plasma levels compared with a well-known HMGCoA reductase inhibitor. Seventy Wistar male adult rats on a fat-enriched diet were treated orally with P. notoginseng pulverized root (43,mg/kg/day or 86,mg/kg/day; 20 animals per group), fluvastatin (3,mg/kg/day; 20 animals) or physiological saline (5,mL/kg/day; 10 animals). The ten rats on a normocaloric diet were also treated with 5,mL/kg/day of physiological saline. After a 28-day treatment, the rats were killed and their blood analysed with standard procedures. Treatment with 43,mg/kg/day of P. notoginseng or 3,mg/kg/day of fluvastatin showed similar activity in decreasing total cholesterol (,23.70%, ,19.29%, respectively) and triglycerides (,21.59%, ,18.55%). The most evident effect of P. notoginseng was the reduction of fibrinogenaemia in treated rats compared with the control values (,38.10%; p,<,0.001), no dose-relationship being shown in this effect. Moreover, no significant variation in HDL cholesterol and glucose levels was observed nor did relevant behavioural changes occur in association with the root intake. Besides a moderate, non dose-related decrease in the plasma lipid levels, P. notoginseng appeared to induce a significant reduction in the rat fibrinogenaemia. Copyright © 2003 John Wiley & Sons, Ltd. [source]

The A370T Variant (StuI Polymorphism) in the LDL Receptor Gene is not Associated with Plasma Lipid Levels or Cardiovascular Risk in UK Men

The effect of hepatic passage on postprandial plasma lipid profile of rainbow trout (Oncorhynchus mykiss) after a single meal

AQUACULTURE NUTRITION, Issue 5 2010
E.J. ELIASON
Abstract For the first time, pre- and post-hepatic plasma lipid profiles were monitored following a single meal in a free-swimming, non-anaesthetized fish. Rainbow trout (Oncorhynchus mykiss; 700,1500 g; 10 °C) were equipped with cannulae in the dorsal aorta (DA) and hepatic portal vein (HPV). Simultaneous blood samples, taken from both cannulae at 0, 3, 6, 12, 24 and 48 h postprandial, revealed the time course of the plasma lipid profiles following a single meal (1% of body mass). Primarily monounsaturated fatty acids with the exception of 18:1n , 9, increased significantly from baseline by 12 h postprandial without greatly affecting total plasma lipid concentrations. Total plasma lipids then showed a small peak at 24 h postprandial, coinciding with a peak in triacylglycerols. We conclude that assimilation of lipids from the digest into the plasma is slower than reported for proteins and carbohydrates in the same species. Furthermore, as there were no significant differences between the HPV and DA, no measurable effect of hepatic passage on plasma lipid levels was resolved. Therefore, we also conclude that, in contrast to that in higher vertebrates, hepatic passage does not seem to have a major role in rainbow trout for modulating the postprandial plasma profile of lipids. [source]

Effects of Rutin on Lipid Profile in Hypercholesterolaemic Rats

BASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 3 2009
Amir Ziaee
Rutin is found in many plants and is also an important dietary constituent of food and plant-based beverages. Rutin has several pharmacological properties including antioxidant and cardioprotective activities. Also, it was identified that rutin is the major low-density lipoprotein (LDL) antioxidant compound of mulberry in an in vitro study. The effects of rutin were tested by using it as a supplement in a high-cholesterol diet. Male rats were fed a high-cholesterol diet (1 ml/100 g) for 4 weeks with rutin (10 or 100 mg/kg) or rutin 100 mg/kg and lovastatin supplementation to study the hypocholesterolaemic effects of rutin on plasma lipid levels, hepatic enzyme activity, and liver tissue. Feeding the animals a high-cholesterol diet resulted in marked hypercholesterolaemia and increased the serum level of LDL cholesterol (LDL-C). Rutin (at 100 mg/kg) alone or in combination with lovastatin significantly reduced the levels of total cholesterol, and LDL-C and also markedly decreased liver enzymes and weight in animals with a high-cholesterol diet. Our findings show that 100 mg/kg of rutin alone or with lovastatin supplementation lowered liver weight and enzymes as well as plasma total cholesterol and LDL. The hepatic histopathological results reflect the correlation of rutin and lovastatin combination with both liver weight and the levels of plasma total cholesterol and LDL-C. These results indicate that rutin in combination with lovastatin has increased anti-hypercholesterolaemic effects in an animal model. [source]