Using Wistar rats the effect of exercise was studied on the level of lipid peroxides, superoxide dismutase activity in the serum and certain tissues, and the contents of triglycerides (TG), total cholesterol (TChol), cholesterol in high density lipoprotein fractions (HDL -chol and HDL3-chol) and alpha-tocopherol in the serum. Low-grade exercise decreased by about 10% the lipid peroxide level in the serum, the soleus muscle and myocardium. Greater exercise increased the lipid peroxide level in the studied tissues. In the liver the lipid peroxide level rose by 20% independently of the degree of exercise. Superoxide activity increased proportionally to the grade of exercise in the myocardium, the soleus muscle and the liver. The serum alphatocopherol level increased in the groups of animals subjected to exercise. In the group with higher grade of exercise a slight fall of TChol in the serum and a fall of HDL and HDL3, cholesterol.
Introduction: Obesity is a multifactorial disorder leading to disturbances in lipid metabolism and adverse plasma lipid profiles. 75G/A polymorphism in the apolipoprotein AI (apo AI) gene promoter has been shown to affect plasma HDL-cholesterol and apolipoprotein AI concentrations. However, the impact of this genetic variant on lipid profiles in obese subjects has not been well recognized. In the present study the relationship between 75G/A apo AI gene polymorphism (rs 670) and plasma lipids and apo AI concentrations in obese and non-obese males was assessed. Material and Methods: 114 men who were not taking lipid lowering drugs were examined: control group with body mass index (BMI) less than 25 (n = 34), overweight with BMI ranged 25-29 (n = 51) and obese subjects with BMI > 30 (n - 29). The 75G/A gene polymorphism of apo AI was determined by PCR-based method. Results: Higher serum HDL-cholesterol and apo AI concentrations in A allele carriers compared to GG homozygotes were observed in men with proper body mass (p = 0.037 and p = 0.056, respectively) and in overweight subjects (p = 0.0072 and p = 0.018, respectively) but not in obese men. Therefore, interaction may be suggested between 75G/A genetic variants in apo AI gene with obesity and its influence on plasma HDL-cholesterol and apo AI concentrations.
We investigated the influence of high sucrose diet (HSD) after 3 or 5 weeks of administration on paraoxonase 1 (PON1) activity in plasma of normolipidemic rats and the relationship between serum PON1 activity, triacylglycerides (TGs), HDL and total cholesterol vs. the control group of rats fed normal, control diet (CD). Because the data about the influence of gemfibrozil (GEM) on PON1 activity are controversial, we also investigated its effects (administration in the 4th and 5th week in rats on HSD and CD) on plasma PON1 activity and lipid levels in normolipidemic rats, and in rats with hypertriglyceridemia caused by HSD. Our results obtained in rats on HSD show a significant increase of plasma TGs levels by 47 % (P < 0.05) after 5 weeks of treatment, and PON1 activity by 32 % and 23 % (P < 0.05) after 3 and 5 weeks, but without change in lipid levels vs. rats on CD. In the rats on CD and HSD, GEM caused a significant decrease of PON1 activity by 44 % and 33 %, while a significant decrease of TGs level by 38 % (P < 0.05) was measured only in rats on CD. The effects of GEM on total cholesterol, HDL and LDL in both groups of rats were typical for its action on lipoprotein metabolism. Because GEM in the rat liver stimulates proliferation of peroxisomes, β oxidation, and production of H2O2, it is possible that the oxidative stress induced by GEM damages hepatocytes and lowers the synthesis of PON1.
Introduction. Lowlevels of high-density lipoprotein (HDL) cholesterol is a risk factor for coronary artery disease. Besides lifestyle, some gene polymorphisms areknown to be related to the individual HDL-cholesterol concentration. Aim. An apolipoprotein AI gene promoterpolymorphism, related to an adenine (A) to guanine (G) transition 75 base pairs upstream from the transcription initiation site, was studied in the group of healthy men. Methods. Genotyping was performed by polymerase chain reaction method with MspI restriction enzyme. Lipid profile was determined by routine biochemical measurements and apolipoprotein AI concentration was obtain by an immunotubidymetric method. Results. Frequency of the rare A allele was 16% and in the study group only one case of the AA genotype was found, whereas GG variants was observed in 23 participants (68%). Statistically significant differences were noted in HDL concentrations between A allele carriers and GG homozygotes: 56 ± 12 mg/dL vs 46 ± 12 mg/dL, respectively. GG males had also about 20 mg/dL lower apolipoprotein AI levels and about 17 mg/dL higher triglyceride levels. Conclusions. In the studied men of Polish origin the A allele was associated with higher HDL-cholesterol and apolipoprotein AI levels compared to GG homozygotes.
Introduction. A decreased serum high density lipoprotein-cholesterol (HDL-C) is a strong predictor of cardiovascular risk. However, total HDL is a very dynamic, changeable fraction, and does not perform the function of atherosclerosis markers. In the presented study, the pattern of serum lipids, including HDL-C subclasses (HDL2- and HDL3-cholesterol), in a middleaged Polish Lower Silesia population was defined. Materials and method. A group of 746 males and 1,298 females, aged 35–70, were investigated. All subjects were participants in the PURE study. Mean serum lipid levels were determined for groups selected on the basis of gender, age, cigarette smoking, drinking alcohol and place of residence (urban/rural area). The data were analyzed using STATISTICA 6.0 PL. Results. In multiple linear regression models, age was the most important independent and consistent predictor of total cholesterol (TC) and LDL cholesterol (LDL-C). The prevalence of low HDL-C (threshold 40 mg/dL in males, 50 mg/dL in females) was 16.5% for males and 22.6% for females. This gender-conditioned difference in the prevalence of low HDL-C was greater in rural (20.0% vs. 30.9%, respectively, in males and females) in comparison to urban (14.4% vs. 17.1%) areas. The lipid pattern was significantly worse in rural than in urban females. Female rural inhabitants showed higher triglycerides (TG) and lower HDL cholesterol (total and contained in subclasses HDL2 and HDL3). Simultaneously, a higher BMI, higher percent of smokers and drinkers and lower age of smoking female rural inhabitants in comparison to urban females were estimated. In the total population, cigarette smoking or drinking alcohol were associated with significant increases in TC, LDL-C and TG, also with decreased HDL-C (smoking) or HDL2-C (drinking). Two-way analysis of variance showed the existence of interaction between these risk factors in their influence on HDL-C and HDL3-C. Conclusion. In the middle-aged population of the Lower Silesian region in Poland the place of residence (urban/rural area) had a significant impact on the lipid pattern. This pattern is more atherogenic in rural women than in urban women.
The pre-β HDL fraction constitutes a heterogeneous population of discoid nascent HDL particles. They transport from 1 to 25 % of total human plasma apo A-I. Pre-β HDL particles are generated de novo by interaction between ABCA1 transporters and monomolecular lipid-free apo A-I. Most probably, the binding of apo A-I to ABCA1 initiates the generation of the phospholipid-apo A-I complex which induces free cholesterol efflux. The lipid-poor nascent pre-β HDL particle associates with more lipids through exposure to the ABCG1 transporter and apo M. The maturation of pre-β HDL into the spherical α-HDL containing apo A-I is mediated by LCAT, which esterifies free cholesterol and thereby forms a hydrophobic core of the lipoprotein particle. LCAT is also a key factor in promoting the formation of the HDL particle containing apo A-I and apo A-II by fusion of the spherical α-HDL containing apo A-I and the nascent discoid HDL containing apo A-II. The plasma remodelling of mature HDL particles by lipid transfer proteins and hepatic lipase causes the dissociation of lipid-free/lipid-poor apo A-I, which can either interact with ABCA1 transporters and be incorporated back into pre-existing HDL particles, or eventually be catabolized in the kidney. The formation of pre-β HDL and the cycling of apo A-I between the pre-β and α-HDL particles are thought to be crucial mechanisms of reverse cholesterol transport and the expression of ABCA1 in macrophages may play a main role in the protection against atherosclerosis.
The relationship between plasma lipid levels and mortality from cardiovascular diseases has been shown in many studies, but there has been far less investigation into their relationship to non-cardiovascular diseases. The aim of this study was to investigate the lipid profile of individuals with hematological malignancies and its relationship to disease activity. 238 patients were included in the study: 84 with acute leukemia, 62 with non-Hodgkin lymphoma, 35 with Hodgkin’s lymphoma, 32 with multiple myeloma, and 25 with myeloproliferative syndrome. The HDL cholesterol level of the patients differed to that of the individuals in the control group in the active disease period for all the analyzed disorders, but only remained statistically significant in the acute leukemia and non-Hodgkin lymphoma groups during the remission period. Smaller differences were observed for the remaining lipid fractions, except for the triglyceride level, which increased in the active disease period in all the analyzed disorders except non-Hodgkin lymphoma. The most pronounced changes in the lipid fractions occurred in the HDL cholesterol level, and were the most remarkable for acute leukemia.
U mężczyzn z zaawansowaną miażdżycą tętnic udowych oznaczano Ca, Mg, Cu i Zn w surowicy krwi. Oceniono dwa sposoby przygotowania surowicy dla oznaczeń metodą płomieniowej spektroskopii absorpcyjnej. Poziom wszystkich oznaczanych pierwiastków w surowicy krwi chorych z miażdżycą był większy w grupie kontrolnej. Stężenie cholesterolu całkowitego było wyższe a HD Lr cholesterolu niższe u chorych z miażdżycą. Wyniki LDL-cholesterolu nie różniły się od siebie.
W pracy przedstawiono wyniki badań wpływu dichlorfosu, pestycydu fosforoorganicznego, na aktywność reduktazy HMG-CoA, kluczowego enzymu syntezy cholesterolu w wątrobie szczura w warunkach in vivo i in vitro.
Celem badania było porównanie wpływu 4 rodzajów tłuszczów spożywczych (margaryny ze stanolami, masła, oleju słonecznikowego, margaryny miękkiej) oraz diety hodowlanej na wybrane parametry lipidowe: cholesterol całkowity (TC), triacyloglicerole (TG), cholesterol we frakcji HDL (c-HDL) i LDL (c-LDL) w osoczu szczurzym. Rodzaj i poziom tłuszczu w diecie nie miały istotnego wpływu na wskaźnik wydajności wzrostowej oraz stężenie cholesterolu we frakcjach HDL i LDL w grupach karmionych dietami wysokotłuszczowymi. Natomiast zastosowane diety wpłynęły różnie na stężenie cholesterolu całkowitego i triacylogliceroli w badanych grupach zwierząt.
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