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Biomedical subjects

E Tvrzická

Publications and source records attributed to E Tvrzická.

At least 19 recordsLinked to original sources

[Changes in serum and adipose tissue fatty acid composition after low calorie diet with respect to dietary fat content in obese].

BACKGROUND: Recently, a new attention has been paid to beneficial effects of high-fat diet on the body weight reduction and metabolic profile in obese subjects. In this study we compared the effects of two hypocaloric diets with different proportion of fat on fatty acid composition (FA) in blood and adipose tissue (AT). METHODS AND RESULTS: Forty-four obese subjects were submitted to 10 weeks' low-calorie diet. Subjects were randomized into low-fat diet (LFD) (20-25% of energy content) and high-fat diet groups (HFD) (40-45%). Before and at the end of the intervention, samples of blood and subcutaneous AT were taken for the analysis of fatty acid composition. The diet-induced body weight and fat mass reduction were not different between the two diets. Plasma triacylglycerols (TAG) were reduced during HFD only. Both diets reduced proportion of n-3 polyunsaturated fatty acids in AT and of saturated fatty acid in blood TAG, with no difference between the diets. HFD induced a higher increase of monounsaturated fatty acids in blood TAG. No other diet-induced changes were found in proportion of major classes of fatty acids. In respect to individual fatty acids, the diets induced a number of changes in AT and blood, the changes, however, not being different between the diets. CONCLUSION: Hypocaloric diets induce a number of changes in fatty acid composition in blood and adipose tissue, with little differences in respect to the proportion of fat in the diet. The results suggest the diet-induced changes in fatty acid composition are controlled by the calorie deficit of the diet and the proportion of dietary fat plays a minor role.

Adipose Tissue↗

[Nicotinic acid: an unjustly neglected remedy].

In human organism, the administration of nicotinic acid (niacin) leads to two types of effects. Within the physiological range (approximately = 20 mg/day), niacin has a vitamin-like role as pellagra preventing factor. The pharmacological dosage (approximately 0,5-4,5 g/day) substantially influences the plasma lipid and lipoprotein concentrations: decreases VLDL and LDL concentrations, changes the profile of LDL subfractions towards the larger particles as well as particles with lower density; it also profoundly increases the concentration of HDL-C in consequence of elevated concentration of HDL2 subfraction. Niacin as the only hypolipidemic drug reduces the lipoprotein(a) concentration. The hypolipidemic mechanism of niacin is different from that of other hypolipidemic drugs. On the basis of clinically controlled trials (both interventional epidemiological and angiographical), which satisfy the criteria of evidence-based medicine, it is possible to conclude that niacin falls unambiguously into the class of hypolipidemic drugs with proven beneficial effect not only on cardiovascular mortality and morbidity, but also on total mortality. Therefore, niacin should have an indisputable role in the pharmacological control of dyslipidemias. With the respect of basic mechanism (inhibition of the lipolysis of adipose tissue) with subsequent decrease in the concentration of free fatty acids and their flux to liver, niacin fulfils the criteria for pathogenetic treatment of atherogenic dyslipidemia in metabolic syndrome. The prerequisite condition for the niacin treatment is the respect for serious adverse effects and possible health hazards of administration (skin flush, hepatotoxicity and deterioration of glucose homeostasis). Recently discovered extrahypolipidemic effects of niacin (antioxidative activity, facilitation of reverse cholesterol transport, activation of PPAR-gamma, antithrombotic effects) and the introduction of drug forms with sustained (extended resp.) release of active compound (that minimizes the adverse effects and administration hazards) form together the basis for firm statement that the derivatives of nicotinic acid should be introduced to the clinical practice in Czech Republic.

Humans↗

The influence of n-3 polyunsaturated fatty acids and very low calorie diet during a short-term weight reducing regimen on weight loss and serum fatty acid composition in severely obese women.

Polyunsaturated fatty acids of n-3 series (n-3 PUFA) were shown to increase basal fat oxidation in humans. The aim of the study was to compare the effect of n-3 PUFA added to a very low calorie diet (VLCD), with VLCD only during three-week inpatient weight reduction. Twenty severely obese women were randomly assigned to VLCD with n-3 PUFA or with placebo. Fatty acids in serum lipid fractions were quantified by gas chromatography. Differences between the groups were determined using ANOVA. Higher weight (7.55+/-1.77 vs. 6.07+/-2.16 kg, NS), BMI (2.82+/-0.62 vs. 2.22+/-0.74, p<0.05) and hip circumference losses (4.8+/-1.81 vs. 2.5+/-2.51 cm, p<0.05) were found in the n-3 group as compared to the control group. Significantly higher increase in beta-hydroxybutyrate was found in the n-3 group showing higher ketogenesis and possible higher fatty acid oxidation. The increase in beta-hydroxybutyrate significantly correlated with the increase in serum phospholipid arachidonic acid (20:4n-6; r = 0.91, p<0.001). In the n-3 group significantly higher increase was found in n-3 PUFA (eicosapentaenoic acid, 20:5n-3, docosahexaenoic acid, 22:6n-3) in triglycerides and phospholipids. The significant decrease of palmitoleic acid (16:1n-7) and vaccenic acid (18:1n-7) in triglycerides probably reflected lower lipogenesis. A significant negative correlation between BMI change and phospholipid docosahexaenoic acid change was found (r = -0.595, p<0.008). The results suggest that long chain n-3 PUFA enhance weight loss in obese females treated by VLCD. Docosahexaenoate (22:6n-3) seems to be the active component.

3-Hydroxybutyric Acid↗

[Pathophysiology of and clinical significance of polyunsaturated fatty acids n-3 family].

Polyunsaturated fatty acids of n-3 family play an important role in the prevention of ischemic heart disease, as was shown in many epidemiological as well as intervention studies. These fatty acids are essential and human organism is fully dependent on their dietary intake from chloroplast of green plants and fat of aquatic animals. Cardioprotective action of these acids results from their complex effect (antiarrhytmic, antithrombotic, antiinflammatory, hypolipidemic etc.). These acids can, with the exception of glucose homeostasis, favourably influence individual components of the metabolic syndrome. Beneficial effects of n-3 polyunsaturated fatty acids are supposed also in chronic inflammatory and autoimmune diseases, psychiatric-neurological diseases and malignant tumours. In the case of rheumatoid arthritis, antiinflammatory effects of polyunsaturated fatty acids were proven. In general, favourable effects of the optimal income of n-3 polyunsaturated fatty acids can be explained by the influencing of cellular metabolic functions, incorporation into membrane phospholipids, modulation of enzymes and signal molecules as well as by direct impact on gene expression. Polyunsaturated fatty acids of n-3 family have high therapeutic potential, which results from the combined action on different levels of cell functions. In some diseases, their effect is nearly pharmacological - prevention of the sudden death and fatal myocardial infarction, treatment of hyper- and dyslipoproteinemias, suppression of the inflammatory activity in rheumatoid arthritis. In another group of diseases, they have supporting effect (prevention of the arterial hypertension in metabolic syndrome) and, finally, in the last one (psychiatric-neurological diseases and tumours), more data of defined clinical groups are necessary for final evaluation.

Fatty Acids, Omega-3↗

[Insulin resistance, metabolic syndrome and cardiovascular diseases].

The article summarizes the nature and causes of the insulin resistance, its relation to the metabolic syndrome, and to the cardiovascular diseases. Insulin resistance can be defined as a set of abnormal clinical symptoms accompanied by lower tissue sensitivity to insulin. Metabolic syndrome, whose major components are impairments of glucose homeostase, obesity, dyslipidemia and arterial hypertension, represents an important risk factor for the development of diabetes mellitus type 2 and for the development of cardiovascular diseases. Possible factors, which can influence those relations, e.g., chronic inflammations, endothelial dysfunction and oxidation stress are discussed. The primary aims for the positive influencing the metabolic syndrome is the prevention of the development of diabetes mellitus type 2 and that of cardiovascular diseases. To approach those goals, the use of non-pharmacologic means (diet, appropriate physical activity) and pharmacologic (treatment of dyslipidemia, namely by statins and fibrates; management of hypertension, specifically by angiotensin-converging enzyme inhibitors, by angiotensin-receptor blockers, by glitazoe administration and by antithrombotic treatment) can be recommended.

Cardiovascular Diseases↗

Effect of long-term administration of antidepressants on the lipid composition of brain plasma membranes.

The connection between changes in lipid pattern in brain plasma membranes and long-term administration of therapeutically effective doses of antidepressants has not been sufficiently demonstrated so far. Therefore, we analyzed effect of antidepressants that differ in pharmacological selectivity on membrane lipid composition in the rat brain tissue. Laboratory rats were given desipramine, maprotiline, citalopram, moclobemide or lithium for a 4-week period. We observed a significant decrease in phosphatidylethanolamine representation after administration of maprotiline, citalopram and moclobemide when compared with controls. Membrane cholesterol content was decreased after desipramine administration and increased after citalopram or lithium treatment. Electroneutral phospholipids were decreased after the administration of all tested antidepressants except for desipramine. Decrease in phosphatidylserine was found following long-term administration of maprotiline or desipramine; relative representation of phosphatidylinositol was reduced after lithium treatment. Statistically significant negative correlation between cholesterol and electroneutral phospholipids was discovered. Membrane microviscosity evaluated by fluorescence anisotropy of membrane probes was only slightly decreased after desipramine and increased after citalopram administration. Hypothesis was supported that changes in brain neurotransmission produced by antidepressants could be, at least partially, associated with adaptive changes in membrane cholesterol and phospholipids.

Adaptation, Physiological↗

[Effect of n-3 polyunsaturated fatty acids on plasma lipid, LDL lipoperoxidation, homocysteine and inflammation indicators in diabetic dyslipidemia treated with statin + fibrate combination].

BACKGROUND: The aim of the study was to determine how addition of n-3 polyenic fatty acids (PUFA) to the present treatment with statin + fibrate combination in diabetic dyslipidemia effects plasma lipids and lipoproteins, LDL lipoperoxidation, glucose homeostasis, concentration of serum homocysteine and selected inflammation indicators. METHODS AND RESULTS: 24 patients with type 2 diabetes, who after the combined hypolipidemic treatment (pravastatin 20 mg + micronized fenofibrate 200 mg per day) cannot reach the recommended target values for long time, received for three consecutive months supplementation of 3,6 g PUFA n-3 per day or a placebo (olive oil). At the beginning of the study, after three months of PUFA supplementation and after another three months of placebo administration, concentrations of plasma lipids, composition of fatty acids, plasma phosphatidylcholine (PC), cholesterol esters (CE) and triglycerides (TG), concentration of tHcy, conjugated diens (CD) in LDL and selected inflammation indicators (IL-6, TNFalpha, VCAM-1) were determined. n-3 PUFA supplementation resulted in the significant decrease of tHcy concentration (-29%, P < 0.01) and TG (-28%, P < 0.05) in plasma. During the period of placebo administration, values returned to base line levels. CD concentration in LDL after n-3 PUFA increased by 15% (P < 0.15, not significant), meanwhile after the placebo containing oleic acid it decreased by 18% (P < 0.05). CONCLUSIONS: Our results show that n-3 PUFA supplementation together with statin + fibrate combination in DDL patients can significantly decrease the risk of cardiovascular diseases.

Adult↗

Composition of plasma fatty acids and non-cholesterol sterols in anorexia nervosa.

Anorexia nervosa is a model of simple starvation accompanied by secondary hyperlipoproteinemia. The pattern of plasma fatty acids influences the levels of plasma lipids and lipoproteins. The concentration of plasma lathosterol is a surrogate marker of cholesterol synthesis de novo, concentrations of campesterol and beta-sitosterol reflect resorption of exogenous cholesterol. The aim of the study was to evaluate fatty acids in plasma lipid classes and their relationship to plasma lipids, lipoproteins, cholesterol precursors and plant sterols. We examined 16 women with anorexia nervosa and 25 healthy ones. Patients with anorexia nervosa revealed increased concentrations of total cholesterol, triglycerides, HDL-cholesterol, campesterol and beta-sitosterol. Moreover, a decreased content of n-6 polyunsaturated fatty acids was found in all lipid classes. These changes were compensated by an increased content of monounsaturated fatty acids in cholesteryl esters, saturated fatty acids in triglycerides and both monounsaturated and saturated fatty acids in phosphatidylcholine. The most consistent finding in the fatty acid pattern concerned a decreased content of linoleic acid and a raised content of palmitoleic acid in all lipid classes. The changes of plasma lipids and lipoproteins in anorexia nervosa are the result of complex mechanisms including decreased catabolism of triglyceride-rich lipoproteins, normal rate of cholesterol synthesis and increased resorption of exogenous cholesterol.

Adult↗

Corticosteroid effect on Caco-2 cell lipids depends on cell differentiation.

Previous studies from our laboratory have indicated that secondary hyperaldosteronism affects phospholipids of rat colonic enterocytes. To assess whether this represents a direct effect of mineralocorticoids on enterocytes, the role of aldosterone and dexamethasone in the regulation of lipid metabolism was examined in Caco-2 cells during development of their enterocyte phenotype. Differentiation of Caco-2 cells was associated with increased levels of triglycerides (TG) and cholesteryl esters (CE), a decreased content of cholesterol and phospholipids and changes in individual phospholipid classes. The phospholipids of differentiated cells had a higher content of n-6 polyunsaturated fatty acids (PUFA) and lower amounts of monounsaturated (MUFA) and saturated fatty acids than subconfluent undifferentiated cells. Differentiated cells exhibited a higher ability to incorporate [3H]arachidonic acid (AA) into cellular phospholipids and a lower ability for incorporation into TG and CE. Incubation of subconfluent undifferentiated cells with aldosterone or dexamethasone was without effect on the content of lipids, their fatty acids and [3H]AA incorporation. In contrast, aldosterone treatment of differentiated cells diminished the content of TG, increased the content of phospholipids and modulated their fatty acid composition. The percentage of n-6 and n-3 PUFA in phospholipids was increased and that of MUFA decreased, whereas no changes in TG were observed. The incorporation of [3H]AA into phospholipids was increased and into TG decreased and these changes were blocked by spironolactone. Treatment of differentiated cells with dexamethasone increased their CE content but no effect was identified upon other lipids, their fatty acid composition and on the incorporation of [3H]AA. As expected for the involvement of corticosteroid hormones the mineralocorticoid and glucocorticoid receptors were identified in Caco-2 cells by RT-PCR. The results suggest that aldosterone had a profound influence on lipid metabolism in enterocytes and that its effect depends on the stage of differentiation. The aldosterone-dependent changes occurring in phospholipids and their fatty acid composition may reflect a physiologically important phenomenon with long-term consequences for membrane structure and function.

Aldosterone↗

Higher content of 18:1 trans fatty acids in subcutaneous fat of persons with coronarographically documented atherosclerosis of the coronary arteries.

AIM: To identify the total content of trans fatty acid (TFA) isomers and C18:1 trans isomers in subcutaneous fat samples from persons with atherosclerosis of the coronary arteries, as an indicator of dietary exposure. METHODS: Using capillary gas chromatography, the authors determined total content of TFA isomers and C18:1 trans isomers in the subcutaneous fat of 34 patients with ischemic heart disease who had undergone aortocoronary bypass surgery and in 46 patients with no sign of coronary disease. RESULTS: On average, the total TFAs in cardiac patients were 2.88 +/- 1.19% of all fatty acids, in noncardiac patients 2.56 +/- 0.89%. However, the difference is not statistically significant. The average concentration of C18:1 trans in cardiac patients (2.31 +/- 1.09%) was statistically significantly higher (p = 0.05) than in the noncardiac group (1.95 +/- 0.77%). CONCLUSIONS: The results obtained indicate a lower TFA load in comparison with previous studies in other countries. A higher concentration of 18:1 TFAs in the subcutaneous fat of patients with coronary disease might be an impulse to correct the dietary habits of this very high-risk population.

Adipose Tissue↗

[Lipid metabolism in anorexia nervosa].

BACKGROUND: Anorexia nervosa is a model of simple starvation accompanied by secondary hyperlipoproteinemia. Plasma fatty acid pattern influences levels of plasma lipids and lipoproteins. Level of plasma lathosterol represents a marker of cholesterol synthesis de novo; levels of plant sterols reflect resorption of exogenous cholesterol. The aim of the study was to evaluate fatty acids in plasma lipid classes and their relationships to plasma lipids, lipoproteins, lathosterol, campesterol and beta-sitosterol. METHODS AND RESULTS: We examined 16 women with anorexia nervosa and 25 matched controls. Main lipid classes were separated by thin-layer chromatography, fatty acids and non-cholesterol sterols were evaluated by capillary gas chromatography. Patients with anorexia nervosa revealed increased concentrations of total cholesterol, triglycerides, HDL-cholesterol, campesterol and beta-sitosterol; changes in plasma levels of lathosterol did not reach statistical significance. The most consistent finding in fatty acid composition was a decreased content of linoleic acid and raised content of palmitoleic acid in all lipid classes. CONCLUSIONS: Changes of plasma lipids and lipoproteins in anorexia nervosa result from complex mechanisms including increased synthesis of triglyceride-rich lipoproteins along with unchanged cholesterol synthesis rate. Hypercholesterolemia in anorexia nervosa may also result from increased resorption of exogenous cholesterol.

Adult↗

Effect of column and software on gas chromatographic determination of fatty acids.

Four capillary columns (A: CP-WAX 52 CB 25 m x 0.25 mm; B: CP WAX 52 CB 30 m x 0.25 mm; C: CP-WAX 58 CB 25 m x 0.25 mm, Chrompack; D: OMEGAWAX 320 30 m x 0.32 mm, Supelco) and two integration software (Mosaic v.5.10, Chrompack and CSW v.1.7, Data Apex5) were compared for analysis of fatty acids. Column A was mounted stepwise in two different instruments. Fatty acids of blood plasma phosphatidylcholine and standard mixture of saturated fatty acids were analysed as methyl esters under identical chromatographic conditions. Both integrating software did not differ significantly in most results; differences were observed only for minor components: 16:1n9 (0.10+/-0.020 vs. 0.17 +/- 0.005 M%, P < 0.0001, column Al; 0.09 +/- 0.011 vs. 0.16 +/- 0.007 M%, P< 0.0001, column A2; 0.09 +/- 0.010 vs. 0.17 +/- 0.003 M%, P < 0.0001, column C; 0.09 +/ -0.008 vs. 0.19 +/- 0.003 M%, P < 0.0001, column D), 20:0 (0.10+0.001 vs. 0.06 +/- 0.005 M%, P < 0.05, column C) and 20:2n6 (0.43 +/- 0.030 vs. 0.91 +/- 0.016 M%, P < 0.0001, column A2). Increased values for 16:1n9 and 20:2n6 integrated by MOSAIC are caused by cointegration of two poorly resolved peaks: fatty acid and impurity from sample matrix. Lower values for 20:0 are caused by incomplete integration of minor peak. Differences between columns were observed mostly for minor fatty acids. The results indicate that CSW is more suitable software for integration of complicated chromatograms. Linear calibration dependences measured with standard mixture of saturated fatty acids (carbon number 10-24) were observed in wide range of concentrations (three orders). Slope close to unity and minimal value of intercept confirmed theoretical relations when analyses are run under optimal conditions. Use of one column is advisable in small intervention or experimental metabolic studies.

Calibration↗

[Effect of fibrates on VLDL and LDL lipoprotein composition and parameters of their oxidation in hypertriglyceridemia].

BACKGROUND: Meta-analyses of epidemiological studies proved that hypertriacylglycerolemia (HTAG) is an independent CHD risk factor. The VLDL lipoproteins, which are the main TAG carrier, are precursors of atherogenic LDL and their increased concentration is related to the decrease of antiatherogenic HDL, increased ratio of small, dense LDL and represents one of the causes of the endothelial dysfunction. According to some authors, HTAG is one of the factors of the oxidation stress. MATERIAL AND METHODS: 45 patients of the studied group received 200 mg of micronized fenofibrate per day for six weeks. Before the beginning and after the end of treatment, following examinations were carried out: concentration of plasma lipids, lipoproteins, and apolipoproteins, composition of fatty acids (FA) in main lipid plasma classes and LDL (phosphatidylcholine--PC, TAG, cholesteryl esters--CE) and lipoperoxidation in VLDL and LDL, isolated by preparative ultracentrifugation. RESULTS AND CONCLUSIONS: In plasma, the treatment of HTAG led to a significant decrease of TC, TAG and apo-B concentration and to the increase of cholesterol concentration in HDL and in both HDL2 and HDL3 subfractions. In isolated LDL particles we observed a decrease of the TAG portion (by 25%) together with significant lag phase prolongation (by 33%, P < 0.05) and peak time retardation (by 24%, P < 0.05). In VLDL particles the concentration of cholesterol became smaller (by 28%), TAG (by 26%), phospholipids (by 28%) (in all groups P < 0.005) and the lag phase became significantly longer (by 16%, P < 0.01). Treatment with fenofibrate significantly reduced the linoleic acid (18:2n-6) in PC and TAG plasma, CE and TG LDL, in a higher ratio of palmitoleic acid (16:1n-7) in CE LDL, oleic (18:1n-9) in PC LDL, in significant concentration of total monoenic FA in PC and CE LDL and to a significant increase of the concentration of myristic acid (14:0) in CE and myristic and stearic acids (18:0) in TAG LDL. From our results it is possible to conclude that the six-week long treatment of HTAG with micronized phenofibrate led to significant modification of LDL and VLDL composition accompanied by their lower lipoperoxidation indexes. These favourable changes in oxidability were accompanied with changes in the composition of FA in CE, TAG and PC plasma as well as LDL.

Adult↗

The responses of serum and adipose Fatty acids to a one-year weight reduction regimen in female obese monozygotic twins.

We have reported strong intrapair resemblances (IPRs) in serum phosphatidylcholine (PC) fatty acid composition within adult monozygotic twins living apart. This study assessed the contribution of genetic factors to changes in serum and adipose tissue fatty acids resulting from weight loss and followed by a subsequent year of weight maintenance. Eleven pairs of female obese monozygotic twins (age: 38.9 +/- 1.8; BMI: 32.5 +/- 0.9) were recruited for the study. Fasting serum and adipose tissue were obtained after 1 week of inpatient stabilization, after 1 month of inpatient very-low-calorie diet (VLCD), and again after 1 year of outpatient weight maintenance. Fatty acids in serum lipid fractions and adipose tissue were quantitated by gas chromatography. Using multiple regression adjusted for age and initial value, IPRs were determined for the changes induced by VLCD and by the year of weight maintenance. There were few IPRs in nonessential fatty acids. By contrast, there were numerous IPRs for essential fatty acids (EFA), especially in the n-3 family across the VLCD. Following the maintenance year, however, frequent IPRs for nonessential fatty acids were seen, particularly in serum PC, and strong IPRs were seen for 18:3 n-3 and 20:5 n-3 across multiple fractions. These results infer the existence of strong genetic factors determining both the nonessential and EFA compositions of tissue lipids in humans independent of diet. Of particular note were the consistent IPRs for n-3 fatty acids despite dietary stress, indicating that the conservation and distribution of this EFA family are subject to considerable genetic variance in humans.

Adipose Tissue↗

[Effect of nutrition on adipose tissue metabolism in humans].

Lipolysis in adipose tissue and balance between energy intake and expenditure are involved in the regulation of adipose tissue mass. Several recent findings suggest that alterations in the regulation of lipolysis and/or energy balance might contribute to the development of obesity. Hormone-sensitive lipase and uncoupling proteins play important role in regulation of lipolysis in adipose tissue as well as in the regulation of energy balance of various tissues. Mechanisms of the control of expression of genes coding synthesis of these proteins are poorly known. A brief overview of the present knowledge of the effects of nutritional intervention on the regulation of lipolysis in adipose tissue and on the expression of genes of hormone-sensitive lipase and that of uncoupling proteins is given in this article. Results of the authors' studies on the effect of calorie restriction on gene expression in adipose tissue are presented.

Adipose Tissue↗

[Fatty acid composition and parameters of VLDL and LDL in persons with dyslipidemia].

BACKGROUND: Oxidatively modified LDL play an important role in the pathogenesis of endothelial dysfunction, initiation and development of atherosclerosis and stability of the atheromatous plaque. The increased oxidative stress is apparent from a number of deviations, which are part of the insulin resistance syndrome (hypertension, hypoalphacholesterolaemia, diabetes and hyperlipoproteinaemia). The objective of the work was to examine the degree of oxidation and oxidability of LDL and VDL in subjects with dyslipidaemia. METHODS AND RESULTS: In 40 subjects with dyslipidaemia, defined as a triglyceride concentration above 2.30 mmol/l and a drop of HDL cholesterol below 0.90 mmol/l, the authors assessed the fatty acid profile in plasma lipid classes and LDL by capillary gas chromatography. Lipoperoxidation in VLDL and LDL was examined by the method of kinetics of conjugated dienes according to Esterbauser. The results were compared with a group of healthy controls. The group of dyslipidaemic subjects had higher concentrations of NEFA, IRI, blood sugar and uric acid. In these subjects the concentration of conjugated dienes in VLDL was significantly higher and the lag stage in VLDL and LDL was reduced. Both groups differed as to the composition of VLDD and LDL. The group of dyslipidaemic subjects had a higher concentration of cholesterol, phospholipids, triglycerides and apolipoprotein B. A constant finding in the fatty acid profile of all lipid classes was a raised concentration of palmitoleic acid and reduced linoleic acid concentration. CONCLUSIONS: Dyslipidaemic subjects have, as compared with a control group, higher NEFA, IRI and uric acid concentrations. Furthermore they differed not only by the composition of VLDL and LDL but also by a higher degree of VLDL oxidation and reduced resistance to lipoperoxidation of VLDL and LDL particles. A consistent finding in the fatty acid profile was an increased level of palmitoleic acid in all plasma lipid classes and LDL and a drop of linoleic acid in phosphatidylcholine LDL and plasma cholesterolesters.

Adult↗

Aldosterone alters the phospholipid composition of rat colonocytes.

Previous studies have shown that aldosterone treatment of amphibian epithelial cells results not only in stimulation of Na(+) absorption but also in changes in phospholipid composition which are necessary for the mineralocorticoid action of aldosterone. The present study was designed to investigate the effect of aldosterone on phospholipids of mammalian epithelia. Phospholipid and fatty acid composition was examined in colonic epithelium (mineralocorticoid target tissue) and thymus (non-mineralocorticoid but glucocorticoid target tissue) of rats which had received aldosterone or vehicle by a miniosmotic pump for 7 days. Aldosterone increased the mass of colonic phospholipids relative to cellular proteins with concomitant changes in the percentage distribution of fatty acids, whereas the relative distribution of membrane phospholipds was not changed. Phosphatidylcholine increased the content of polyunsaturated and decreased that of monounsaturated fatty acids, which predominantly reflected the accretion of arachidonic and a decrease in oleic and palmitoleic acids. Within the phosphatidylethanolamine subclass, pretreatment of rats with aldosterone decreased the content of monounsaturated fatty acids (predominantly oleic and palmitoleic acid) and of n-3 fatty acids, and increased the content of saturated fatty acids (palmitic acid). The saturated-to-nonsaturated fatty acid ratio also significantly increased after aldosterone treatment. No changes in thymic phospholipids were seen. The results are consistent with the contention that aldosterone specifically modulates phospholipid concentration and metabolism in mineralocorticoid target tissue. The changes in phospholipid content and its fatty acid composition during the fully developed effect of aldosterone may reflect a physiologically important phenomenon with long-term consequences for membrane structure and function.

Aldosterone↗