Biomedical subjects

A T Høstmark

Publications and source records attributed to A T Høstmark.

At least 19 recordsLinked to original sources

PubMed2001

Effect of acupuncture on smoking cessation or reduction: an 8-month and 5-year follow-up study.

BACKGROUND: This study was undertaken to examine whether acupuncture treatment may have a long-term effect on smoking cessation or reduction. METHODS: Altogether 46 healthy men and women who reported smoking 20 +/- 6 cigarettes per day (mean +/- SD) volunteered in the study. They were randomly assigned to a test group (TG) or to a control group (CG) in which presumed anti-smoking acupoints were stimulated (TG) or acupuncture was applied to acupoints considered to have no effect on smoking cessation (CG). Before each treatment, after the last one, and 8 months and 5 years after the last one, each subject answered questionnaires about his or her smoking habits and attitudes. Blood samples for measuring variables related to smoking, i.e., serum cotinine and serum thiocyanate, were taken. RESULTS: During the treatment period the reported cigarette consumption fell on average by 14 (TG) and 7 (CG) cigarettes per day (P < 0.001). For both groups the reported cigarette consumption rose on average by 5-7 cigarettes during the following 8 months, and there was no systematic change thereafter. Consequently, TG showed a maintained reduction in smoking; no lasting effect was seen for CG. The TG reported that cigarettes tasted worse than before the treatments, and also the desire to smoke fell. For TG the serum concentration of cotinine fell, and the values correlated with the reported smoking. CONCLUSIONS: This study confirms that adequate acupuncture treatment may help motivated smokers to reduce their smoking, or even quit smoking completely, and the effect may last for at least 5 years. Acupuncture may affect the subjects' smoking by reducing their taste of tobacco and their desire to smoke. Different acupoints have different effects on smoking cessation.

Acupuncture↗

PubMed2001

Active recovery and post-exercise white blood cell count, free fatty acids, and hormones in endurance athletes.

Strenuous endurance exercise in fasted subjects is accompanied by increased plasma levels of catecholamines, leucocytosis, low insulin, and elevated plasma free fatty acids (FFA). Immediately after such exercise, plasma FFA may rise to high and potentially harmful levels, whereas the white blood cell count (WBCC) rapidly decreases towards or below baseline values. The present work investigated how active recovery (AR) for 15 min at 50% of maximal oxygen consumption (VO2max), after 60 min of uphill running at 83% of VO2max, influenced plasma FFA, lymphocyte, neutrophil, granulocyte, and monocyte count, as well as adrenaline, noradrenaline, insulin and cortisol concentrations until 120 min post-exercise. Thirteen endurance athletes participated in the study [24.2 (3.7) years, 1.82 (0.06) m, 76.7 (7.9) kg and VO2max 69.2 (6.8) ml min-1 kg-1]. In a randomized order, the subjects completed two sets of strenuous workouts, followed by either AR or complete rest in the supine position (RR). Compared with RR, AR strongly counteracted the rapid increase in plasma FFA 5 min post-exercise. The decreases in neutrophil and monocyte counts post-exercise were nullified by AR, and the cell count stayed above resting values throughout the observation period. AR also counteracted the rapid return of hormone concentration towards baseline levels. It would appear that active recovery at low intensity after strenuous exercise can maintain sufficient adrenergic activation to counteract the post-exercise drop in WBCC. However, in spite of keeping the catecholamine concentration high and insulin levels low, AR can also maintain a low plasma FFA concentration, probably because of the continued use of FFA in muscle. It remains to be elucidated whether the observed high FFA and low WBCC values after RR have a negative effect on health. If so, AR could be a preventive measure.

Adult↗

PubMed2001

Apoptotic effects of dichloro stearic and dichloro myristic acid in human hepatoma cells (HepG2).

Chlorinated fatty acids represent the major fraction of extractable organically bound chlorine in fish. After dietary intake such fatty acids may accumulate in adipose tissue, and even be transferred from mother to child via breast milk. We have previously reported that 9,10-dichloro stearic acid and 5,6-dichloro myristic acid inhibited cell growth. The aim of the present work was to investigate whether the growth inhibitory effect of these modified fatty acids might involve apoptosis. Human hepatoma cells (HepG2) were cultured for 4 days before addition of chlorinated fatty acids, and then cultured for another day before harvested. Morphological analysis was mainly done by light microscopy. In addition, fluorescence microscopy and electrophoretic analysis of DNA were carried out. The effect of 0.3 and 0.6 mmol/l was studied. Both chlorinated fatty acids seemed to cause a concentration-dependent increase in the relative abundance of pycnotic and broken nuclei, as well as nuclear fragments, with the strongest effect of dichloro stearic acid. Apoptosis by the chlorinated fatty acids was however less than that of docosahexaenoic acid, a known apoptosis effector. In conclusion, chlorinated fatty acids seem to possess the ability to cause apoptosis.

Apoptosis↗

PubMed2001

Effect of long-term storage on the concentration of albumin and free fatty acids in human sera.

Stored sera from healthy persons can be used to study relationships between blood variables at the time of sampling and disease appearing several years later but storage may influence the variables. In this work we measured the concentration of albumin and free fatty acids (FFA) in samples from the JANUS serum bank of Norway. Sera from blood donors and persons participating in health screening programs have been added to the bank since 1973. The concentration of albumin and FFA was measured in 443 JANUS bank sera. The material was divided into quartiles according to the length of storage: <3 years (n = 110), 3-6 years (n = 110), 6-12 years (n = 115) and >12 years (n = 108). Albumin was measured colorometrically using the bromcresol green method and FFA was determined enzymatically. The serum albumin concentrations (mean +/- SEM) in the four groups were 55.8+/-0.6, 56.2+/-0.5, 59.9+/-0.6 and 59.5+/-0.6 g/L. The values of groups 3 and 4 were significantly higher than those of groups 1 and 2 (p<0.001). The serum FFA concentrations in the four groups were 0.56+/-0.03, 0.64+/-0.03, 0.77+/-0.03 and 0.85+/-0.04 mmol/L, i.e. a significant storage effect. The Scheffé multiple comparison test showed that FFA values in groups 3 and 4 were significantly higher than those in groups 1 and 2 (p <0.001 for group 4 vs. 1 and 2, and 3 vs. 1; p<0.04 for group 3 vs. 2) Serum FFA and albumin levels were positively associated (r = 0.489, p <0.01). Using linear regression analysis, it was estimated that serum albumin values increased by 0.28 g/L per year (i.e. 0.5%) and FFA by 0.02 mmol/L (i.e. 3.8%). Thus, measured by standard methods, serum FFA and albumin could increase in response to several years of storage at -25 degrees C. It is suggested that the storage time dependent increase in FFA is due to FFA liberation from lipoprotein triglycerides, whereas the apparent increase in albumin concentration possibly could be attributed to an unfolding of the protein, allowing more bromcresol green to be bound.

Blood Preservation↗

PubMed2001

Predictors of restenosis after coronary angioplasty. A study on demographic and metabolic variables.

OBJECTIVE: The major concern about percutaneous transluminal coronary angioplasty (PTCA) is the high incidence of restenosis. METHODS: Demographic, clinical and biochemical data were recorded 2 weeks prior to PTCA in 388 patients fulfilling the criteria for initial stenosis, successful PTCA, and angiographic follow-up after 6 months. Restenosis was evaluated by quantitative coronary angiography. RESULTS: Variables predictive of restenosis in univariate analysis were diabetes mellitus, male gender, and the levels of high density lipoprotein (HDL) cholesterol, apolipoprotein A1 (Apo A1) and thio-barbituric acid-reactive substances (TBARS). In trend analysis through quartiles TBARS and fasting glucose levels were significantly associated with restenosis (p = 0.016 and 0.044, respectively), whereas the negative predictivity of Apo A1 and HDL-cholesterol were of borderline significance. In multivariate analysis male gender and diabetes mellitus showed predictivity of significance, and a negative predictivity was also apparent for HDL-cholesterol. CONCLUSION: We conclude that diabetes mellitus, male gender, and low HDL-cholesterol are predictors of restenosis 6 months after PTCA. In addition, TBARS may be a marker for the development of restenosis after PTCA.

Adult↗

PubMed2001

Lipid peroxidation and growth inhibition of human microvascular endothelial cells.

Peroxidation products of polyunsaturated fatty acids may cause growth inhibition of cells in culture. This study was carried out to elucidate to what extent peroxidation products may be found in growth media, with and without cells and albumin, using thiobarbituric acid-reactive substances (TBARS) and protein carbonyl groups as measures of peroxidation. The growth of human microvascular endothelial cells was studied as influenced by docosahexaenoic (C22:6, n - 3), arachidonic acid (C20:4. n - 6), and serum albumin. Cell growth was strongly inhibited by the fatty acids, and the inhibition was related to the concentration of TBARS in the medium. Defatted albumin (0.5 g/100 ml) nullified the increase of TBARS in the medium and released the growth inhibition by the fatty acids. With polyunsaturated fatty acids (PUFA) there was a time- and concentration-dependent increase in media TBARS, observed both with and without cells, but the TBARS increase was somewhat greater in the presence of cells. Surprisingly, TBARS in cell-free media also increased somewhat upon increasing the albumin concentration from 0.5 to 5 g/100 ml, and the TBARS increase differed among various preparations of albumin. Unexpectedly, the albumin that had not been defatted gave the lowest TBARS values. The amount of protein carbonyl groups did not differ among various albumin preparations. It is concluded that PUFA may autooxidize in media used for cell cultures, and thereby cause an unspecific growth inhibition, which can be prevented by a low albumin concentration. However, even defatted albumin preparations may contain lipid peroxidation products, the causes and implications of which remain to be elucidated.

Arachidonic Acid↗

PubMed2000

[Physical activity, overweight and obesity].

Regular physical activity has profound effects on body composition and the utilisation of nutrients and help to maintain and increase skeletal muscle mass, with increased resting metabolic rate and enhanced capacity for lipid oxidation during rest and exercise. Regular exercise may also prevent or limit the loss of lean tissue (fat-free mass, FFM) during slimming regimens. Increased physical activity induces a number of favourable changes in the metabolism of lipoproteins: serum triglycerides are lowered by the increased lipolytic activity, the HDL concentration increases and the concentration of small dense LDL decreases. In addition, the enhanced metabolic capacity of skeletal muscle (metabolic fitness) will favorably influence risk factors such as insulin resistance and hypertension. Because regular physical activity has favorable effects on several of the comorbid conditions of obesity, particularly cardiovascular disease and type 2 diabetes, it is not surprising that the mortality rates seem to be lower in the overweight and moderately obese individuals who are physically fit compared with the unfit. The treatment of overweight and obese persons should perhaps be more focused on the level of regular physical activity than on body weight per se. For most of those who wish to reduce their body weight, it is recommended that they combine regular physical activity with a somewhat reduced energy intake, in particular of food rich in fat. Emphasis should be on promoting relatively low-intensity, long-duration physical activity which can be conveniently incorporated into daily life.

Body Composition↗

PubMed2000

Active recovery reduces the decrease in circulating white blood cells after exercise.

This study was conducted to examine the effects of different recovery regimens on white blood cell count (WBCC) and muscle enzyme activities following strenuous, submaximal, steady state workouts on a treadmill. Fourteen endurance trained, healthy, non-smoking college-aged males participated in the study. The workouts were followed by either 15-min of rest recovery (RR), or active recovery (AR). The AR consisted of running at 50% of VO2max whereas RR implied complete rest. Seven subjects completed two sets of 60-min running at 70% of VO2max (moderate intensity group, MI) followed by either RR or AR. The other seven completed two sets of 30-min running at 80% of VO2max (high intensity group, HI) followed by either RR or AR. Blood samples were drawn at rest, immediately after exercise, and at 15- and 120-min post-exercise (PE). Blood lactate concentrations increased throughout the running trials. Creatine kinase (CK), lactate dehydrogenase (LD), white blood cell count (WBCC) and thrombocyte count increased between rest and 0-min PE (p<0.05). Between 0-15-min PE, there were several significant differences between RR and AR in the HI-trial. RR was associated with a 35% reduction in WBCC, compared to only 6% decrease in AR (p<0.02). Neither during 15-120-min PE this period, nor in the 120-min sample alone, were there any significant differences in WBCC between the RR and AR experiments. In conclusion, the results show that AR as opposed to rest recovery prevents the initial 0-15-min PE fall in WBCC after strenuous endurance exercise.

Adult↗

PubMed2000

Active recovery counteracts the post-exercise rise in plasma-free fatty acids.

The present study investigated the effect of active recovery (AR) as compared to rest recovery (RR) upon FFA concentrations following moderate- (MI) or high-intensity (HI) running. Fourteen well-trained males (23.7 +/- 6 years, VáO2max = 69.5 +/- 1.8ml á min-1 kg-1) were randomly assigned into two trials (HI = 30 min at 82% of VáO2max; MI = 60 min at 75% of VáO2max). Within each group, the subject completed two sets of experiments of running followed by either AR (15 min running at 50% of VáO2max) or RR (complete rest in the supine position). Plasma volume changes after the exercise did not deviate between the AR or RR trials. In both the HI and MI trials, AR resulted in lower FFA peaks and lower overall FFA concentrations while performing AR (p <.05). However, upon discontinuing AR, there was a rise in the FFA concentration. At 120-min post-exercise, the FFA concentrations after AR and RR were not significantly different. The changes in the FFA/albumin ratio were similar to the FFA responses. It is concluded that AR may counteract the rise in FFA 5-15 minutes after exercise.

Adult↗

PubMed1999

Luminal loss and restenosis after coronary angioplasty. The role of lipoproteins and lipids.

AIMS: Lipoproteins and lipids, especially lipoprotein(a), have been studied as risk factors for restenosis after coronary angioplasty with conflicting results. We investigated the association between serum levels of lipoprotein(a) apolipoprotein A-1, apolipoprotein B-100, total-cholesterol, high density lipoprotein-cholesterol, triglycerides, and coronary luminal loss and restenosis after angioplasty. METHODS: The lipoproteins and lipids were measured in 305 consecutive patients who underwent successful angioplasty and reangiography 20+/-3 weeks after angioplasty. Single-vessel dilatation was performed in 251 patients. Luminal loss was defined as minimal luminal diameter post-angioplasty minus minimal luminal diameter at follow-up, divided by the interpolated reference diameter of the vessel. Restenosis was defined according to three dichotomous categorical criteria: (1) >50% diameter stenosis at follow-up (2) loss of >50% of the gain achieved by angioplasty, (3) the need for target vessel revascularization. RESULTS: There was no significant association between the serum levels of lipoproteins and lipids and luminal loss. Univariate analysis did not show any significant difference in the serum levels of any of the lipoproteins and lipids between the restenosis and no-restenosis groups. Multivariate analysis revealed that only the angiographic variables (luminal gain and post-angioplasty minimal luminal diameter) were associated with luminal loss and restenosis after angioplasty. CONCLUSION: Lipoproteins and lipids were neither associated with luminal loss nor independent risk factors for restenosis after angioplasty.

Amlodipine↗

PubMed1999

Short-term effects of exercise on plasma very low density lipoproteins (VLDL) and fatty acids.

PURPOSE: In the fasted state the lipid fuels for muscle metabolism are free fatty acids (FFA) released either from intramuscular triglycerides (TG), plasma albumin, or TG in circulating very low density lipoproteins (VLDL). The purposes of this study were to determine the influence of acute exercise of moderate intensity on 1) plasma total concentration of TG and VLDL components, 2) the plasma concentration and distribution of individual albumin-bound long-chain FFA, and 3) lipid peroxidation as measured by thiobarbituric acid reactive substances (TBARS). METHODS: Eight healthy male subjects each participated in one exercise (EX) and one rest (RE) experiment. In EX the subjects exercised for 90 min at 58+/-5% (mean +/- SD) of maximal O2 uptake on a cycle ergometer followed by 4.5 h bedrest. RE followed the same protocol, but without exercise. RESULTS: In EX there was no immediate change in VLDL concentration during the exercise. After exercise there was a decrease in VLDL, VLDL-TG, -cholesterol, -protein and -phospholipids compared with those after RE. There was no change in percentage composition of VLDL as result of exercise. Total plasma FFA concentration increased appreciably during exercise and remained elevated for several hours postexercise. There was no correlation between the change in FFA concentration and VLDL-TG. There was a significant positive correlation between the exercise-related increments in the various long-chain FFA, but the effect varied so that the relative abundance of oleic acid increased and that of stearic and arachidonic acid decreased during exercise. Plasma TBARS concentration increased during the day in both experiments. CONCLUSION: The results indicate that there is a delay in the effect of an exercise bout on plasma VLDL and confirm that exercise affects various FFA in plasma differentially.

Adult↗

PubMed1999

Growth-modulating effects of dichloro myristic and dichloro stearic acid in cell cultures.

Chloro-containing fatty acids are a major fraction of extractable, organically bound chlorine in fish. It has been suggested that dichloro stearic acid (9,10-dichlorooctadecanoic acid) (C18) is metabolized to dichloro myristic acid (5,6-dichlorotetradecanoic acid) (C14) which accumulates in tissues. Hence, the biological effects of the C18 dichloro fatty acid could be due to formation of the C14 dichloro fatty acid. In this study we have compared the effects of dichloro stearic and dichloro myristic acid on growth of three widely differing cell lines. Both fatty acids inhibited cell growth; however, dichloro myristic acid had a weaker growth inhibitory effect than dichloro stearic acid. Dichloro myristic acid had a biphasic effect (i.e. growth was stimulated at low concentrations, followed by inhibition at higher concentrations) on the growth of human hepatoma cells and immortalized human kidney epithelial cells, but no such effect on human microvascular endothelial cells. The order of potency for growth inhibition by dichloro myristic acid was consistently human hepatoma cells>immortalized human kidney epithelial cells >human microvascular endothelial cells, whereas the relative potency of dichloro stearic acid was variable. Albumin alone stimulated cell growth and had a stronger protective effect against growth inhibition by dichloro myristic acid than against that of dichloro stearic acid. It seems unlikely that a major part of the effect of dichloro stearic acid on cell growth is caused by conversion to dichloro myristic acid.

Analysis of Variance↗

PubMed1999

The effect of supplementation with omega-3 fatty acids on soluble markers of endothelial function in patients with coronary heart disease.

During progression of atherosclerosis the overlying endothelial cells alter their expression of some surface molecules. Circulating levels of such molecules may be quantified. We investigated the effect of omega-3 fatty acids (n-3 FA) on the levels of tissue plasminogen activator antigen, von Willebrand factor, and the soluble forms of thrombomodulin, P-selectin, E-selectin, and vascular cell adhesion molecule-1 in 54 patients with coronary heart disease. Twenty-three of the patients had taken 5.1 g/d n-3 FA for 6 months (group I) and 31 were given corn oil as placebo (group II). For another 4 weeks ("the study period") they all got 5.1 g/d of n-3 FA. Compliance was confirmed by demonstration of changes in relevant fatty acids in serum phospholipids. At baseline, significant differences between the groups were found with lower median values of von Willebrand factor (128% versus 147%) and soluble thrombomodulin (24.9 versus 32.5 ng/mL) and higher median values of soluble E-selectin (41.4 versus 35.5 ng/mL) and soluble vascular cell adhesion molecule-1 (573 versus 473 ng/mL) in group I. During the study period differences in changes between the groups were found; tissue plasminogen activator antigen and soluble thrombomodulin decreased (P for difference between the groups 0.001 and 0.015, respectively), whereas soluble E-selectin and soluble vascular cell adhesion molecule-1 increased (P for difference between the groups <0.01 for both) in group II relative to group I. Our results indicate that n-3 FA supplementation decreases hemostatic markers of atherosclerosis, whereas markers of inflammation may be increased. The latter may be the result of lipid peroxidation as a simultaneous decrease of vitamin E and increase in thiobarbituric acid-reactive substances were observed.

Adult↗

PubMed1998

Effect of beta-adrenoceptor blockade on postexercise oxygen consumption and triglyceride/fatty acid cycling.

In the recovery period after strenuous exercise, there is increased O2 uptake, termed the excess postexercise O2 consumption (EPOC). One of the mechanisms suggested to explain EPOC is activation of the triglyceride/fatty acid (TG/FA) cycle by catecholamines. The purpose of this study was to determine the effect of selective beta1- and nonselective beta-adrenoceptor blockade on EPOC and the TG/FA cycle. Seven healthy young men each participated in three control and three exercise experiments in a randomized and balanced sequence. In the exercise experiments, subjects exercised for 90 minutes at 58% +/- 2% (mean +/- SD) of maximal O2 uptake on a cycle ergometer, followed by a 4.5-hour bedrest. The control experiments followed the same protocol, but without exercise. In one control and one exercise experiment, the selective beta1-adrenoceptor antagonist atenolol (0.062 mg.kg(-1) body weight) was administered intravenously immediately after the exercise (EXAT) and at the corresponding time in the rest-control experiment (REAT). In a second set of control and exercise experiments, the nonselective beta-adrenoceptor antagonist propranolol (0.15 mg.kg(-1) body weight) was administered (REPRO and EXPRO). In a third set of rest and exercise experiments, an injection of saline was given instead of beta-antagonist (RE and EX). TG/FA cycling was calculated by combining results obtained with a two-stage glycerol infusion and indirect calorimetry. O2 uptake was significantly increased above control levels throughout the recovery period after exercise with the nonselective beta-adrenoceptor antagonist, beta1-adrenoceptor antagonist, and saline. However, there was no difference between the time course or magnitude of EPOC in the three situations. After 4.5 hours of bedrest, the mean increase in O2 uptake was 8% to 9% in all three conditions. TG/FA cycling was increased after exercise, but no effects of beta-antagonists were observed. We conclude that EPOC and the rate of TG/FA cycling are not attenuated by selective beta1- or nonselective beta-adrenoceptor blockade after an acute prolonged exercise protocol.

Adrenergic beta-Antagonists↗

PubMed1998

Adrenergic control of post-exercise metabolism.

After strenuous exercise there is a sustained increase in resting O2 consumption. The magnitude and duration of the excess post-exercise O2 consumption (EPOC) is a function of exercise intensity and exercise duration. Some of the mechanisms underlying the rapid EPOC component (<1 h) are well defined, while the mechanisms causing the prolonged EPOC component (>1 h) are not fully understood. It has been suggested that beta-adrenergic stimulation is of importance for the prolonged component. There is an increased level of plasma adrenaline and noradrenaline during exercise, and it is shown that catecholamines stimulate energy expenditure through beta-adrenoceptors. After exercise an increased fat oxidation and an increased rate of triglyceride fatty acid (TG-FA) cycling may account for a significant part of the prolonged EPOC component. These processes may be stimulated by catecholamines. However, the return of plasma concentration of catecholamines to resting levels after exercise is more rapid than the return of O2 uptake. But plasma concentration of catecholamines may be an insensitive indicator of sympathetic activity, since the clearance rate of catecholamines is high. Also, the sensitivity to catecholamines may be increased after exercise. A decreased post-exercise O2 uptake has been shown when beta-blockade is administered in dogs before the exercise bout. In a pilot study in humans, administration of beta-antagonist after exercise did not seem to change EPOC.

Animals↗

PubMed1998

Bone mineral density and menstrual irregularities. A comparative study on cortical and trabecular bone structures in runners with alleged normal eating behavior.

Bone mineral density (BMD), and associated biochemical and endocrine markers were compared in a group of runners with menstrual dysfunction (IR, n=13), and a group of performance matched eumenorrheic runners (R, n=15). All subjects claimed to have normal eating habits. Body height and weight, body mass index, and amount of body fat were similar. The IR group consisted of 5 presently oligomenorrheic (O) and 8 presently amenorrheic (A) runners. The BMD values of the athletes were additionally compared with corresponding values in a reference group (C) of healthy age matched controls (n=54). BMD values were significantly lower in IR compared with R on all measuring sites: Total body (-9%, p=0.03), femoral neck (-11%, p=0.01), lumbar spine (-12%, p=0.001), lower leg (-6.5%, p=0.03) and arms (-7%, p=0.01). In addition, IR athletes had lower total body (-5%, p=0.01), and lumbar spine BMD (-10%, p=0.001) than C. No differences were observed in serum IGF-1, SHBG, testosterone and cortisol, or in the biochemical marker of bone formation (osteocalcin) and bone resorption (1 CTP). Values of serum E2, FSH and LH were low in IR and normal in R. TSH was in the normal range in both groups, but f-T4 was significantly lower in IR than in R. The athletes were furthermore grouped according to past and present menstrual dysfunction severity. At all measuring sites, with the exception of the lower leg, increasing menstrual dysfunction severity was linearly associated with declining BMD values (p<0.05). In conclusion, even highly conditioned cortical bone tissue seems to be negatively related to menstrual disorders, which may serve to explain the high incidence of stress fractures in athletes with menstrual disorders. Single measurements of biochemical markers of bone resorption and formation may not reflect the current bone status.

Adipose Tissue↗

PubMed1998

Growth modulating effects of chlorinated oleic acid in cell cultures.

Chlorinated fatty acids represent a major fraction of extractable, organically bound chlorine in fish. After dietary intake such fatty acids may be transferred from the mother to the foetus through the placenta, and via breast milk to the child. In the present work we have studied the effect of chlorinated oleic acid on the growth of three widely differing types of cells in culture. Chlorinated oleic acid inhibited growth of Human Microvascular Endothelial Cells (HMVEC), Immortilized Human Kidney Epithelial (IHKE) cells, and human Hepatoma cells (HepG2). The order of potency was: HMVEC > IHKE > HepG2. Vitamin E counteracted the inhibitory effect of chlorinated oleic acid on HepG2 cells, but did not significantly affect the fatty acid effect on HMVEC or IHKE. Defatted serum albumin stimulated the growth of HMVEC and IHKE. With HMVEC there was no major interaction between the effect of albumin and chlorinated oleic acid on cell growth. In contrast, with IHKE albumin at low concentration abolished the growth inhibiting effect of chlorinated oleic acid and appreciably counteracted growth inhibition by the fatty acid of HepG2. We conclude that the growth modulation by chlorinated oleic acid and its interaction with vitamin E and albumin are cell specific.

Albumins↗

PubMed1997

Omega-3 fatty acid supplementation does not improve maximal aerobic power, anaerobic threshold and running performance in well-trained soccer players.

In a randomized, placebo-controlled study the effect of 10 weeks of supplementation with either 5.2 g of a concentrated fish oil triglyceride (Triomar) enriched in omega-3 fatty acids (1.60 g/day EPA and 1.04 g/ day DHA) or 5.2 g corn oil (serving as placebo) on maximal aerobic power, anaerobic threshold and running performance was assessed in 28 well-trained male soccer players (18-35 years). Supplements were given as 650-mg capsules. Capsule assignment was randomized to one omega-3 group (n = 15), given eight Triomar capsules per day, and one placebo group (n = 13), given eight capsules of corn oil per day. During the 10-week supplementation period the subjects maintained their usual diets and training regimes. Red blood cell (RBC) osmotic fragility, triglycerides and fatty acid composition in plasma were assessed before and after the supplementation period. The pre- and post-supplementation tests of maximal aerobic power, anaerobic power and running performance showed no significant difference between the two groups. Subjects in the omega-3 group had significantly reduced plasma triglycerides, rose EPA (175%) and DHA (40%) in the total lipid fraction of plasma after supplementation. RBC osmotic fragility did not change. In conclusion, the results do not support the hypothesis that endurance athletes can improve maximal aerobic performance by omega 3-fatty acid supplementation.

Adult↗