Conversion of alpha-linolenic acid to eicosapentaenoic,docosapentaenoic and docosahexaenoic acids in young women

The extent to which women of reproductive age are able to convert the n-3 fatty acid alpha-linolenic acid (ALNA) to eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA) and docosahexaenoic acid (DHA) was investigated in vivo by measuring the concentrations of labelled fatty acids in plasma for 21 d following the ingestion of [U-13C]ALNA (700 mg). [13C]ALNA excursion was greatest in cholesteryl ester (CE) (224 (sem 70) micromol/l over 21 d) compared with triacylglycerol (9-fold), non-esterified fatty acids (37-fold) and phosphatidylcholine (PC, 7-fold). EPA excursion was similar in both PC (42 (sem 8) micromol/l) and CE (42 (sem 9) micromol/l) over 21 d. In contrast both [13C]DPA and [13C]DHA were detected predominately in PC (18 (sem 4) and 27 (sem 7) micromol/l over 21 d, respectively). Estimated net fractional ALNA inter-conversion was EPA 21 %, DPA 6 % and DHA 9 %. Approximately 22 % of administered [13C]ALNA was recovered as 13CO2 on breath over the first 24 h of the study. These results suggest differential partitioning of ALNA, EPA and DHA between plasma lipid classes, which may facilitate targeting of individual n-3 fatty acids to specific tissues. Comparison with previous studies suggests that women may possess a greater capacity for ALNA conversion than men. Such metabolic capacity may be important for meeting the demands of the fetus and neonate for DHA during pregnancy and lactation. Differences in DHA status between women both in the non-pregnant state and in pregnancy may reflect variations in metabolic capacity for DHA synthesis.     

Brain metabolism of alpha-linolenic acid during development.

To date, experimental models for evaluation of the relative contribution of conversion of 18:3n-3 to 22:6n-3 in brain, particularly during crucial stages of rapid brain growth, have limitations that preclude a definitive resolution of the relative contribution of conversion in brain per se compared with dependence on extracerebral sources of 22:6n-3. Clearly, brain in the neonatal period has substantial capacity for delta 6- and delta 5-desaturation that equals or surpasses that of immature liver. Furthermore, activity in brain is much less susceptible than that in liver to dietary fluctuations. Studies with cultured cells of neural origin provide valuable insight into relative contributions of alternate pathways and into molecular mechanisms of regulation of desaturation and chain elongation but obviously have limitations when trying to extrapolate this to the intact animal. Some investigators have concluded that 22:6n-3 for brain phospholipids may be derived primarily from liver and dietary sources; at the same time, brain has the capacity for formation of 22:6n-3 should 18:3n-3 be the primary dietary component of the n-3 family. Whereas 18:3n-3 itself appears not to be essential for esterification to brain membrane phospholipids, 22:6n-3 is clearly a vital and quantitatively significant component. Potentially, brain can convert 18:3n-3 to more polyunsaturated derivates during the growth period when the products are most needed and other sources such as diet or conversion by liver may be restrictive.     

Circulating linoleic acid and alpha-linolenic acid and glucose metabolism: the Hoorn Study

Purpose

Data on the relation between linoleic acid (LA) and alpha-linolenic acid (ALA) and type 2 diabetes mellitus (T2DM) risk are scarce and inconsistent. The aim of this study was to investigate the association of serum LA and ALA with fasting and 2 h post-load plasma glucose and glycated hemoglobin (HbA1c).

Method

This study included 667 participants from third examination (2000) of the population-based Hoorn study in which individuals with glucose intolerance were overrepresented. Fatty acid profiles in serum total lipids were measured at baseline, in 2000. Diabetes risk markers were measured at baseline and follow-up in 2008. Linear regression models were used in cross-sectional and prospective analyses.

Results

In cross-sectional analyses (n = 667), serum LA was inversely associated with plasma glucose, both in fasting conditions (B = ?0.024 [?0.045, ?0.002]) and 2 h after glucose tolerance test (B = ?0.099 [?0.158, ?0.039]), but not with HbA1c (B = 0.000 [?0.014, 0.013]), after adjustment for relevant factors. In prospective analyses (n = 257), serum LA was not associated with fasting (B = 0.003 [?0.019, 0.025]) or post-load glucose (B = ?0.026 [?0.100, 0.049]). Furthermore, no significant associations were found between serum ALA and glucose metabolism in cross-sectional or prospective analyses.

Conclusions

In this study, serum LA was inversely associated with fasting and post-load glucose in cross-sectional, but not in prospective analyses. Further studies are needed to elucidate the exact role of serum LA and ALA levels and dietary polyunsaturated fatty acids in glucose metabolism.

     

Effect of dietary alpha-linolenic acid on thrombotic risk factors in vegetarian men

BACKGROUND: Vegetarians have lower platelet and plasma concentrations of n-3 polyunsaturated fatty acids (PUFAs) than do omnivores. We recently showed that male vegetarians have higher platelet aggregability than do omnivores. OBJECTIVE: We investigated whether male vegetarians (n = 17) who consumed an increased amount of dietary alpha-linolenic acid (ALA) showed any changes in their tissue profile of PUFAs, plasma thromboxane concentrations, platelet aggregability, or hemostatic factors. DESIGN: During the study, all subjects maintained their habitual vegetarian diets except that a proportion of dietary fat was replaced with vegetable oils and margarines that were provided. Initially, all subjects consumed a low-ALA diet (containing safflower oil and safflower oil-based margarine) for 14 d; they then consumed either a moderate-ALA diet (containing canola oil and canola oil-based margarine) or a high-ALA diet (containing linseed oil and linseed oil-based margarine) for 28 d. Blood samples were collected at day 0 (baseline), day 14, and day 42. RESULTS: Eicosapentaenoic acid, docosapentaenoic acid, total n-3 PUFAs, and the ratio of n-3 to n-6 PUFAs were significantly increased (P < 0.05), whereas the ratio of arachidonic acid to eicosapentaenoic acid was decreased (P < 0.05), in platelet phospholipids, plasma phospholipids, and triacylglycerols after either the moderate-ALA or high-ALA diet compared with the low-ALA diet. No significant differences were observed in thrombotic risk factors. CONCLUSION: ALA from vegetable oils (canola and linseed) has a beneficial effect on n-3 PUFA concentrations of platelet phospholipids and plasma lipids in vegetarian males.     

Effects of casein and soy-protein on alpha-linolenic acid metabolism in rats.

In order to study the effects of different proteins on alpha-linolenic acid (alpha-LnA) metabolism, rats were given the diet added respectively with milk casein and soy-protein isolate (SPI) as sources of proteins and perilla oil as a source of lipid. The results obtained are as follows. The ratio of (C20:3 + C20:4)/C18:2 in liver microsomal PL, liver PE fraction, and kidney PE and PC fractions was significantly lowered by the SPI treatment when compared to the casein treatment, similarly to the already established results. In the liver microsomal PL and PE and PC fractions of liver and kidney in rats treated with SPI, there was also observed a significant decrease or a decrease tendency in the (C20:4 + C20:5)/C18:3 ratio. A similar tendency was again shown in the sigma (n-3)M/C18:3 ratio indicating metabolic conversion from C18:3(n-3) to C22:6. On the other hand, contrary to the ratios of (C20:3 + C20:4)/C18:2, sigma (n-3)M/C18:3, and (C20:3 + C20:5)/C18:3, the (C22:5 + C22:6)/C20:5 ratio which is the parameter for metabolic conversion of C20:5(n-3) was elevated in the PE and PC fraction of liver, heart and kidney in the SPI group compared to the casein group. Then, further analysis of the metabolic process from C20:5 to C22:6 showed that the C22:5/C20:5 ratio increased while the C22:6/C22:5 ratio decreased in the SPI group compared to the casein group. Based on these results, it is assumed that the metabolic process from C18:3(n-3) to C20:5(n-3) and from C22:5 to C22:6 is affected by SPI but that the elongation process from C20:5(n-3) to C22:5(n-3), on the contrary, is rather accelerated by SPI.     

Eicosapentaenoic acid decreases postprandial β-hydroxybutyrate and free fatty acid responses in healthy young and elderly

ObjectivesWe investigated whether a dietary supplement rich in eicosapentaenoic acid (EPA) increases fasting plasma ketones or postprandial ketone responses in healthy young and elderly subjects.MethodsTen young (22 ± 1 y old) and 10 elderly (75 ± 1 y old) subjects were recruited and participated in two identical study days, one before and one 6 wk after providing an EPA-enriched supplement (1.4 g/d of EPA and 0.2 g/d of docosahexaenoic acid). On the study days, blood samples were collected at fasting and every hour for 6 h after giving a breakfast. Fasting and postprandial plasma β-hydroxybutyrate (β-OHB), free fatty acid (FFA), triacylglycerol, glucose, and insulin responses were measured. Fatty acid profiles were assessed in fasting plasma samples before and after the EPA supplement.ResultsAfter the EPA supplement, postprandial plasma β-OHB responses decreased by 44% in the young and by 24% in the elderly subjects, in addition to 20% and 34% lower FFA responses in the young and elderly adults, respectively. β-OHB and FFAs were positively and significantly correlated in young but not in elderly subjects before and after the EPA supplement. In both groups, postprandial plasma triacylglycerols, glucose, and insulin were not significantly different after the intake of the EPA supplement. Before and after the EPA supplement, fasting plasma EPA was 50% higher in the elderly but increased by about five times in both groups after intake of the EPA supplement.ConclusionContrary to our expectations, EPA supplementation lowered postprandial β-OHB response and, in the elderly subjects, the concentration of postprandial β-OHB was not lowered after intake of the EPA supplement.     

Dietary alpha-linolenic acid reduces inflammatory and lipid cardiovascular risk factors in hypercholesterolemic men and women

Alpha-linolenic acid (ALA) reduces cardiovascular disease (CVD) risk, possibly by favorably changing vascular inflammation and endothelial dysfunction. Inflammatory markers and lipids and lipoproteins were assessed in hypercholesterolemic subjects (n = 23) fed 2 diets low in saturated fat and cholesterol, and high in PUFA varying in ALA (ALA Diet) and linoleic acid (LA Diet) compared with an average American diet (AAD). The ALA Diet provided 17% energy from PUFA (10.5% LA; 6.5% ALA); the LA Diet provided 16.4% energy from PUFA (12.6% LA; 3.6% ALA); and the AAD provided 8.7% energy from PUFA (7.7% LA; 0.8% ALA). The ALA Diet decreased C-reactive protein (CRP, P < 0.01), whereas the LA Diet tended to decrease CRP (P = 0.08). Although the 2 high-PUFA diets similarly decreased intercellular cell adhesion molecule-1 vs. AAD (-19.1% by the ALA Diet, P < 0.01; -11.0% by the LA Diet, P < 0.01), the ALA Diet decreased vascular cell adhesion molecule-1 (VCAM-1, -15.6% vs. -3.1%, P < 0.01) and E-selectin (-14.6% vs. -8.1%, P < 0.01) more than the LA Diet. Changes in CRP and VCAM-1 were inversely associated with changes in serum eicosapentaenoic acid (EPA) (r = -0.496, P = 0.016; r = -0.418, P = 0.047), or EPA plus docosapentaenoic acid (r = -0.409, P = 0.053; r = -0.357, P = 0.091) after subjects consumed the ALA Diet. The 2 high-PUFA diets decreased serum total cholesterol, LDL cholesterol and triglycerides similarly (P < 0.05); the ALA Diet decreased HDL cholesterol and apolipoprotein AI compared with the AAD (P < 0.05). ALA appears to decrease CVD risk by inhibiting vascular inflammation and endothelial activation beyond its lipid-lowering effects.     

Dietary alpha-linolenic acid is as effective as oleic acid and linoleic acid in lowering blood cholesterol in normolipidemic men.

The effect of dietary oleic acid (OA), linoleic acid (LA), and linolenic acid (LNA) on plasma lipid metabolism was studied in eight normolipidemic men. A mixed-fat diet composed of conventional foods was fed during 6-d pre- and post-experimental periods. The same basic diet but with 75% of the fat (26% of total energy) provided by sunflower and olive; canola; soybean; and sunflower, olive, and flax oils was fed during four 18-d experimental periods. Mean plasma total cholesterol (-18%), low-density-lipoprotein-cholesterol, (-22%) and very-low-density-lipoprotein-cholesterol (-41%) concentrations were significantly (P less than 0.004) lower after the experimental diets than after the mixed-fat diet. Mean serum apolipoprotein B (-19%) and apolipoprotein A-I (-9%) concentrations were also significantly (P less than 0.0007) lower after the experimental diets. The experimental diets were equally effective in lowering total and lipoprotein cholesterol and apolipoprotein concentrations in plasma, indicating that dietary OA, LA, and LNA were equally hypocholesterolemic.     

Efficiency of conversion of alpha-linolenic acid to long chain n-3 fatty acids in man

Alpha-linolenic acid (18:3n-3) is the major n-3 (omega 3) fatty acid in the human diet. It is derived mainly from terrestrial plant consumption and it has long been thought that its major biochemical role is as the principal precursor for long chain polyunsaturated fatty acids, of which eicosapentaenoic (20:5n-3) and docosahexaenoic acid (22:6n-3) are the most prevalent. For infants, n-3 long chain polyunsaturated fatty acids are required for rapid growth of neural tissue in the perinatal period and a nutritional supply is particularly important for development of premature infants. For adults, n-3 long chain polyunsaturated fatty acid supplementation is implicated in improving a wide range of clinical pathologies involving cardiac, kidney, and neural tissues. Studies generally agree that whole body conversion of 18:3n-3 to 22:6n-3 is below 5% in humans, and depends on the concentration of n-6 fatty acids and long chain polyunsaturated fatty acids in the diet. Complete oxidation of dietary 18:3n-3 to CO2 accounts for about 25% of 18:3n-3 in the first 24 h, reaching 60% by 7 days. Much of the remaining 18:3n-3 serves as a source of acetate for synthesis of saturates and monounsaturates, with very little stored as 18:3n-3. In term and preterm infants, studies show wide variability in the plasma kinetics of 13C n-3 long chain polyunsaturated fatty acids after 13C-18:3n-3 dosing, suggesting wide variability among human infants in the development of biosynthetic capability to convert 18:3n-3 to 22:6n3. Tracer studies show that humans of all ages can perform the conversion of 18:3n-3 to 22:6n3. Further studies are required to establish quantitatively the partitioning of dietary 18:3n-3 among metabolic pathways and the influence of other dietary components and of physiological states on these processes.     

Conversion of alpha-linolenic acid in humans is influenced by the absolute amounts of alpha-linolenic acid and linoleic acid in the diet and not by their ratio

BACKGROUND: Human in vivo data on dietary determinants of alpha-linolenic acid (ALA; 18:3n-3) metabolism are scarce. OBJECTIVE: We examined whether intakes of ALA or linoleic acid (LA; 18:2n-6) or their ratio influences ALA metabolism. DESIGN: During 4 wk, 29 subjects received a control diet (7% of energy from LA, 0.4% of energy from ALA, ALA-to-LA ratio = 1:19). For the next 6 wk, a control diet, a low-LA diet (3% of energy from LA, 0.4% of energy from ALA, ratio = 1:7), or a high-ALA diet (7% of energy from LA, 1.1% of energy from ALA, ratio = 1:7) was consumed. Ten days before the end of each dietary period, [U-13C]ALA was administered orally for 9 d. ALA oxidation was determined from breath. Conversion was estimated by using compartmental modeling of [13C]- and [12C]n-3 fatty acid concentrations in fasting plasma phospholipids. RESULTS: Compared with the control group, ALA incorporation into phospholipids increased by 3.6% in the low-LA group (P = 0.012) and decreased by 8.0% in the high-ALA group (P < 0.001). In absolute amounts, it increased by 34.3 mg (P = 0.020) in the low-LA group but hardly changed in the high-ALA group. Nearly all ALA from the plasma phospholipid pool was converted into eicosapentaenoic acid. Conversion of eicosapentaenoic acid into docosapentaenoic acid and docosahexaenoic acid hardly changed in the 3 groups and was <0.1% of dietary ALA. In absolute amounts, it was unchanged in the low-LA group, but increased from 0.7 to 1.9 mg (P = 0.001) in the high-ALA group. ALA oxidation was unchanged by the dietary interventions. CONCLUSION: The amounts of ALA and LA in the diet, but not their ratio, determine ALA conversion.     

Dietary intakes of arachidonic acid and alpha-linolenic acid are associated with reduced risk of hip fracture in older adults

PUFA are hypothesized to influence bone health, but longitudinal studies on hip fracture risk are lacking. We examined associations between intakes of PUFA and fish, and hip fracture risk among older adults (n = 904) in the Framingham Osteoporosis Study. Participants (mean age ~75 y at baseline) were followed for incident hip fracture from the time they completed the baseline exam (1988-1989) until December 31, 2005. HR and 95% CI were estimated for energy-adjusted dietary fatty acid exposure variables [(n-3) fatty acids: α-linolenic acid (ALA), EPA, DHA, EPA+DHA; (n-6) fatty acids: linoleic acid, arachidonic acid (AA); and the (n-6):(n-3) ratio] and fish intake categories, adjusting for potential confounders and covariates. Protective associations were observed between intakes of ALA (P-trend = 0.02) and hip fracture risk in a combined sample of women and men and between intakes of AA (P-trend = 0.05) and hip fracture risk in men only. Participants in the highest quartile of ALA intake had a 54% lower risk of hip fracture than those in the lowest quartile (Q4 vs. Q1: HR = 0.46; 95% CI = 0.26-0.83). Men in the highest quartile of AA intake had an 80% lower risk of hip fracture than those in the lowest quartile (Q4 vs. Q1: HR = 0.20; 95% CI = 0.04-0.96). No significant associations were observed among intakes of EPA, DHA, EPA+DHA, or fish. These findings suggest dietary ALA may reduce hip fracture risk in women and men and dietary AA may reduce hip fracture risk in men.     

Dietary trans alpha-linolenic acid from deodorised rapeseed oil and plasma lipids and lipoproteins in healthy men: the TransLinE Study

TRANS: isomers of alpha-linolenic acid, which are formed by deodorization of refined vegetable oils, can be found in significant amounts in edible oils. Effects of trans alpha-linolenic acid on plasma lipoproteins are unknown. We therefore investigated the effects of trans alpha-linolenic acid on plasma lipids and lipoproteins in healthy European men. Eighty-eight healthy men from three European countries (France, Scotland, UK and the Netherlands) first consumed for 6 weeks a diet with experimental oils 'free' of trans fatty acids (run-in period). For the next 6 weeks, they were randomly allocated to a diet with experimental oils 'high' or 'low' in trans alpha-linolenic acid. Daily total trans alpha-linolenic acid intake in the high trans group was 1410 (range 583-2642) mg. Experimental oils were provided as such, or incorporated into margarines, cheeses, muffins and biscuits. The high trans alpha-linolenic acid diet significantly increased the plasma LDL-:HDL-cholesterol ratio by 8.1 % (95 % CI 1.4, 15.3; and the total cholesterol:HDL-cholesterol ratio by 5.1 % (95 % CI 0.4, 9.9; compared with the low-trans diet. This was largely explained by an increase in LDL-cholesterol on the high-trans diet, while no change was observed in the low-trans group (mean treatment effect of 4.7 % (95 % CI -0.8, 10.5; No effects were found on total cholesterol and HDL-cholesterol, triacylglycerols, apolipoprotein B and A-1, and lipoprotein(a) concentrations. In conclusion, trans alpha-linolenic acid may increase plasma LDL-:HDL-cholesterol and total cholesterol:HDL-cholesterol ratios. Whether diet-induced changes in these ratios truly affects the risk for CHD remains to be established.     

Dietary alpha-linolenic acid and immunocompetence in humans.

We examined the effect of dietary alpha-linolenic acid (ALA) on the indices of immunocompetence in 10 healthy free-living men (age 21-37 y) who consumed all meals at the Western Human Nutrition Research Center for 126 d. There was a stabilization period of 14 d at the start when all 10 subjects consumed basal diet (BD) and there were two intervention periods of 56 d each. Five of the subjects consumed the basal diet and the other five consumed flax-seed-oil diet (FD) during each intervention period. Feeding of FD suppressed the proliferation of peripheral blood mononuclear cells when they were cultured with phytohemagglutinin-P (P = 0.041) and concanavalin A (P = 0.054) and the delayed hypersensitivity response to seven recall antigens (NS). Concentrations of immunoglobulins in serum, C3, C4, salivary IgA, the numbers of helper cells, suppressor cells, and total T and B cells in the peripheral blood were not affected by the diets.     

High cholesterol intake modifies chylomicron metabolism in normolipidemic young men

Whether the consumption of egg yolk, which has a very high cholesterol content without excess saturated fats, has deleterious effects on lipid metabolism is controversial. Absorbed dietary cholesterol enters the bloodstream as chylomicrons, but the effects of regular consumption of large amounts of cholesterol on the metabolism of this lipoprotein have not been explored even though the accumulation of chylomicron remnants is associated with coronary artery disease (CAD). We investigated the effects of high dietary cholesterol on chylomicron metabolism in normolipidemic, healthy young men. The plasma kinetics of a chylomicron-like emulsion, doubly-labeled with 14C-cholesteryl ester (14C-CE) and 3H-triolein (3H-TG) were assessed in 25 men (17-22 y old, BMI 24.1 +/- 3.4 kg/m2). One group (n = 13) consumed 174 +/- 41 mg cholesterol/d and no egg yolk. The other group (n = 12) consumed 3 whole eggs/d for a total cholesterol intake of 804 +/- 40 mg/d. The nutritional composition of diets was the same for both groups, including total lipids and saturated fat, which comprised 25 and 7%, respectively, of energy intake. Serum LDL and HDL cholesterol and apoprotein B concentrations were higher in the group consuming the high-cholesterol diet (P < 0.05), but serum triacylglycerol, apo AI, and lipoprotein (a) did not differ between the 2 groups. The fractional clearance rate (FCR) of the 14C-CE emulsion, obtained by compartmental analysis, was 52% slower in the high-cholesterol than in the low-cholesterol group (P < 0.001); the 3H-TG FCR did not differ between the groups. Finally, we concluded that high cholesterol intakes increase the residence time of chylomicron remnants, as indicated by the 14C-CE kinetics, which may have undesirable effects related to the development of CAD.     

Decreasing linoleic acid with constant alpha-linolenic acid in dietary fats increases (n-3) eicosapentaenoic acid in plasma phospholipids in healthy men

High linoleic acid (LA) intakes have been suggested to reduce alpha-linolenic acid [ALA, 18:3(n-3)] metabolism to eicosapentaenoic acid [EPA, 20:5(n-3)] and docosahexaenoic acid [DHA, 22:6(n-3)], and favor high arachidonic acid [ARA, 20:4(n-6)]. We used a randomized cross-over study with men (n = 22) to compare the effect of replacing vegetable oils high in LA with oils low in LA in foods, while maintaining constant ALA, for 4 wk each, on plasma (n-3) fatty acids. Nonvegetable sources of fat, except fish and seafoods, were unrestricted. We determined plasma phospholipid fatty acids at wk 0, 2, 4, 6, and 8, and triglycerides, cholesterol, serum CRP, and IL-6, and platelet aggregation at wk 0, 4, and 8. LA and ALA intakes were 3.8 +/- 0.12% and 1.0 +/- 0.05%, and 10.5 +/- 0.53% and 1.1 +/- 0.06% energy with LA:ALA ratios of 4:0 and 10:1 during the low and high LA diets, respectively. The plasma phospholipid LA was higher and EPA was lower during the high than during the low LA diet period (P < 0.001), but DHA declined over the 8-wk period (r = -0.425, P < 0.001). The plasma phospholipid ARA:EPA ratios were (mean +/- SEM) 20.7 +/- 1.52 and 12.9 +/- 1.01 after 4 wk consuming the high or low LA diets, respectively (P < 0.001); LA was inversely associated with EPA (r = -0.729, P < 0.001) but positively associated with ARA:EPA (r = 0.432, P < 0.001). LA intake did not influence ALA, ARA, DPA, DHA, or total, LDL or HDL cholesterol, CRP or IL-6, or platelet aggregation. In conclusion, high LA intakes decrease plasma phospholipid EPA and increase the ARA:EPA ratio, but do not favor higher ARA.     

Physiological effects of diet enriched in essential fatty acids in young men

The investigations were carried out on healthy young males aged 20-21 years. Those young men, whose previously different diets were determined by the dietary habits of their families, were selected and grouped under uniform conditions (feeding, housing, physical activity). After 4 months staying under these uniform conditions their diet was changed adding E.F.A. to their previous food rations. Food rations enriched with E.F.A. were given to these young males for 3 months. Then E.F.A. additions to the diet was stopped and the observed subjects received food rations, identical as during the initial 4-month period prior to E.F.A. enrichment, these rations were given during 5 months. Immediately after grouping these men were subjected to biochemical investigation of the serum and to anthropometric and general medical examinations (examination I). The subsequent examinations (II, III, IV) were carried out while the subjects were living under uniform conditions: II) after 4 months on the diet without E.F.A. enrichment, III) after 3 months on the diet enriched with E.F.A., and IV) after 5 months of diet without E.F.A. enrichment (after withdrawal of additional E.F.A.). The investigations were begun on 97 young males (examination I). The consecutive examinations (II, III, IV) were carried out on smaller groups of subjects for reasons on with the authors had no influence. During the experiment, 2-3 times in a month, sample of daily food rations given to the studied subjects and residual food on the plates were taken for analysis. This was done for determination of actual food intake. Through the whole period of the experiment the observed subjects were inquired about additional food consumed. The biochemical investigations of the nutritional state of these young subjects included hematological indices, serum proteins, selected biochemical components in the serum, activity of certain enzymes in the serum, serum lipid components and serum level of certain vitamins. The results of these investigations show the enrichment of diets during 3 months with vegetable fats (sunflower oil, margarine containing 40% of E.F.A.) for increasing the amount of E.F.A. in the whole daily food (together with additional food calculated on the basis of inquiry information) from 14.7 g to 27.7 g (3,2% kcal and 5,8% kcal respectively) has a favorable effect on selected serum lipids. The following changes appeared: decrease of total lipid level, total cholesterol level, cholesterol content of beta and prebeta-lipoproteins levels, free fatty acid level and the favorable changes in the composition of fatty acid in total lipid and selected lipid fractions in the serum. Food enrichment with E.F.A. led to rise the level of linoleic acid and total E.F.A. level and to fall the level of saturated fatty acids. The ratio of polyunsaturated to saturated fatty acids changes favorably both in total serum lipids and in different lipid fraction...     

Trans-10,cis-12 conjugated linoleic acid suppresses the desaturation of linoleic and alpha-linolenic acids in HepG2 cells

The objective of this study was to determine the effects of cis-9,trans-11 and trans-10,cis-12 CLA on the fatty acid desaturation in a human hepatoma cell line, HepG2. Therefore, experiments were conducted in which HepG2 cells were incubated with various concentrations of those fatty acids and the concentrations of fatty acids in various lipid fractions of HepG2 cells were determined. In the presence of linoleic acid as substrate, cells treated with 25 micromol/L of trans-10,cis-12 CLA had lower ratios of dihomo-gamma-linoleic acid to linoleic acid and of arachidonic acid to linoleic acid in phospholipids than control cells; with alpha-linolenic acid as substrate, they had a lower ratio of eicosapentaenoic acid to alpha-linolenic acid in phospholipids than control cells. Cells treated with cis-9,trans-11 CLA did not differ in these ratios from control cells. Cells treated with trans-10,cis-12 CLA had also a markedly lower ratio of monounsaturated fatty acids (MUFA) to saturated fatty acids (SFA) in lipids than control cells; cells treated with cis-9,trans-11 CLA had a slightly lower MUFA:SFA ratio than control cells. These findings suggest that trans-10,cis-12 CLA suppresses Delta9-, Delta6- and Delta5-desaturation in HepG2 cells; cis-9,trans-11 CLA slightly reduces Delta9-desaturation but does not inhibit Delta6- and Delta5-desaturation. Moreover, HepG2 cells treated with 100 micromol/L of trans-10,cis-12 CLA released larger amounts of 6-keto-prostaglandin F(1alpha) and prostaglandin F(2alpha) than control cells. Treatment of cells with cis-9,trans-11 CLA did not alter the release of these eicosanoids compared with control cells. In conclusion, this study suggests that trans-10,cis-12 CLA has significant effects on the metabolism of essential fatty acids in HepG2 cells, whereas cis-9, trans-11 CLA does not have any effect in this respect.