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PubMed1982

Perturbation of the metabolism of essential fatty acids by dietary partially hydrogenated vegetable oil.

Rats were fed purified diets containing (i) partially hydrogenated soybean oil as source of isomeric octadecenoic acids, (ii) hydrogenated coconut oil as source of saturated fatty acids, and (iii) a low level of corn oil as low-fat control. All diets contained 18% of the linoleate requirement. Rat liver and heart phospholipids were analyzed by gas/liquid chromatography for fatty acids, and liver, microsomes were assayed for desaturase (acyl-CoA, hydrogen-donor: oxidoreductase, EC 1.14.99.5) activities. Products of desaturation reactions measured analytically provided more information with greater statistical significance than did the enzymatic assays. Rats fed isomeric octadecenoic acids showed more severe essential fatty acid deficiency than did saturated-fat and control groups. The suppression of linoleate metabolites was largely due to decreased delta 5 and delta 6 desaturase activities. At several levels of linoleate, the deficiency was more severe at the higher level of isomeric octadecenoic acids. Increasing the intake of linoleate to 7.5% of calories did not suppress deposition of isomeric unsaturated acids in tissue lipids.

Animals↗
PubMed1997

Ursodeoxycholic acid improves the hepatic metabolism of essential fatty acids and retinol in children with cystic fibrosis.

OBJECTIVE: Several clinical trials of ursodeoxycholic acid (UDCA) have shown improvement of liver-function test results in cystic fibrosis (CF) with liver disease; however, there is no evidence that the long-term course will be affected. In view of the observations that UDCA can change the lipid profile and that patients with CF and liver disease are more likely to have essential fatty acid (EFA) deficiency, we elected to examine changes in the lipid profile and in the status of fat-soluble vitamins in response to UDCA. METHODS: Nineteen children with CF and liver dysfunction were recruited for a double-blind, crossover study of 1 year's duration, followed by treatment of the entire group. UDCA was administered at a dosage of 15 mg/kg per day, which, in the absence of a 50% decrease of alanine transaminase or aspartate transaminase or both within 2 months, was increased to 30 mg/kg per day. RESULTS: At entry, all patients had biochemical evidence of EFA deficiency. The lipid profiles during an average period of 25 months of follow-up showed a significant decrease in triglycerides (p <0.002), cholesterol (p <0.02), and total fatty acids (p <0.006). In addition, UDCA therapy led to an improvement in EFA status, as indicated by an increase (p <0.05) in the n-6 fatty acid concentration and a reduction (p <0.04) in the 20:3n-9/20:4n-6 fatty acid ratio. Although no change in vitamin E levels was observed, retinol metabolism was altered. There was an increase (p <0.02) in the unesterified retinol/retinol binding protein molar ratio in the absence of a difference in retinol binding protein concentration. Furthermore, retinyl esters, which normally account for less than 3% of circulating retinol, decreased (p <0.05) from 13.7% +/- 3.6% to 8.1% +/- 1.7%. CONCLUSIONS: This study confirms that UDCA alters lipoprotein metabolism and shows that it improves the EFA and retinol status of patients with CF and liver disease.

Adolescent↗
PubMed1990

Abnormal fatty acid profile in chronic hemodialysis patients: possible deficiency of essential fatty acids.

Plasma fatty acid profiles from maintenance hemodialysis patients (n = 9) were compared with those from healthy volunteers (n = 9). Hemodialysis patients had significantly higher levels of oleic acid, 15.3 +/- 1.1 vs. 8.9 +/- 0.6% (p less than 0.0001), and lower levels of arachidonic acid (6.0 +/- 0.5 vs. 8.4 +/- 0.3%, p less than 0.0009). Linolenic and linoleic acids, the essential fatty acid and precursors of arachidonic acid, were also significantly lower than normal in the dialysis group. These data show that dialysis patients have fatty acid abnormalities suggesting relative depletion of essential fatty acids. These observations are important because these abnormalities may play an important role in the pathogenesis of some common clinical conditions associated with uremia, such as a constellation of skin problems, fragility of erythrocytes, lipid anomalies and hormonal aberrations.

Adult↗
PubMed1983

[Essential fatty acids: its transformations and functions].

Essential fatty acids, in animals, pertain to two different fatty acid families: the linoleic and the linolenic. These, and the non-essential families of oleic and palmitoleic are produced by action of the enzymes proper. The lack of essential fatty acids produces typical symptoms that are accompanied by fatty acid compositions, also typical, utilized with diagnostic value. The biological effects of essential fatty acids can be specific and nonspecific. The latter manifest themselves particularly in the phospholipid composition and, therefore, in the structure and fluency of the membranes. In contrast, specific essential fatty acids act in the formation of prostaglandins, prostacyclins, tromboxans and leucotriens. Each essential fatty acid produces specific effects, depending on the prostanoids formed and the tissue in question.

Animals↗
PubMed1987

Protection of the gastric mucosa by linoleic acid--a nutrient essential fatty acid.

We studied whether linoleic acid, a precursor for arachidonic acid and prostaglandins, could protect the gastric mucosa against ethanol-induced injury. Fasted male rats received intragastric pretreatment with 1 ml of one of: a) solubilizer; b) solubilized linoleic acid (74 mg); or c) solubilized oleic acid (74 mg) (a nonessential fatty acid). One hour later, 2 ml 100% ethanol was given intragastrically. Three hours after ethanol administration, the gastric mucosa was assessed for gross necrosis and for histologic changes. Three hours after ethanol administration in solubilizer, pretreated-group gross mucosal necrosis involved 35 +/- 3% of total mucosal area, while deep histologic necrosis involved 52 +/- 4% of the mucosal strip length. Pretreatment with linoleic acid (but not oleic acid) significantly reduced gross histologic necrosis, to 2.3 +/- 0.5%, and deep histologic necrosis to 4 +/- 2% (both p less than 0.001 versus solubilizer group). The protective action of linoleic acid was significantly reduced (greater than 10-fold) by pretreatment with indomethacin (prostaglandins synthetase inhibitor), suggesting prostaglandins as mediators of protection. The present study showed that effective protection of the gastric mucosa against ethanol injury can be achieved by intragastric administration of linoleic acid, a dietary essential fatty acid.

Animals↗
PubMed1980

[Clinical significance of essential fatty acids (author's transl)].

Essential fatty acids are important constituents of human nutrition. They lower cholesterol and phospholipid levels in serum. They are structural parts of cell membranes, affecting the function of membrane-bound enzymes and transport systems and modulating cellular immune response. Prostaglandins, prostacyclin and thromboxane, the metabolites of essential fatty acids, are active compounds in the cardio-vascular system, the lung, in the uro-genital and gastro-intestinal tract, in the inflammatory response and platelet aggregation.

Cardiovascular Physiological Phenomena↗
PubMed1985

Contrasting effects of low or high copper intake on rat tissue lipid essential fatty acid composition.

The effects of low copper intake or copper supplementation on the metabolism of stearic acid have been studied previously, but their effects on essential fatty acids have not been reported. Male Sprague-Dawley rats were fed for 12 weeks on pelleted semi-synthetic diets containing less than 1 mg/kg copper (low copper), 6 mg/kg (copper control), or 250 mg/kg copper (copper supplemented). The fatty acid composition of the total phopholipids and triglycerides of plasma, liver, heart and adipose tissue was analyzed by gas liquid chromatography. In low copper rats compared to controls, palmitic and oleic acids were decreased but stearic acid and docosahexaenoic acid were increased in plasma, liver and heart phopholipids. Arachidonic acid was also increased in plasma and liver phospholipids in low copper rats. In liver triglycerides, linoleic and arachidonic acids were increased but palmitic and oleic acid were decreased in low copper rats. Copper supplementation had the opposite effect; palmitic and oleic acids were increased in phospholipids and triglycerides whereas essential fatty acids were generally decreased. Hence, copper not only has a direct effect on the desaturation of stearic acid but also has significant effects on the tissue lipid composition of essential fatty acids.

Adipose Tissue↗
PubMed2002

Nitric oxide as the mediator of the antiosteoporotic actions of estrogen, statins, and essential fatty acids.

Estrogen, statins, and essential fatty acids and their metabolites can prevent osteoporosis. However, it is not certain how these three structurally different agents can have the same beneficial action. It is suggested that all three, in addition to their other modes of action in the prevention of osteoporosis, have the ability to augment constitutional (or endothelial) nitric oxide generation, which is known to be beneficial in osteoporosis. If so, it will be interesting to study whether nitric oxide donors and/or nitric oxide precursors can be given together with estrogen, statins, or essential fatty acids to potentiate their benefit in osteoporosis.

Drug Synergism↗
PubMed1992

Nonessential fatty acids in formula fat blends influence essential fatty acid metabolism and composition in plasma and organ lipid classes in piglets.

The n-6 and n-3 fatty acid status of developing organs is the cumulative result of the diet lipid composition and many complex events of lipid metabolism. Little information is available, however, on the potential effects of the saturated fatty acid chain length (8:0-16:0) or oleic acid (18:1) content of the diet on the subsequent metabolism of the essential fatty acids 18:2n-6 and 18:3n-3 and their elongated/desaturated products. The effects of feeding piglets formulas with fat blends containing either coconut oil (12:0 + 14:0) or medium chain triglycerides (MCT, 8:0 + 10:0) but similar levels of 18:1, 18:2n-6 and 18:3n-3, or MCT with high or low 18:1 but constant 18:2n-6 and 18:3n-3 on the fatty acid composition of plasma, liver and kidney triglycerides, phospholipids and cholesteryl esters, and of brain total lipid, were studied. Diet-induced changes in the fatty acid composition of lipid classes were generally similar for plasma, liver and kidney. Dietary 18:1 content was reflected in tissue lipids and was inversely associated with levels of 18:2n-6. Lower percentage of 18:2n-6, however, was not associated with lower levels of its elongated/desaturated product 20:4n-6 but was associated with higher levels of 22:6n-3. Feeding coconut oil vs. MCT resulted in lower 18:1 levels in all lipids, and higher percentages of 20:4n-6 in tissue phospholipid. Increasing the dietary n-6/n-3 ratio from 5 to 8 significantly increased tissue percentage of 18:2n-6 and decreased phospholipid 22:6n-3.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1999

Metabolism of n-3 and n-6 fatty acids in Atlantic salmon liver: stimulation by essential fatty acid deficiency.

Oxidation, esterification, desaturation, and elongation of [1-14C]18:2n-6 and [1-14C]18:3n-3 were studied using hepatocytes from Atlantic salmon (Salmo salar L.) maintained on diets deficient in n-3 and n-6 polyunsaturated fatty acids (PUFA) or supplemented with n-3 PUFA. For both dietary groups, radioactivity from 18:3n-3 was incorporated into lipid fractions two to three times faster than from 18:2n-6, and essential fatty acids (EFA) deficiency doubled the incorporation. Oxidation to CO2 was very low and was independent of substrate or diet, whereas oxidation to acid-soluble products was stimulated by EFA deficiency. Products from 18:2n-6 were mainly 18:3n-6, 20:3n-6, and 20:4n-6, with minor amounts of 20:2n-6 and 22:5n-6. Products from 18:3n-3 were mainly 18:4n-3, 20:5n-3, and 22:6n-3, with small amounts of 20:3n-3. The percentage of 22:6n-3 in the polar lipid fraction of EFA-deficient hepatocytes was fourfold higher than in n-3 PUFA-supplemented cells. This correlated well with our other results obtained after abdominal injection of [1-14C]18:3n-3 and [1-14C]18:2n-6. In hepatocytes incubated with [4,5-3H]-22:6n-3, 20:5n-3 was the main product. This retroconversion was increased by EFA deficiency, as was peroxisomal betaoxidation activity. This study shows that 18:2n-6 and 18:3n-3 can be elongated and desaturated in Atlantic salmon liver, and that this conversion and the activity of retroconversion of very long chain PUFA is markedly enhanced by EFA deficiency.

Animals↗
PubMed1976

Linoleic acid desaturation activity of liver microsomes of essential fatty acid deficient and sufficient rats.

Studies were carried out to relate the changes of the fatty acid and lipid composition of rat microsomes with the modification of the activity of the linoleic acid desaturation evoked by an essential fatty acid deficient diet. Two steps were shown in the progression of the essential fatty acid deficienty. In a first step shown at three days of essential fatty acid deficiency the fatty acid composition was changed by decreasing linoleic and arachidonic acids and increasing oleic and eicosatrienoic (-9) acids. No change was found in the lipid distribution and approximate V and Km of the linoleic acid desaturation. In this first step the unsaturated/saturated fatty acids ratio fell in spite of the synthesis of eicosatrienoic (n-9) acid that was produced without any change of enzyme activity. In a second step shown at 15 days of essential fatty acid deficiency the change of the fatty acid composition was greater but the unsaturated/saturated acid ratio was restored. An increase of triacylglycerols and a decrease of phospholipids was also detected together with an enhanced activity of linoleic acid desaturation (higher approximate V) and a higher approximate Km. The increase of the V of linoleic acid desaturation is considered to be evoked by an increased level of active delta-6 desaturase. The increased activity of the delta-6 desaturase in this second period is a secondary and important response of the cell to maintain the unsaturated : saturated acid ratio and fluidity of the membrane.

Animals↗
PubMed2005

[No effect of supplement of essential fatty acids on lateral epicondylitis].

BACKGROUND: Essential fatty acids influence the production of prostaglandins, which is suggested to be of importance for the development of chronic degenerative changes in tendons. Clinical studies indicate that treatment with essential fatty acids, vitamins and minerals may be effective against tendon diseases. This randomised trial was performed to evaluate the effect of an essential fatty acid supplement on pain in lateral epicondylitis. MATERIAL AND METHODS: 55 patients with unilateral epicondylitis were treated with eccentric training of the wrist extensor muscles for 6 months. 50% of the patients were randomised to 8 weeks of peroral supplement with essential fatty acids, 50% to placebo supplement. RESULTS: Reported pain declined throughout the study period, with a mean pain level reported on a 10 cm visual analogue scale of 4.9 cm (95% CI 4.3-5.1 cm) at inclusion and 0.95 cm (95% CI 0.5-1.1 cm) at 6 months. Maximal grip force of afflicted arm increased about 23%. No differences in pain reduction or force increase were found between the supplement and the placebo groups. CONCLUSION: Reported pain was reduced and force increased gradually over 6 months with eccentric training. No additional effect was observed with a fatty acid supplement.

Administration, Oral↗
PubMed1998

Essential fatty acid status in cell membranes and plasma of patients with primary Sjogren's syndrome. Correlations to clinical and immunologic variables using a new model for classification and assessment of disease manifestations.

In 41 primary Sjögren's syndrome patients we compared fatty acid levels within erythrocyte phospholipids, plasma phospholipids, plasma triglycerides and plasma cholesterol esters, with the immunopathological and clinical disease status. Docosahexaenoic acid was the essential fatty acid (EFA), the levels of which correlated (inversely) most closely with the clinical disease status (r=-0.33 to -0.50). Levels of dihomogammalinolenic acid and eicosapentaenoic acid correlated inversely to levels of IgM rheumatoid factors (r=-0.33) and anti-SSA/Ro antibodies (r=-0.40) respectively. Moreover, levels of anti-SSA/Ro antibodies (r=-0.34-0.40) correlated with levels of the proinflammatory arachidonic acid. Sigma n-3 EFA/sigma n-6 EFA ratios correlated significantly to the quantitative estimates of immunopathological and clinical disease status. Our data are in agreement with current understanding of pro- and anti-immunoinflammatory roles within EFA metabolism, and support the rationale for intervention studies.

8,11,14-Eicosatrienoic Acid↗
PubMed2002

Assessment of essential fatty acid and omega3-fatty acid status by measurement of erythrocyte 20:3omega9 (Mead acid), 22:5omega6/20:4omega6 and 22:5omega6/22:6omega3.

BACKGROUND: Early suspicion of essential fatty acid deficiency (EFAD) or omega3-deficiency may rather focus on polyunsaturated fatty acid (PUFA) or long-chain PUFA (LCP) analyses than clinical symptoms. We determined cut-off values for biochemical EFAD, omega3-and omega3/22:6omega3 [docosahexaenoic acid (DHA)]-deficiency by measurement of erythrocyte 20:3omega9 (Mead acid), 22:5omega6/20:4omega6 and 22:5omega6/22:6omega3, respectively. METHODS: Cut-off values, based on 97.5 percentiles, derived from an apparently healthy omnivorous group (six Dominica breast-fed newborns, 32 breast-fed and 27 formula+LCP-fed Dutch low-birth-weight infants, 31 Jerusalem infants, 33 Dutch 3.5-year-old infants, 69 omnivorous Dutch adults and seven Dominica mothers) and an apparently healthy group with low dietary LCP intake (81 formula-fed Dutch low-birth-weight infants, 12 Dutch vegans). Cut-off values were evaluated by their application in an EFAD suspected group of 108, mostly malnourished, Pakistani children, three pediatric patients with chronic fat-malabsorption (abetal-ipoproteinemia, congenital jejunal and biliary atresia) and one patient with a peroxisomal beta-oxidation disorder. RESULTS: Erythrocyte 20:3omega9, 22:5omega6/20:4omega6 and 22:5omega6/22:6omega3 proved age-dependent up to 0.2 years. Cut-off values for ages above 0.2 years were: 0.46mol% 20:3omega9 for EFAD, 0.068mol/mol 22:5omega6/20:4omega6 for omega3-deficiency, 0.22mol/mol 22:5omega6/22:6omega3 for omega3/DHA-marginality and 0.48mol/mol 22:5omega6/22:6omega3 for omega3/DHA-deficiency. Use of RBC 20:3omega9 and 22:5omega6/20:4omega6 cut-off values identified 20.4% of the Pakistani subjects as EFAD+omega3-deficient, 12.9% as EFAD+omega3-sufficient, 38.9% as EFA-sufficient+omega3-deficient and 27.8% as EFA-sufficient+omega3-sufficient. The patient with the peroxisomal disorder was classified as EFA-sufficient, omega3-sufficient (based on RBC 22:5omega6/20:4omega6) and omega3/DHA-deficient (based on RBC 22:5omega6/22:6omega3). The three other pediatric patients were classified as EFAD, omega3-deficient and omega3/DHA-deficient. CONCLUSION: Use of the combination of the present cut-off values for EFA, omega3 and omega3/DHA status assessment, as based on 97.5 percentiles, may serve for PUFA supplement intervention until better concepts have emerged.

8,11,14-Eicosatrienoic Acid↗