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PubMed2001

Essential fatty acid deficiency in relation to genotype in patients with cystic fibrosis.

OBJECTIVE: To determine if the serum phospholipid fatty acid pattern in patients with cystic fibrosis (CF) was related to the major cystic fibrosis transmembrane conductance regulator gene mutations. METHODS: Patients with CF (n = 110) aged 3 months to 56 years were studied. Serum samples were analyzed for phospholipid fatty acid with gas-liquid chromatography, and cystic fibrosis transmembrane conductance regulator mutations were determined with standard methods. RESULTS: Patients with CF had significantly lower molar percentages of linoleic acid and docosahexaenoic acid in the serum phospholipid than healthy controls (mean +/- standard deviation, 20.3 +/- 4.5 and 2.6 +/- 0.9 vs 22.4 +/- 2.2 and 3.1 +/- 0.7, respectively; P <.001). Palmitoleic and oleic acids were significantly increased (P <.001) but arachidonic acid was not different from controls. Homozygotes for DeltaF508 and heterozygotes/homozygotes for 394delTT showed significantly lower concentrations of linoleic acid and docosahexaenoic acid than the other groups. Low values were not correlated to anthropometric data or lung function. Patients with pancreatic insufficiency showed similar differences to those with sufficient pancreatic function, reflecting the different genotypes. CONCLUSION: Serum concentrations of linoleic acid and docosahexaenoic acid were significantly lower in patients with severe cystic fibrosis transmembrane conductance regulator mutations, suggesting an association between the basic defect and abnormal essential fatty acid metabolism in CF patients.

Adolescent↗
PubMedDate not supplied

Replacement of long-chain triglyceride with medium-chain triglyceride/long-chain triglyceride lipid emulsion in patients receiving long-term parenteral nutrition: effects on essential fatty acid status and plasma vitamin K1 levels.

BACKGROUND: In long-term parenteral nutrition (LTPN) patients, the use of a 50:50 mixture of medium- and long-chain triglyceride emulsion (MCT/LCT) has been suggested to prevent or correct fatty liver infiltration. However, the use of MCT/LCT lipid emulsion results in a 50% reduction of essential fatty acids and vitamin K1 supply and could induce essential fatty acid and vitamin K1 deficiencies. This study evaluated the effect of a long-term infusion of MCT/LCT lipid emulsion on plasma fatty acid (FA) and vitamin K1 levels on LTPN patients. METHODS: In a prospective nonrandomized crossover study, we measured plasma phospholipid FA composition by gas chromatography and vitamin K1 levels by high-performance liquid chromatography in 11 LTPN patients before and after a 4-month replacement of the usual 20% LCT lipid emulsion (20% Lipoven; Fresenius-Kabi France, Sèvres, France) by a 20% MCT/LCT lipid emulsion (Medialipide B; Braun Medical, Boulogne, France). RESULTS: Patient received LTPN for 46 +/- 40 months; IV lipid emulsion was 827 +/- 336 mL/week. MCT/LCT lipid substitution did not change most of the essential plasma fatty acid concentrations and did not induce essential fatty acid deficiency. With both lipid emulsions, the triene/tetraene (20:3n-9/20:4n-6) ratio remained within the normal ranges. However, with MCT/LCT lipid emulsion, 22:4n-6 (LCT: 0.50 +/- 0.12; MCT/LCT: 0.63 +/- 0.11%) and 22:5n-6 (LCT: 0.32 +/- 0.11; MCT/LCT: 0.48 +/- 0.15%) increased significantly (p = .022 and 0.011, respectively). Plasma vitamin K1 levels decreased drastically with MCT/LCT lipid emulsion. CONCLUSIONS: An amount of 2.85 +/- 1.55 g x kg(-1) week(-1) of MCT/LCT lipid emulsion neither induced essential fatty acid deficiency nor improved the fatty acid disturbances usually observed in LTPN patients but did induce a drop in plasma vitamin K1 levels.

Adult↗
PubMed1999

Essential fatty acids profile and lipid peroxides in severe pre-eclampsia.

There is increasing evidence that an imbalance between products of arachidonic acid metabolism (such as prostaglandins, prostacyclin and thromboxane A2) and lipid peroxidation products might have a role in the pathogenesis of pre-eclampsia. In order to study some of the changes taking place in pre-eclampsia, the plasma concentrations of essential fatty acids and lipid peroxidation products [measured as thiobarbituric-acid (TBA)-reactive substance] were evaluated in 25 patients with severe pre-eclampsia and 20 normal pregnant control subjects. Arachidonic acid concentration (median and range) was significantly higher in the pre-eclamptic group (14.1; 11.0-19.8 micrograms/L) compared with the normal pregnant subjects (2.5; 2.0-4.4 micrograms/L). Plasma concentration of TBA-reactive substance was also significantly higher in the pre-eclamptic cases (14.8; 13.4-16.8 vs 11.4; 9.0-12.8). These results suggest that arachidonic acid and lipid peroxidation products may play a role in the pathogenesis of pre-eclampsia.

Arachidonic Acid↗
PubMed2005

Hypoxia/reoxygenation alters essential fatty acids metabolism in cultured rat cardiomyocytes: protection by antioxidants.

BACKGROUND AND AIMS: Peroxidation of membrane lipids, altering cell integrity and function, plays an important part in the onset and development of cardiac damage following ischemia and reperfusion. Cells maintain their membrane lipid homeostasis by substituting peroxidized lipids with new polyunsaturated fatty acids. The microsomal enzymatic system converting essential fatty acids to highly unsaturated fatty acids (HUFAs) contributes to this repairing mechanism. The membrane of the endoplasmic reticulum could be one of the potential targets of free radicals generated in ischemia/reperfusion, thus causing a reduced efficacy of the system required for HUFA biosynthesis. To verify this hypothesis, and the consequent modification in fatty acid composition, we exposed cultured rat cardiomyocytes to different periods of hypoxia (H), eventually followed by reoxygenation (R). Furthermore, the effectiveness of antioxidants like alpha-tocopherol and a green tea extract in counteracting H/R damage towards HUFA biosynthesis was tested. METHODS AND RESULTS: Linoleic (LA) and alpha-linolenic acid (ALA) conversion was measured by pre-labelling cells with [1-14C]LA or [1-14C]ALA for 1 h; total lipid fatty acid composition was determined by gas chromatographic analysis. H profoundly affected HUFA biosynthesis, and this effect was much more evident on LA than on ALA. Conversion of both substrates was partially restored during R due to the readmission of the final acceptor of the desaturating complex. Fatty acid composition data were in agreement with the modifications observed in essential fatty acid conversion. Antioxidant protection appeared to be related to the duration of H, and to be more effective during H than during R. CONCLUSION: This study points out the importance of possessing good antioxidant defenses not only after, but mainly prior to the onset of H.

Animals↗
PubMed1988

Essential fatty acid deficiency reduces the inflammatory cell invasion in rabbit hydronephrosis resulting in suppression of the exaggerated eicosanoid production.

The rabbit hydronephrotic kidney (HNK) is a model of renal inflammation characterized by a marked increase in arachidonic acid metabolism which is temporally associated with an inflammatory cell influx into the injured tissue. The HNK exhibits an exaggerated elaboration of eicosanoids ex vivo in response to inflammatory agonists (bradykinin and the chemotactic peptide, n-formyl-methionyl-leucyl-phenylalanine). Essential fatty acid (EFA) deficiency [i.e., deprivation of (n-6) fatty acids] attenuated markedly the ex vivo elaboration of eicosanoids and prevented the enhancement of the microsomal cyclooxygenase and thromboxane synthase activity associated with 3 days of ureter occlusion. In contrast, postobstructive release prevented the ex vivo elaboration of eicosanoids by the HNK. When the HNK was assessed morphologically by electron microscopy, both EFA deficiency and postobstructive release markedly reduced the population of interstitial macrophages normally seen in the HNK. Apparently, EFA deficiency blocked the influx of macrophages whereas postobstructive release resulted in the efflux of macrophages from the HNK. Because EFA deficiency has been shown to inhibit the synthesis of leukotriene B4, a potential chemotaxin, it was hypothesized that EFA deficiency might prevent the influx of macrophages due to an inhibition of leukotriene B4 synthesis. Indeed, EFA deficiency suppressed the synthesis of this eicosanoid in blood whereas prostaglandin E2 and thromboxane A2 production were unaffected. In summary, this study demonstrates that EFA deficiency prevents the influx of macrophages into the HNK and prevents the enhanced arachidonate metabolism which normally occurs after ureter obstruction. A potential role for leukotriene B4 as a chemotactic agent in this model of renal inflammation also is suggested.

Animals↗
PubMed1999

The impairment of essential fatty acid metabolism as a key factor in doxorubicin-induced damage in cultured rat cardiomyocytes.

The clinical use of the antitumoral doxorubicin (DOX) is limited by its cardiotoxicity, which is mediated through different mechanisms. The membrane lipid peroxidation induced by DOX may cause disruption of the unsaturated fatty acyl chains; in the endoplasmic reticulum, containing the system catalyzing the desaturation/elongation of fatty acids, DOX could interfere with the metabolism of linoleic and alpha-linolenic acids. Using primary cultures of neonatal rat cardiomyocytes we demonstrated that the exposure to different concentrations of DOX (10(-5) and 10(-7) M) for 24 h caused an increase in the production of conjugated dienes, an impairment in the desaturation/elongation of essential fatty acids, and a reduction in the cellular content of highly unsaturated fatty acids. Conversely, 1 h exposure to 10(-5) M DOX was sufficient to induce alterations in the desaturation/elongation of linoleic and alpha-linolenic acids, but did not cause either formation of conjugated dienes or modification of the fatty acyl pattern. Therefore, DOX has a dual negative effect, depending on its concentration and on the time of exposure, one directed against the membrane highly unsaturated fatty acids, the other against the system which is required for the synthesis of these fatty acids themselves. These two effects synergically act in causing heart cell damage.

Animals↗
PubMed1983

Comparison of Intralipid 10% and Intralipid 20% as a source of energy and essential fatty acids--a multicenter study.

A multicenter clinical study was done which directly compared efficacy and safety of Intralipid 10% and Intralipid 20%. Twenty-nine patients received the 10% concentration, 30 patients received the 20% concentration. Both groups of patients received equivalent amounts of calories, amino acids, dextrose and fat for seven day study periods. Analysis of nitrogen balance data showed that the two preparations were equally effective in maintaining nitrogen balance. Both concentrations of fat emulsion were effective in reversing or correcting the changes of essential fatty acid deficiency. Analysis of clinical laboratory data indicated that both preparations were equally well tolerated by the patients. No adverse effects attributed to the fat emulsions were observed.

Adult↗
PubMed1995

Essential fatty acids in pregnancy and early human development.

Essential fatty acids (EFA) are vitally important structural elements of cell membranes and, therefore, instrumental in the formation of new tissues. The primary EFA cannot be synthesized by man and, consequently, humans depend on dietary sources for an adequate EFA supply. Fetal development is associated with a high EFA requirement, and for its EFA supply, the developing fetus depends on the availability of maternal EFA. At delivery, a strong correlation is observed between the relative amounts of the various EFA in maternal and umbilical plasma phospholipids (PL), which underlines this fetal dependence. In a longitudinal study, we observed that, in women, the EFA status progressively decreases during pregnancy. This particularly holds for cervonic acid (CA, 22:6n-3, also named Docosahexaenoic acid, DHA), the major structural and functional EFA in the CNS. In addition, evidence was obtained for CA mobilization from maternal stores during pregnancy. Furthermore, the maternal CA status appeared significantly higher in primigravida than in multigravida. This was associated with a tendency for the first child of a given woman to have a higher CA status than her following children. This suggests that maternal CA mobilization during pregnancy occurs from a pool that is not easily replenished after pregnancy. The fetal CA status of premature infants is positively related to head circumference, birth weight and birth length. This may imply that increasing the fetal CA status could promote fetal growth and, thereby, improve the general prognosis of prematures. In conclusion, our data suggest that increasing the maternal EFA intake during pregnancy may be beneficial to both mother and child.(ABSTRACT TRUNCATED AT 250 WORDS)

Docosahexaenoic Acids↗
PubMed1983

Ethanol, essential fatty acids and prostaglandins.

In the body the essential fatty acid (EFA) linoleic acid (18:2, omega-6) is desaturated and chain elongated to form homo-gamma-linoleic acid (20:3, omega-6) and arachidonic acid (20:4, omega-6). Apart from their structural function in cell membranes, the EFAs serve as precursors to the prostaglandins and related substances. The prostaglandins can, in general terms, be described as a defensive regulatory system of importance for cardiovascular, gastrointestinal and urogenital function. Acute intake of ethanol gives facial flushing, inhibition of platelet aggregation and elevation of tissue c-AMP. These effects are consistent with release of vasodilatory and antiaggregating PGs. In epidemiological studies, moderate ethanol intake offers some protection against coronary heart disease. Chronic intake high doses of ethanol is associated with damage to, e.g., liver, heart, brain, immunoregulation and various hormonal systems. Decreased tissue levels of 18:2, 20:4 and PGs have been observed both in animals and man. The conversion of 18:2 to 20:4 is inhibited by chronic ethanol exposure. It is suggested that ethanol depletes the PG precursor pool by a dual mechanism of releasing precursor acids and by inhibiting their synthesis. This would lead to a functional EFA-deficiency, manifested by a hypoactive PG system.

Alcoholism↗
PubMed1980

Experimental wound healing in essential fatty acid deficiency.

Clinical reports have suggested that essential fatty acid deficiency (EFAD) may cause delayed healing. One hundred weanling rats were placed on normal or EFAD diets. After 4 wk in control and 6 wk in EFAD animals comparative studies were performed as follows: (1) skin and fascial incisions were tested for tensile strength up to 5 wk, (2) single layer small bowel, (3) colonic anastomoses were studied for anastomotic bursting strength to 14 days, ana (4) 20% partial thickness burns were followed to healing and autoradiographic analysis of healing epiothelium performed. After 4 wk on diet, EFAD rats showed chemical and clinical evidence of deficiency, while control rats remained normal. There was no significant difference in tensile strength of ventral skin incisions with underlying fascial incisions between control and EFAD rats during the study, but solitary dorsal skin incisions were significantly stronger after three weeks in control animals. Bursting pressures in colonic and small bowel anastomoses were not significantly different between control and EFAD groups. However, colonic suture line disruption occurred in 42% of EFAD rats as opposed to 17% of control animals. Highly significant differences in the healing rate of partial-thickness burns were noted. Control rats healed completely by 21 days while EFAD rats had not completely healed at 120 days postburn. Observation of the burn wounds indicated that wound contraction was impaired. These studies suggest that skin healing is the prime area affected by EFAD although colonic healing may have been affected as well.

Animals↗
PubMed1989

Essential fatty acids and immune response.

The implication that essential fatty acids (EFA) can affect immune response was based on the observation that EFA deficiency can accentuate or improve symptoms of certain autoimmune diseases in animals, and that supplementation of linoleic acid to animals reversed such effects. Furthermore, treatment of animals with cyclooxygenase inhibitors abrogated the effect of linoleic acid. Administration of cyclooxygenase inhibitors to animals enhanced both cell-mediated and humoral immune responses. In vitro studies have shown that prostaglandin E (PGE) group inhibits both T and B lymphocyte functions; it is suggested that effects of EFA on immune response are, in part, mediated through eicosanoids. Growing evidence now suggests that the PGE group of prostaglandins can serve as a negative feedback modulator of immune response. However, in vitro effects of other cyclooxygenase-derived products, such as PGI2 and thromboxane A2 (TXA2) have not been well established, perhaps because of their instability in aqueous media. Unlike the PGE group, some of lipoxygenase-derived products of arachidonic acid have shown immunostimulatory effects, as assessed by lymphokine production in vitro. Whether such effects can be seen in vivo remains to be determined. Some lipoxygenase-derived products with strong chemotactic action may indirectly influence immune response by modulating the population of antigen-presenting macrophages in tissues. Thus, the net effect of eicosanoids synthesized in macrophages on modulating immune response may depend on relative amounts of cyclooxygenase-derived products as compared with lipoxygenase-derived products. Macrophages are the major source of eicosanoids among immunocompetent cells. The profile of eicosanoids, produced in vitro by macrophages, varies with type of stimuli and anatomical sites. It can also be affected by the fatty acid composition of tissue lipids, which in turn can be modified by the composition of dietary EFA. Whether manipulating dietary EFA can modulate immune response in normal humans and animals needs to be determined.

Animals↗
PubMed1991

Essential fatty acids in Alzheimer's disease.

Concentrations of essential fatty acids (EFAs) in plasma and red blood cell phospholipids were found to be abnormal in patients with Alzheimer's disease. A double-blind, placebo-controlled trial of treatment with EFAs plus appropriate antioxidants was carried out in 36 patients with Alzheimer's disease. After 20 weeks both the EFA and placebo groups had improved, but the degree of improvement was consistently greater in the EFA group.

Alzheimer Disease↗
PubMed1987

Essential fatty acid status in southern Thai preschool children.

Essential fatty acid (EFA) status was assessed in 15 Southern Thai preschool children. The mean (+/- SD) serum linoleate (18:2 n-6), arachidonate (20:4 n-6), linolenate (18:3 n-3), eicosapentaenoate (20:5 n-3), and docosahexaenoate (22:6 n-3) percentages in the preschool children were 21.7 +/- 4.0, 6.0 +/- 1.2, 0.4 +/- 0.1, 1.2 +/- 0.8, and 4.4 +/- 1.3, respectively. Since EFA composition of total serum lipids in healthy children are not available and age and sex do not largely influence these parameters, the results of the preschool children were compared with those of 10 healthy Bangkok adults. The corresponding figures of the aforementioned fatty acids in adults were 34.9 +/- 8.5, 4.6 +/- 1.5, 0.8 +/- 0.4, 0.5 +/- 0.4, and 1.6 +/- 0.8, respectively. The data indicate linoleate and linolenate depletion in the preschool children. This was due to their low fat intake and lack of consumption of vegetable oil rich in linoleic and linolenic acids. Their high serum arachidonate percentage was probably due to the increased conversion of 18:2 n-6 to 20:4 n-6 in the presence of linolenate depletion. The significantly higher serum 20:5 n-3 and 22:6 n-3 percentages in the preschool children should be due to direct consumption of these two n-3 fatty acids from fish intake.

Arachidonic Acid↗
PubMed1990

[Essential fatty acids and the skin].

Metabolism of the essential fatty acids (AGE) in an organism leads to synthesis of eicosanoids, which have various biological properties. Linoleic acid plays an important part in maintenance of epidermal integrity by intervening in the cohesion of the stratum corneum and in prevention of transepidermal water loss. Metabolites of arachidonic acid (mostly those obtained by the lipoxygenase pathway) are important agents in causing many inflammatory skin reactions concurrent with development of skin diseases such as psoriasis and atopic dermatitis. Pharmacological and dietetic control of the metabolism of arachidonic acid is a new and interesting therapeutic concept in the care of skin diseases. Also, fish oil, which is rich in linoleic acid and poor in arachidonic acid, seems to be useful in basal treatment of psoriasis. The value of evening primrose oil, which is rich in gamma-linoleic acid, in the treatment of atopic dermatitis is discussed.

Acne Vulgaris↗
PubMed1972

Very low density lipoproteins and lipoprotein lipase in serum of rats deficient in essential fatty acids.

Rats fed a diet deficient in essential fatty acids have a low level of serum very low density lipoproteins (VLDL). It was found that after intraperitoneal injection of heparin, deficient rats had a higher level of lipoprotein lipase activity in their plasma than did normal rats. VLDL isolated from serum of normal and deficient rats were compared as substrates for postheparin lipase of rat plasma. There was no significant difference in V(max) between the two preparations of lipoproteins, but the apparent K(m) for lipoproteins from deficient animals was significantly less than that for normal animals. These observations suggest that the low concentration of VLDL in deficient rats may be explained (a) by an increased activity of lipoprotein lipase in the tissues of these animals and (b) by the VLDL of deficient rats being more rapidly hydrolyzed at low concentrations by lipoprotein lipase than VLDL from normal rats.

Animals↗
PubMed1991

Interactions between n-3 and n-6 essential fatty acids (EFAs) in the regulation of cardiovascular disorders and inflammation.

Much attention has recently been paid to the possible benefits of increasing the intake of eicosapentaenoic acid (EPA) by consuming fish oil. However, this can have adverse effects such as raising cholesterol levels in patients with hyperlipidaemia and causing a deterioration in glucose tolerance. High doses of EPA given to Westerners also lower levels of dihomogammalinolenic acid (DGLA), a substance with a wide range of desirable cardiovascular and antiinflammatory actions. This lowering of DGLA does not occur in Eskimos who consume large amounts of EPA, indicating that there may be differences in essential fatty acid metabolism between Westerners and Eskimos. Therapeutic strategies are required which raise both EPA and DGLA and which do not raise EPA at the cost of lowering DGLA.

8,11,14-Eicosatrienoic Acid↗
PubMed1984

Essential fatty acid deficiency: a suggestion concerning experimental design.

In experiments on essential fatty acid deficiency, various strategems have been used to balance the deficient and control groups for all nutrients except essential fatty acids. We suggest the use of a single fat-free diet for both groups, with essential fatty acids administered parenterally to the control (nondeficient) group once each week.

Animals↗
PubMed1988

Essential fatty acid deficiency and neutrophil function: studies of lipid-free total parenteral nutrition in monkeys.

Linoleic acid (18:2 omega 6), the obligate precursor of arachidonic acid (20:4 omega 6), is an essential nutrient for humans and other mammals. Because arachidonic acid release and metabolism are components of neutrophil activation by certain stimuli, we questioned whether neutrophils depleted of arachidonate as a result of essential fatty acid deficiency might be functionally impaired. We examined this possibility by producing essential fatty acid deficiency in monkeys with lipid-free total parenteral nutrition (TPN). Rhesus and African green monkeys were given calorically equal TPN for up to 23 days with and without a vegetable fat emulsion rich in linoleic acid. Fatty acids were analyzed in total lipid extracts of serum and isolated blood neutrophils by gas-liquid chromatography. Although fatty acids in the serum and neutrophils of monkeys given TPN with lipid did not change, linoleic acid levels decreased by at least 60% in serum and 50% in neutrophils from animals given TPN with no lipid. Moreover, arachidonate levels in neutrophil lipids decreased by at least 50% within 12 days of lipid-free TPN, and the abnormal fatty acid 20:3 omega 9 (characteristic of essential fatty acid deficiency) appeared and steadily increased with time. These biochemical signs of omega 6 fatty acid deficiency were associated with impaired neutrophil function in vitro. Both migration responses and superoxide generation stimulated by N-formyl-methionyl-leucyl-phenylalanine were significantly decreased by 12 days of lipid-free TPN, as was the capacity of activated cells to synthesize leukotriene B4. In contrast, functional responses of fatty acid-deficient neutrophils to leukotriene B4 and phorbol myristate acetate, which have little or no effect on arachidonate release or metabolism, were not significantly altered. These findings indicate that endogenous supplies of arachidonic acid and other essential omega 6 fatty acids influence the functional responsiveness of neutrophils. These studies also indicate that altered neutrophil function is a feature of essential fatty acid deficiency and that it may contribute to the increased risk of infection and decreased inflammatory responses observed in this condition.

Animals↗