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PubMed1990

Essential-fatty-acid metabolites in plasma phospholipids in patients with ichthyosis vulgaris, acne vulgaris and psoriasis.

The concentration of essential fatty acids (EFAs) and their metabolites in plasma phospholipids were measured by gas chromatography in normal individuals, and in patients with ichthyosis vulgaris, acne vulgaris or psoriasis. In all three patient groups, concentrations of arachidonic acid (20:4 omega 6) and docosapentaenoic acid (22:5 omega 6) were significantly below those in controls, suggesting that these abnormalities may occur in many skin diseases. Concentrations of dihomogammalinolenic acid (20:3 omega 6) were low in ichthyosis, normal in acne and elevated in psoriasis. Thus ichthyosis, acne and psoriasis each had a characteristic pattern of EFA metabolites.

Acne Vulgaris↗
PubMed1974

Studies of the hepatic excretory defects in essential fatty acid deficiency. Their possible relationship to the genesis of cholesterol gallstones.

Male hamsters were fed normal and essential fatty acid (EFA)-deficient diets for at least 12 wk before bile duct cannulation. With [32P]phosphate, hepatic synthesis of lecithin was similar, but biliary excretion of newly synthesized lecithin was significantly reduced in EFA-deficient compared to that in normal hamsters. Hepatic uptake of intravenously infused taurocholate (TC) and taurochenodeoxycholate (TCDC) were similar in both groups of animals. However, biliary excretion of intravenously infused TC was significantly reduced in EFA-deficient hamsters, whereas that of TCDC-was unchanged. The absolute rate of biliary cholesterol excretion was similar in both groups. Canalicular bile flow, as measured by [14C]erythritol clearance after functional nephrectomy, was significantly lower, with both the bile salt-dependent and independent fractions of this flow being diminished in EFA-deficient hamsters infused with TC. It is concluded that EFA deficiency leads to impaired biliary excretion of taurocholate, lecithin, and water, while cholesterol transport is unaffected, and thus results in supersaturation of bile with respect to cholesterol and production of lithogenic bile.

Animals↗
PubMed2005

Simultaneous quantitative determination of deuterium- and carbon-13-labeled essential fatty acids in rat plasma.

This study reports methods for the quantitative determination of stable isotope-labeled essential fatty acids (EFAs) as well as an experiment in which deuterium-labeled linoleic acid (18:2n-6) and alpha-linolenic acid (18:3n-3) were compared with those labeled with carbon-13 in rat plasma in vivo. Standard curves were constructed to compensate for concentration and plasma matrix effects. It was observed that endogenous pools of fatty acids had a greater suppressing effect on the measurements of 13C-U-labeled EFAs relative to those labeled with 2H5. Using these methods, the in vivo metabolism of orally administered deuterated-linolenate, 13C-U-labeled linolenate, deuterated-linoleate, and 13C-U-labeled linoleate was compared in adult rats (n = 11). There were no significant differences in the concentrations of the 2H versus 13C isotopomers of 18:2n-6, 18:3n-3, arachidonic acid (20:4n-6), and docosahexaenoic acid (22:6n-3) in rat plasma samples at 24 h after dosing. Thus, there appears to be little isotope effect for 2H5- versus 13C-U-labeled EFAs when the data are calculated using the conventional standard curves and corrected for endogenous fatty acid pool size and matrix effects.

Animals↗
PubMedDate not supplied

Natural killer cell functions are related to the cell membrane composition of essential fatty acids: differences in healthy persons and patients with primary Sjögren's syndrome.

To examine whether abnormalities in essential fatty acid (EFA) metabolism are associated with the impaired natural killer (NK) cell functions in primary Sjögren's syndrome, we measured the levels of phospholipid fatty acids in blood mononuclear cells with (MD) and without monocyte depletion (MC), and NK cell activity before and after indomethacin-boosting. We found MD levels of 20:3n6 (dihommo-gamma-linolenic acid), and basal and indomethacin-enhanced NK cell activity significantly reduced, in 10 primary Sjögren's syndrome patients as compared with 10 healthy controls. In the controls the relative (%) increase in indomethacin-enhanced NK cell activity correlated with the level of MD 18:2n6 (linoleic acid) (r = 0.97, p less than 0.001). In the patients the relative (%) indomethacin-enhanced NK cell activity correlated with the 20:4n6 (arachidonic acid)/20:3n6 ratio in the MC (r = 0.90, p less than 0.001). This ratio has been assumed to be an important determinant for the production of prostaglandin 1 and 2. The present data suggest that in healthy persons, as opposed to primary Sjögren's syndrome patients, the level of MD 18:2n6 is a determinant for the sensitivity of NK cells to monocyte-derived prostaglandins. Furthermore, in patients with primary Sjögren's syndrome the MC levels of 20:3n6 and 20:4n6 may be regulating factors for the production of NK cell suppressing prostaglandins.

Adult↗
PubMed1991

Adipose tissue essential fatty acid composition in patients with atopic eczema.

We have measured adipose tissue total lipid and plasma phospholipid essential fatty acid composition by capillary column gas chromatography in patients with atopic eczema. In both adipose tissue and plasma phospholipids there was a significant elevation of linoleic acid in patients compared to a control group (adipose tissue P less than 0.05; plasma P less than 0.001), and a substantially higher ratio of linoleic acid to the sum of its longer chain highly unsaturated derived fatty acids, dihomogamma linolenic acid and arachidonic acid. These findings add support to the proposition that patients with atopic eczema have a defect in the conversion of linoleic acid.

Adipose Tissue↗
PubMed1986

Essential fatty acid uptake and esterification in primary culture of rat hepatocytes.

Primary cultures of adult rat hepatocytes were used to compare the uptake and esterification of essential polyunsaturated fatty acids (18:2, 20:3 and 20:4 of the n-6 series) with those of palmitic and oleic acids. The uptake of unesterified fatty acids was linearly related to the free fatty acid/albumin molar ratio for 14 h and did not depend on the unbound free fatty acid level. Whatever the initial free fatty acid/albumin molar ratio, it dropped to 0.5 +/- 0.1 mM after 14 h, thus showing that hepatocytes have a high capacity for clearing free fatty acids from the medium at high free fatty acid/albumin molar ratios. The free fatty acid uptake become saturable when the free fatty acid and albumin concentrations were raised and the free fatty acid/albumin ratio remained constant. This strongly suggests that albumin-hepatocyte interaction mediates free fatty acid uptake. This uptake was identical whatever the fatty acid tested and did not depend on the relative amounts of fatty acids when they were added simultaneously. Triacylglycerol accumulation and synthesis, monitored by labelled fatty acids, were related to the free fatty acid/albumin molar ratio and exhibited no specificity for the series of fatty acids tested. Triacylglycerols were enriched in all the fatty acids tested by up to 60%, and fatty acid incorporation into diacylglycerols and triacylglycerols reflected the free fatty acid composition of the medium. By contrast, neither the level nor the synthesis of phospholipids varied with free fatty acid/albumin, but the rate of phospholipid turnover depended on the fatty acids tested. Accumulation of these acids was smaller in phospholipids than in triacylglycerols. When linoleic and arachidonic acids were added together, phospholipids (especially phosphatidylethanolamine and phosphatidylinositol) were more enriched in arachidonic acid than triacylglycerols. This might be due to the specificity for fatty acid of the enzymes involved in phospholipid metabolism.

Animals↗
PubMed1997

Essential fatty acids, immune function, and exercise.

The immunologic response to exercise comprises numerous alterations within the immune system, but how these processes are regulated is still largely unknown. Exercise-related immunological changes include signs of inflammation, such as release of inflammatory mediators, activation of various white blood cell lines and complement, and induction of acute phase proteins. Nevertheless, signs of immunosuppression, such as decreased T and B cell function or impaired cytotoxic or phagocytic activity, can also be observed. Some data suggest that essential fatty acids help regulate inflammatory processes, modulating both cytokine release and the acute phase response. Positive effects of changing dietary essential fatty acids have been demonstrated in chronic inflammatory diseases. In contrast, little is known about the contribution of fatty acids to the exercise-induced immunologic reaction. Essential fatty acids may determine alterations within the immune system following exercise. Therefore, future studies are necessary to evaluate the influence of the fatty acid composition on the inflammatory or immunosuppressive component following heavy exertion.

Acute-Phase Reaction↗
PubMed2003

Red blood cell membrane essential fatty acid metabolism in early psychotic patients following antipsychotic drug treatment.

A role of indices of oxidative stress, oxidative injury, and abnormal membrane phospholipid, specifically the phospholipid essential polyunsaturated fatty acids (EPUFAs) metabolism has been suggested based on studies in separate groups of patients with or without medication. The current study investigated the relationship between these biochemical measures in first-episode psychotic patients (N=16) at baseline and after 6 months of antipsychotic treatment (N=5 each with risperidone and olanzapine) and compared them to matched normal subjects. The indices of oxidative stress included: antioxidant enzymes; superoxide dismutase, glutathione peroxidase and catalase; and the oxidative injury as the levels of plasma lipid peroxides. The key membrane EPUFA's been; linolenic acid, arachidonic acid, nervonic acid, docosapentaenoic acid and docosahexaenoic acid. Furthermore, the changes in these biochemical measures were correlated with clinical symptomatology. Data indicated that, at baseline, reduced levels of antioxidant enzymes were associated with increased plasma lipid peroxides and reduced membrane EPUFAs, particularly omega-3 fatty acids. Furthermore, these biochemical measures normalized after 6 months of antipsychotic treatment. Parallel-improved psychopathology indicated that membrane EPUFA status might be partly affected by oxidative damage, which together may contribute to the pathophysiology and thereby, psychopathology of schizophrenia. These data also support the augmentation of antipsychotic treatment by supplementation with a combination of antioxidants and omega-3 fatty acids.

Adult↗
PubMedDate not supplied

Effects of protein kinase Cbeta inhibition on neurovascular dysfunction in diabetic rats: interaction with oxidative stress and essential fatty acid dysmetabolism.

BACKGROUND: Elevated protein kinase C (PKC) activity is thought to play a substantial role in the aetiology of diabetic microvascular complications, the PKCbeta isoform being identified as particularly important. Neuropathy has a vascular component; therefore, one aim was to assess whether the PKCbeta inhibitor, LY333531, could correct nerve conduction velocity (NCV) and perfusion deficits in diabetic rats. Neurovascular dysfunction also depends on oxidant stress and impaired omega-6 essential fatty acid metabolism; correctable by antioxidant and gamma-linolenic acid (GLA) treatments, respectively. A second aim was to assess whether there were interactions between these mechanisms and PKCbeta-mediated effects. METHODS: Diabetes was induced by streptozotocin; duration was 8 weeks. NCV was monitored and blood flow was assessed by hydrogen clearance microelectrode polarography. RESULTS: Diabetes caused 19.7% and 13.9% reductions in sciatic motor and saphenous sensory NCV, respectively. Two weeks of LY333531 treatment dose-dependently corrected these deficits. A dose of 10 mg kg(-1) day(-1) gave non-diabetic NCV values and also completely corrected a 50% diabetic reduction in sciatic endoneurial blood flow. Low-dose (0.25 mg kg(-1) day(-1)) LY333531 had modest effects ( approximately 20% correction) on NCV and sciatic perfusion. However, when combined with equi-effective doses of the antioxidants vitamin E or alpha-lipoic acid, or GLA, motor and sensory NCV and sciatic nerve perfusion were in the non-diabetic range. The joint effect was equivalent to that of the 10 mg kg(-1) day(-1) LY333531 dose, demonstrating synergism between PKCbeta, oxidative stress and essential fatty acid mechanisms. CONCLUSIONS: LY333531, alone or combined with antioxidants or GLA, could form the basis for therapeutic intervention in neuropathy, which requires assessment in clinical trials.

Animals↗
PubMed1978

Cerebral prostaglandin synthesis during the dietary and pathological stresses of essential fatty acid deficiency and experimental allergic encephalomyelitis.

Rats of the Lewis strain were fed diets adequate or deficient in essential fatty acids (EFA). At 70-80 days of age experimental allergic encephalomyelitis (EAE) was induced using adjuvants containing either Mycobacterium butyricum or Mycobacterium tuberculois H37Ra. When the former Mycobacterium was used, the incidence of EAE was greater in the EFA-deficient than in EFA-adequate controls; but when the rats challenged with M. tuberculosis, the incidence of the disease was the same in both dietary groups. Brain slices from EFA-deficient rats had a marginally depressed synthesis of prostaglandin F (PGF) compared to that of controls. Immunochallenge with adjuvant alone or adjuvant plus antigen tended to depress further PGF synthesis by brain slices from EFA-deficient rats and significantly depressed synthesis by slices from rats receiving adequate EFA. Whether or not rats were paralyzed had no effect on PGF synthesis when the diet was adequate in EFA, but a significant difference was seen in the EFA-deficient group. The results indicate a possible role for PGF synthesis in the degree of susceptibility of the rats to EAE under different dietary regimens.

Animals↗
PubMed1992

Effects of dietary essential fatty acid deficiency on the development of the rat thymus and immune system.

The paper describes an effect of essential fatty acid (EFA) deficiency on the development of the rat thymus and pups' immune system. From birth until being weaned (22nd day), the pups were hand-fed artificial milk diets containing a low (EFA-D) or high (EFA-R) proportion of EFA in the lipid fraction. The weight parameters of the body, thymus and spleen, the fatty acid composition of the individual thymus phospholipid subclasses, and mitogen-induced proliferation of thymus and spleen lymphocytes were studied. The results show that the total body weight of the EFA-deficient (EFA-D) fed animals was significantly decreased in comparison with the EFA-rich (EFA-R) and rat milk hand-fed animals. For the EFA-D group of young rats a high level of the (n-9) and (n-7) series fatty acids [mainly oleic 18:1(n-9) and eicosatrienoic 20:3(n-9) acids] was characteristic of the fatty acids in phosphatidylcholine and phosphatidylethanolamine in the thymus, compensating for the reduction of the content of arachidonic acid 20:4(n-6). The biochemical index of the EFA nutritional deficit in the thymus tissue was observable as early as on day 7. The mitogen-induced (Con A) proliferation of the thymus and spleen lymphocytes was decreased both on the 30th and 40th day of life. The results show that the EFA nutritional deficit in the early postnatal period caused damage to the structure of thymus in the young rats, most probably as a result of the change in the composition of the lipid fraction. These changes also affected the development of the immune system of the whole organism.

Animals↗