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PubMed1990

Lipid and cell metabolic changes associated with essential fatty acid enrichment of articular chondrocytes.

Observations of impaired chondrocyte metabolism in essential fatty acid (EFA) deficiency as well as EFA protection against development of osteoarthrosis in inbred mice suggest the existence of a relationship between EFA, chondrocyte metabolism, and cartilage degeneration. To explore this relationship further, the fatty acid content of lipids in normal fetal bovine chondrocytes was manipulated by in vitro exposure to media supplemented with 100 microM arachidonic acid (20:4) or oleic acid (18:1). Chondrocytes rapidly and differentially incorporated both fatty acids into their lipid pools. The predominant acceptor was triacylglycerols. A 980% enrichment of arachidonic acid was associated with increased concentrations of fatty acids, increased 35SO4 and [3H]proline incorporation into matrix macromolecules (170% and 54-103%, respectively), and a 24-fold elevation in chondrocyte prostaglandin synthesis. No metabolic effects elicited observed in cells enriched by 377% with 18:1 oleic acid. The metabolic effects elicited by 20:4 arachidonic acid were abolished by pretreatment of cells with indomethacin, suggesting that the cellular responses to essential fatty acid loading may be associated with induced increases in prostaglandin synthesis. The data indicate that excessive in vitro accumulation of arachidonic acid is associated with an increase in synthetic activity that is causally related to increased prostaglandin synthesis and elevated levels of cellular fatty acids.

Animals↗
PubMed1997

Essential fatty acid status in children with cholestasis, in relation to serum bilirubin concentration.

The liver plays a central role in the metabolism of polyunsaturated fatty acids. We studied the relationship between essential fatty acid (EFA) status and indicators of liver function in 15 children with chronic cholestasis aged 9 months to 3.4 years (median, 1.3 years). Compared with 13 control children, the patients studied had low percentage values of phospholipid EFAs, particularly of the omega-6 fatty acids linoleic acid (18:2omega-6) and arachidonic acid (20:4omega-6). Fatty acid values exhibited an inverse relationship to serum bile acids, as well as to serum bilirubin. Bilirubin values were unrelated to the EFA precursors linoleic acid and alpha-linolenic acid but correlated inversely with the long-chain metabolites arachidonic acid (r = -0.75; p = 0.001), docosapentaenoic acid (22:5omega-3; r = -0.63; p = 0.01), and docosahexaenoic acid (22:6omega-3; r = 0.72; p = 0.002). We conclude that children with chronic cholestasis are at a high risk for EFA deficiency, which increases with progressive elevation of serum bilirubin. Hepatic conversion of essential precursor fatty acids into their long-chain metabolites may be increasingly impaired with advancing severity of liver disease.

Arachidonic Acid↗
PubMed1979

Effects of essential fatty acid deficiency, and various levels of dietary polyunsaturated fatty acids, on humoral immunity in mice.

Six experiments were conducted to determine the influence of an essential fatty acid deficient diet (EFAD), and various levels of dietary polyunsaturated fatty acids, on humoral immunity in mice. The results indicated that: 1) Consumption of diets deficient in essential fatty acids (0% corn oil) significantly reduced the humoral response. This reduction was demonstrated after feeding the essential fatty acid deficient diet for only 28 days; and preceded the effects of essential fatty acid deficiency on growth or appearance. 2) Reduced antibody response was demonstrated against T-cell dependent and T-cell independent antigens, and in both primary and secondary responses of mice fed the essential fatty acid deficient diet. 3) After 56 days of feeding the EFAD diet (0% corn oil), mice switched to the control diet (13% corn oil) for 7 days demonstrated full recovery of the humoral response. 4) Diets containing various levels of polyunsaturated fatty acids (from 2 to 70% of energy from corn oil) did not adversely affect the humoral response. The results support the hypothesis that essential fatty acids play a crucial role in maintaining the functional integrity of humoral immunity.

Animals↗
PubMed1995

Nutritional modulation of guinea pig skin hyperproliferation by essential fatty acid deficiency is associated with selective down regulation of protein kinase C-beta.

In a previous study we demonstrated that 13-hydroxyoctadecadienoic acid (13-HODE), a 15-lipoxygenase metabolite of linoleic acid is incorporated into epidermal phosphatidyl 4,5-bisphosphate (PtdIns 4,5-P2) and released as 13-HODE-containing-diacylglycerol (13-HODE-DAG). In vitro, 13-HODE-DAG was shown to selectively inhibit epidermal total protein kinase C (PKC-beta) activity. To determine whether these observations are relevant in vivo, guinea pigs were made essential fatty acid deficient (EFAD) by feeding them a basal diet supplemented with 4% hydrogenated coconut oil for 8 wk. Tissue levels of putative 13-HODE-DAG, protein kinase C (PKC) isozymes and tissue hyperproliferation were determined in the epidermal preparations from skin of control safflower oil-fed guinea pigs, those fed EFAD diet and those fed EFAD diet followed by the control diet for 2 wk. Our data revealed that cutaneous 13-HODE and 13-HODE-DAG were significantly lower in EFAD animals than in safflower-fed controls. These reductions were associated with both elevated epidermal hyperproliferation and elevated expressions and activities of PKC-alpha and beta-isozymes. Refeeding the animals with safflower oil for 2 wk replenished tissue levels of 13-HODE-DAG, which inversely correlated with the selective down regulation of PKC-beta expression and activity and the reversal of hyperproliferation. In contrast, although, the expression and activity of PKC-alpha was elevated in the epidermis of the EFAD guinea pigs, this elevated PKC-alpha expression was not down regulated after refeeding the safflower oil diet to the animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animal Nutritional Physiological Phenomena↗
PubMed1978

Essential fatty acid deficiency in infants receiving parenteral nutrition.

The clinical and biochemical features of essential fatty acid deficiency are described in an infant with gastroschisis who required long-term (6 mo) parenteral nutrition. The deficiency responded to therapy with Intralipid, topical sunflower oil, and breast milk. In a prospective study of three infants with gastroschisis, biochemical essential fatty acid deficiency developed in each during the first week of lipid-free parenteral nutrition; clinical signs of the deficiency were absent. The biochemical features were progressive in the one patient followed for 19 days, and were associated with a decrease in weight gain. Both the deficiency and weight gain were corrected by Intralipid. Biochemical essential fatty acid deficiency did not develop in three other gastroschisis infants who were given prophylactic Intralipid (two patients) or topical sunflower oil (one patient). We conclude that all infants on parenteral nutrition should receive a source of linoleic acid to prevent essential fatty acid deficiency.

Abdominal Muscles↗
PubMed1986

Essential fatty acids and acne.

Acne is characterized by hyperkeratosis of the follicular epithelium, leading to horny impactions that may lie dormant as open or closed comedones or may cause inflammation of the follicle. Although persons with acne have consistently been observed to have elevated levels of sebum secretion, no mechanism relating sebum secretion rates to comedogenesis is known. Acne patients have also been shown to have low levels of linoleic acid in their skin surface lipids. To explain this observation, the hypothesis is advanced that the linoleate concentration in human sebum depends on the quantity of linoleic acid present in each sebaceous cell at the commencement of its differentiation and on the extent to which this initial charge is diluted by subsequent endogenous lipid synthesis in each sebaceous cell. A corollary hypothesis holds that low concentrations of linoleate in sebum impose a state of essential fatty acid deficiency on the cells of the follicular epithelium and induce the characteristic response of hyperkeratosis. Both hypotheses could hold, without there being a systemic deficiency of linoleic acid, simply as the result of elevated lipogenesis in individual sebaceous cells.

Acne Vulgaris↗
PubMed1981

Effect of some dietary additions to either an arginine-devoid diet or a diet supplemented with orotic acid refed after starvation on liver lipid content during essential fatty acid deficiency in rats.

Refeeding either an arginine-devoid diet or a 14% casein diet supplemented with 1% orotic acid for 7 days to starved rats caused an increase in liver lipid content which was prevented by the addition of adenine, allopurinol and safflower oil, but not guanine, cytosine, thymine and uracil. When rats were refed the arginine-devoid diet unsupplemented or supplemented with guanine, cytosine, thymine and uracil, their serum triglyceride and cholesterol decreased or tended to decrease as compared with those of rats refed the arginine-devoid diet supplemented with either adenine or allopurinol or rats refed the arginine-supplemented diet. Furthermore, triglyceride and cholesterol in serum of rats refed the arginine-devoid diet supplemented with either adenine or allopurinol increased as compared with those of rats refed the arginine-supplemented diet. The addition of either adenine or allopurinol to the arginine-devoid diet resulted in lowered lipid content in the liver as compared with the arginine-supplemented diet. Thus, when the arginine-devoid diet unsupplemented or supplemented with arginine, adenine and allopurinol was refed, liver lipid content was inversely related to the serum triglyceride level.

Adenine↗
PubMedDate not supplied

Essential fatty acids prevent slowed nerve conduction in streptozotocin diabetic rats.

Rats were given streptozotocin to induce insulin-dependent diabetes or citrate buffer alone in two experiments. Initially, the effect of 5 wks of dietary gamma-linolenic acid (GLA) plus eicosapentaenoic acid (EPA) on cutaneous nerve conduction velocity (CV) was examined. CV was determined by direct stimulation and recording from saphenous nerve under urethane anesthesia. Secondly, a 5 weeks study of supplementing the diet with GLA, GLA and EPA, or hydrogenated coconut oil (HC) was done. In addition, motor nerve CV was determined by directly stimulating sciatic nerve and recording from gastrocnemius muscle. The acute diabetes led to weight loss, and elevated blood glucose and glycosylated hemoglobin levels. Essential fatty acid (EFA) supplementation had no effect on any of these measures of severity of diabetes. In diabetic rats without EFA supplementation, CV of the myelinated fibers fell by 19-21%, while those receiving both GLA and EPA had normal CV. In diabetic rats receiving GLA alone, CV fell by 5-7%, which was significantly less than those without EFA supplementation (p less than 0.01 for cutaneous, and p less than 0.001 for motor nerves).

Animals↗
PubMed1986

Apparent in vivo retroconversion of dietary arachidonic to linoleic acid in essential fatty acid-deficient rats.

Essential fatty acid-deficient rats were fed ethyl [U-14C]arachidonate (308 dpm/nmol) and when a decrease in the transepidermal water loss was seen, the epidermal sphingolipids, acylglucosylceramide and acylceramide were isolated. [14C]Linoleic acid (approx. 130 dpm/nmol) was present in both lipid classes, while the substrate was only detected in the former. These results intimate that in vivo retroconversion of arachidonic to linoleic acid can be induced in the rat.

Animals↗
PubMed1998

The inadequacy of the essential fatty acid content of present preterm feeds.

UNLABELLED: Arachidonic (AA) and docosahexaenoic (DHA) acids are major components of endothelial, pulmonary and neuro-visual cell membranes. Preterm babies may be born with deficits of both AA and DHA. There is evidence that their endogenous anti-oxidant enzymes defence systems have only reached half the activity expected at term. Yet they are exposed to an oxygen tension greater than physiologically anticipated at this time, and the superoxide dismutase shows no evidence of significant catch-up. After birth, present enteral and parenteral feeds for the preterm baby result in a further drop of AA and DHA plasma proportions to a quarter or third of the intra-uterine expectation. At the same time, the proportion of linoleic acid (LA), the precursor for AA, rises in the plasma phosphoglycerides four-fold, thus denying the preterm infant the provision with which the placenta would have perfused the fetus to meet the very rapid demand for endothelial and neural growth. From the biochemistry it is predictable that this situation could lead to fragile cell membranes, leakage, rupture with peroxidation resulting in the formation of inflammatory and vasoconstrictive agents. CONCLUSION: The essential fatty acid content of current enteral and parenteral feeds for preterm infants is incorrectly formulated.

Arachidonic Acids↗
PubMed2003

Phosphatidylethanolamine-N-methyltransferase activity and dietary choline regulate liver-plasma lipid flux and essential fatty acid metabolism in mice.

Phosphatidylethanolamine-N-methyltransferase (PEMT) catalyzes the methylation of phosphatidylethanolamine to form phosphatidylcholine (PC) and represents one of the two major pathways for PC biosynthesis. Mice with a homozygous disruption of the PEMT gene are dependent on the 1,2-diacylglycerol cholinephosphotransferase (CDP-choline) pathway for the synthesis of PC and develop severe liver steatosis when fed a diet deficient in choline. The present study used quantitative lipid metabolite profiling to characterize lipid metabolism in PEMT-deficient mice fed diets containing varying concentrations of choline. Choline supplementation restored liver, but not plasma PC concentrations of PEMT-deficient mice to levels commensurate with control mice. Choline supplementation also restored plasma triglyceride concentrations to normal levels, but did not restore plasma cholesterol ester concentrations in the PEMT-deficient mice to those equal to control mice. PEMT-deficient mice also had substantially diminished concentrations of docosahexaenoic acid [22:6(n-3)] and arachidonic acid [20:4(n-6)] in plasma, independent of choline status. Thus, choline supplementation rescued some but not all of the phenotypes induced by the knockout. These findings indicate that PEMT activity functions beyond its recognized role as a compensatory pathway for PC biosynthesis and that, in contrast, PEMT activity is involved in many physiologic processes including the flux of lipid between liver and plasma and the delivery of essential fatty acids to blood and peripheral tissues via the liver-derived lipoproteins.

Animals↗
PubMed2005

Effects of essential fatty acid deficiency on periodontal tissue adaptation to spontaneous tooth migration.

Essential fatty acids (EFAs) play a significant role in bone metabolism. Herein we studied the adaptation of alveolar bone to physiologic tooth drift in young rats deprived of essential fatty acids from birth. Reductions in femur size and trabecular bone volume reflected body growth impairment. Along the alveolar wall, osteoclastic resorption and bone formation were depressed, disrupting the adaptive deformation of the tooth socket to ongoing migration. As a result, the periodontal ligament narrowed considerably, and further adaptation was achieved through root resorption. Essential fatty acid deficiency (EFAD), did not affect precursor recruitment or differentiation in the periodontal ligament (PDL), but caused redistribution of nonspecific-esterase (NSE)-positive osteoclast precursors and tartrate-resistant acid phosphatase (TRAP)-positive pre-osteoclasts between the bone compartment (which was depleted) and the root compartment (which was enriched). EFAD had also a marked effect on the PDL vasculature; the number of vessels was reduced, whereas their size was markedly increased. As a whole, our results show that EFAD disturbs alveolar bone adaptation to drift, but that a reaction (detrimental to root integrity) prevents root collision with the bone surface, thereby preserving the PDL as a source of precursor cells for bone and cementum homeostasis. Moreover, our results confirm that although alveolar bone resorption is arachidonic acid-dependent, the factors activating root resorption are different.

Animals↗
PubMed1990

Paradoxical effects of essential fatty acid supplementation on lipid profiles and sweat electrolytes in cystic fibrosis.

Supplements of evening primrose oil (Oenothera biennis), which contains at least 72% linoleic (18:2n-6) and 7% gamma-linolenic (18:3 n-6) acids (expressed as % fatty acid methyl esters) were given to sixteen cystic fibrosis patients for a period of 12 months. Clinical observations showed no significant changes in patients' weights or respiratory function throughout. Linoleic acid levels in plasma and erythrocyte membranes increased significantly during the first 6 months but this increase was not sustained at its initial level. After supplementation was discontinued reversion to baseline (low) levels occurred within 4 months. Levels of plasma prostaglandins (PG) and urinary PG metabolites varied among individuals over a wide range, and urinary PGF2 alpha metabolites fell during the supplementation. There was a significant fall in sweat sodium concentrations after 6 weeks of supplementation, but sweat chloride was unchanged. It is not known whether the effect of essential fatty acids on sweat Na+ reflects changes in cell membrane conformation or if there is a direct effect on Na+ pump activity.

Adolescent↗
PubMed1980

[Recent developments in the concept of essential fatty acids in fish].

In fish, essential acids belong to the n-3 series. In trout, carp and salmon a dietary supply of 0.7 to 1% linolenate allows to prevent any symptoms of deficiency and ensures a normal growth. This is not the case for see fish such as daurade and turbot, where a supply of a similar proportion of n-3 high polyunsaturated fatty acids (HPUFA) appears to be necessary. However, recent experiments show that this requirement for HPUFA is not specific, since they can be replaced by linolenate in the turbot provided that the linolenate dietary amount is substantially higher than in the trout. The 6-desaturase activity seems to be lower in see fish than in freshwater fish and there is a good agreement between the nutritional tests of growth rate of fish and the biological tests of bioconversion rate of linolenate into HPUFA. Fish seem to be a highly valuable tool for determining the role and mechanism of action of essential fatty acids. In our opinion it is very interesting to use differences between fish and mammals to apprehend all the specific biological processes related to the presence of essential fatty acids in the organism.

Animals↗
PubMed1993

Placebo-controlled trial of essential fatty acid supplementation in atopic dermatitis.

Treatment of atopic dermatitis with essential fatty acids remains controversial. A double-blind, placebo-controlled, parallel-group study was done to investigate the response of patients with atopic dermatitis to essential fatty acid supplements. Patients with atopic dermatitis were randomised to receive evening primrose oil, evening primrose oil and fish oil, or placebo for 16 weeks. Disease activity was monitored by clinical severity scores recorded by the investigator, topical steroid requirement, and symptom scores recorded by subjects. Of 123 subjects recruited, 102 completed the treatment period. No improvement with active treatment was demonstrated. Our study, which avoided the methodological and analytical problems of previous studies, found no effect of essential fatty acid supplementation in atopic dermatitis.

Adult↗
PubMed1996

Metabolism of orally fed [3H]-eicosapentaenoic and [14C]-arachidonic acid in essential fatty acid-deficient rats.

The metabolism of individual polyunsaturated fatty acids (PUFA) may be influenced differently by nutritional status and nutritional intake. In normal rats, radioactive arachidonic acid (20:4(n-6), is preferentially retained in tissue phospholipids compared to linoleic (18:2(n-6), or eicosapentaenoic acid (20:5(n-3). This study compares the fate of 20:4(n-6) and 20:5(n-3) acids in essential fatty acid-deficient (EFAD) rats. [3H]-20:5 and [14C]-20:4 were fed in a fish oil emulsion to EFAD rats. Tissue lipids were analysed for radioactivity at 1, 2 and 4 h. The conversion of [3H]-20:5 to docosapentaenoic acid (22:5) and docosahexaenoic acid (22:6) was examined using high performance liquid chromatography (HPLC). The recovery of 3H in small intestine was lower than that of 14C (26 vs. 36% after 4 h, p < 0.001), but was higher in the liver (26 of 3H vs. 22% of 14C, p < 0.01), kidneys (1.5 vs. 1.2%, p < 0.001) and colon (0.3 vs. 0.2%, p = 0.01). The percentages of 3H and 14C in phospholipids were investigated in intestine and liver, and were higher in EFAD rats than in normal rats, particularly for phosphatidylethanolamine (PE). The proportions of [3H]-20:5 transformed to 22:5 and 22:6 did not exceed 7% in the intestine and 10% in the liver. In conclusion, the metabolism of dietary fatty acids 20:4 and 20:5 differed less than in normal rats, mainly due to the preferential retention of both fatty acids in phospholipids.

Animals↗
PubMed2003

Smoking, gender, and dietary influences on erythrocyte essential fatty acid composition among patients with schizophrenia or schizoaffective disorder.

BACKGROUND: Prior reports of decreased levels of essential fatty acids among schizophrenic patients have generated several hypotheses proposing inherent abnormalities in phospholipid and fatty acid metabolism and have provided the basis for treatment trials; however, these essential fatty acid aberrations may be attributable to uncontrolled factors, such as smoking, rather than abnormalities inherent to schizophrenia. METHODS: Erythrocyte fatty acid compositions were quantified in 72 medicated schizophrenic or schizoaffective patients both at baseline and after 16 weeks of supplementation with 3 g/day of either ethyl-eicosapentaenoic acid or placebo. Current smoking status, gender, dietary survey, and Montgomery Asburg Depression Rating Scale, Repeatable Battery for the Assessment of Neuropsychological Status, Abnormal Involuntary Movement Scale, and Positive and Negative Syndrome Scale scores were assessed. RESULTS: Schizophrenic patients who smoked had lower baseline erythrocyte docosahexaenoic acid percent (2.98 +/-.7 vs. 3.59 +/- 1.2, p <.005) and eicosapentaenoic acid (EPA) percent (.39 +/-.13 vs. 47 +/-.22, p <.05), compared with nonsmokers, with a significant gender interaction (p <.01) in multivariate analyses of variance. Baseline arachidonic acid did not differ. Smokers reported lower dietary intake (percent total fat) of linolenic acid (F = 10.1, p <.003) compared with nonsmokers. Nonsmoking women reported greater dietary intake of EPA compared with smoking men or nonsmokers of either gender. CONCLUSIONS: Smoking status, gender, and dietary intake significantly predicted erythrocyte polyunsaturated fatty acid status among schizophrenic patients. No evidence was found for subgroups of schizophrenia or relationships to specific symptom severity on the basis of erythrocyte fatty acids. Prior reports of abnormalities of essential fatty acid metabolism among schizophrenic patients may have been an artifact of patients' smoking behavior and differences in dietary intake of omega-3 fatty acids.

Adolescent↗