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PubMed1998

Uptake and metabolism of structured triglyceride by Caco-2 cells: reversal of essential fatty acid deficiency.

Structured lipids have been proposed as efficient vehicles for the supplementation of essential fatty acids (EFA) to patients with malabsorption. We investigated how a novel structured triglyceride (STG), containing purely octanoic acid in the sn-1/sn-3 and [14C]linoleic acid in the sn-2 positions, was incorporated into different lipid classes in Caco-2 cells. We also evaluated the contribution of gastric lipase in the uptake and metabolism of [14C]linoleic acid from the STG. We furthermore determined the potential of the STG to correct EFA deficiency induced in Caco-2 cells. The absorption of STG by Caco-2 cells was significantly greater compared with that of triolein. The addition of human gastric lipase significantly enhanced cellular uptake of the labeled substrate, reflecting the stereoselectivity of gastric lipase to hydrolyze medium chain FA. Analysis of the intracellular lipids synthesized revealed a predominance of phospholipids-monoglycerides. Most of the radioactivity in the lipoproteins isolated from Caco-2 cells was recovered in TG-rich lipoproteins (45%) and to a lesser extent in the high-density lipoprotein (36%) and low-density lipoprotein (17%) fractions. The administration of STG to Caco-2 cells rendered EFA deficient produced a marked increase of the cellular level of linoleic and arachidonic acids. This resulted in a lower ratio of 20:3(n-9) to 20:4(n-6), reflecting the correction of EFA deficiency in Caco-2 cells. Our data demonstrate that STG, in the presence of gastric lipase, have beneficial effects on lipid incorporation, lipoprotein production, and EFA status, utilizing Caco-2 cells as a model of EFA deficiency.

Biological Transport↗
PubMed1979

Adenine nucleotide translocation in liver mitochondria isolated from rats deficient in essential fatty acids.

Adenine nucleotide content and adenine nucleotide transport were evaluated in rats deficient in essential fatty acids (EFA) and in control rats. ADP uptake by EFA-deficient mitochondria was altered in a manner similar to the alteration produced by treatment of normal mitochondria with uncoupler. The uptake of ATP by EFA-deficient mitochondria was more rapid than that of normal mitochondria, but similar to that of normal mitochondria treated with uncoupler (DNP). Both uptake of ADP and uptake of ATP by EFA-deficient mitochondria were atractyloside sensitive. Total adenine nucleotide content of liver mitochondria from EFA-deficient rats was similar to that of liver mitochondria from control animals, but the content of ATP in EFA-deficient mitochondria was significantly higher than that of normal mitochondria. There was a negative correlation between the concentration of linoleic acid in total mitochondria lipids and ATP content of mitochondria.

Adenine Nucleotides↗
PubMed1985

Nutrition and immunity: the immunoregulatory effect of n-6 essential fatty acids is mediated through prostaglandin E.

Suppression of cell-mediated immune responses by essential fatty acids (EFA) was demonstrated in mice maintained on a standard laboratory diet for rodents. Daily oral administration of EFA at doses ranging from 125 to 750 mg/kg body weight significantly suppressed local host-versus-graft and graft-versus-host reactions as measured by popliteal lymph node assay. Studies employing immune sera directed against E-type prostaglandin demonstrated that n-6 EFA-induced suppression was mediated through prostaglandin E1. In titration experiments the effect of n-6 EFA on the reactions was dose dependent with enhancement of the responses at low concentrations and suppression at high concentrations.

Alprostadil↗
PubMedDate not supplied

Clinical aspects of essential fatty acid metabolism: Jonathan Rhoads Lecture.

The clinical implications of the metabolism of the 2 essential fatty acids, linoleic and alpha-linolenic acid, are most clearly related to the membrane phospholipid concentrations of their elongation and desaturation products, arachidonic, eicosapentaenoic, and docosahexaenoic acid. Levels of these very long chain polyunsaturated fatty acids can be altered by diet, prematurity, and disease which can affect growth (nutritional repletion) and the intensity and character of systemic inflammation as well as cognitive and visual function in infants.

Adult↗
PubMed1979

Essential fatty acid deficiency: a consequence of fat-free total parenteral nutrition.

A case of essential fatty acid deficiency (EFAD) associated with fat-free total parenteral nutrition (TPN) therapy in a 53-year-old white male is reported. The patient's tube feedings (Sustacal) were discontinued and a fat-free TPN solution of 25% dextrose injection, 4.25% amino acid injection (Freamine II) and appropriate electrolytes, vitamins and minerals was started when an upper GI study showed complete obstruction of his esophageal-colonic anastomosis. After nearly 1.5 months of fat-free TPN therapy, a diffuse scaly rash appeared on the patient's elbows, groin, arms and legs, and plasma fatty acid analysis showed a gross fatty acid deficiency. One liter of 10% soybean oil emulsion (Intralipid) then was added to 3 liters of TPN daily; linoleic acid accounted for 12% of the total calories of this solution. After 14 days of Intralipid therapy, the patient's skin lesions had cleared and plasma fatty acids had returned to normal. The patient was discharged on tube feedings of Sustacal providing sufficient linoleic acid (8.4% of calories) to prevent recurrence of EFAD. The pathophysiology, diagnosis and treatment of EFAD, and the role of linoleic acid in the disease are reviewed. TPN protocols should include recommendations for administration of linoleic acid to all patients receiving continuous infusion of fat-free TPN.

Fatty Acids, Essential↗
PubMed1992

Essential fatty acid deficiency normalizes function and histology in rat nephrotoxic nephritis.

The central lipid abnormality in essential fatty acid deficiency (EFAD) is the lack of availability of arachidonic acid. To examine the role of total eicosanoid's biosyntheses in the pathology and pathophysiology of glomerulonephritis, EFAD was induced in weanling rats, which were then subjected to antiglomerular basement membrane antibody (NTS)-induced injury in adulthood. Glomerular dynamics (as assessed by micropuncture), quantitative histology, and eicosanoid generation rates were measured at two hours and two weeks post-NTS, and compared to those of standard diet-fed (STD) controls. Two hours post-NTS, and despite the occurrence of proteinuria in both EFAD and STD animals, glomerular dynamics were essentially normal in EFAD rats, whereas STD animals had reduced values for glomerular filtration rate (GFR) and renal plasma flow rate (RPF). At two weeks, severe histologic changes were observed in STD animals including mesangial and stalk hypercellularity, moderate sclerosis, and interstitial nephritis, coupled with heavy proteinuria and reduced GFR and RPF. In dramatic contrast, EFAD rats displayed totally normal glomerular structures and functions. In parallel, glomerular generation rates of prostaglandin E2 and thromboxane A2 were suppressed markedly in EFAD rats. Thus, EFAD confers complete protection against the histopathologic and functional sequelae of immune-initiated injury in the glomerulus. The data suggest that the initial wave of complement-induced neutrophil infiltration (with resultant proteinuria) is not sufficient to perpetuate injury into the more destructive chronic phases. The results provide strong impetus for the design of more specific interventional therapies targeting the various enzymes and products of arachidonic acid metabolism in the attempts to control glomerular inflammation.

Acute Disease↗
PubMed1991

Essential fatty acid deficiency associated with the use of a medium-chain-triglyceride infant formula in pediatric hepatobiliary disease.

Serum phospholipid fatty acid patterns were determined by gas chromatography in four infants with hepatobiliary disease receiving a formula with a high content of medium-chain-triglyceride (MCT) oil. All four infants demonstrated signs of essential fatty acid deficiency, characterized by decreased arachidonic acid and increased palmitoleic and oleic acids. All had substantial concentrations of the pathologic triene 5,8,11-eicosatrienoic acid. Three of four had decreased linoleic acid concentrations and abnormal ratios of triene to tetraene (5,8,11-eicosatrienoic acid: arachidonic acid), greater than 0.38. One patient may have experienced growth failure due to abnormal essential fatty acid status. Infants with the potential for fat malabsorption should only receive MCT-oil feedings with well above the generally recommended requirements for linoleic acid (3% of total caloric intake).

Cholestasis↗
PubMed1980

Essential fatty acid deficiency and plasma triglyceride turnover in rats.

Hepatic triglyceride secretion in essential fatty acid-deficient rats was examined by three separate techniques in an effort to resolve conflicting evidence on the question of whether essential fatty acid deficiency altered hepatic triglyceride secretion in vivo. First, plasma triglyceride turnover was measured by intravenous injection of [2-3H]glycerol trioleate. Equations of the kinetics were formulated based on a single, open pool model. Turnover rates and pool sizes of plasma triglyceride were calculated from these equations. Second, [2-3H]glycerol was injected, and apparent rate constants for plasma triglyceride secretion and clearance were calculated by kinetic analysis. Third, Triton WR-1339 was used to inhibit lipoprotein clearance from blood plasma, and rates of plasma triglyceride accumulation were measured. The results of these studies showed that the rate of hepatic triglyceride secretion was 2-3 times greater in essential fatty acid-deficient rats than in nondeficient controls. The increase in triglyceride secretion, as well as the higher level of liver triglyceride typical of essential fatty acid-deficient rats, could be caused by increased lipogenesis and increased mobilization of fatty acids from adipose tissues.

Animals↗
PubMed2002

Essential fatty acids given from conception prevent topographies of motor deficit in a transgenic model of Huntington's disease.

Transgenic R6/1 mice incorporate a human genomic fragment containing promoter elements exon 1 and a portion of intron 2 of the Huntingtin gene responsible for Huntington's disease. They develop late-onset neurological deficits in a manner similar to the motor abnormalities of the disorder. As essential fatty acids are phospholipid components of cell membranes which may influence cell death and movement disorder phenotype, R6/1 and normal mice were randomised to receive a mixture of essential fatty acids or placebo on alternate days throughout life. Over mid-adulthood, topographical assessment of behaviour revealed R6/1 transgenics to evidence progressive shortening of stride length, with progressive reductions in locomotion, elements of rearing, sniffing, sifting and chewing, and an increase in grooming. These deficits were either not evident or materially diminished in R6/1 transgenics receiving essential fatty acids. R6/1 transgenics also showed reductions in body weight and in brain dopamine D(1)-like and D(2)-like quantitative receptor autoradiography which were unaltered by essential fatty acids.These findings indicate that early and sustained treatment with essential fatty acids are able to protect against motor deficits in R6/1 transgenic mice expressing exon 1 and a portion of intron 2 of the Huntingtin gene, and suggest that essential fatty acids may have therapeutic potential in Huntington's disease.

Aging↗
PubMed1991

Effect of essential fatty acid deficiency on lipid composition of basolateral plasma membrane of pig intestinal mucosal cells.

The effect of essential fatty acid (EFA) deficiency on the lipid composition of basolateral plasma membranes (BPM) from intestinal mucosal cells was investigated in weaning pigs fed control or EFA-deficient diets for 12 weeks. The phospholipid and cholesterol contents relative to protein were similar in both groups, showing a cholesterol/phospholipid molar ratio of 0.6. The distribution of phospholipid classes was also unaffected by the diet. In contrast, fatty acid profiles of the two phospholipid main classes, phosphatidylcholine and phosphatidyl-ethanolamine were altered by EFA deficiency. Linoleic acid (18:2n-6) was largely reduced, whereas arachidonic acid (20:4n-6) only slightly decreased in EFA-deficient pigs. The unsaturation index was essentially maintained by high levels of oleic acid (18:1n-9) and by conversion of oleic acid to 5,8,11-eicosatrienoic acid (20:3n-9). Finally, during the period of EFA deficiency, the lipid composition of BPM of the intestinal mucosal cells was little affected, suggesting a preferential uptake of 20:4n-6 and (or) precursor mobilized from other tissues. However, an effect of dietary treatment on the function of membrane-associated proteins cannot be ruled out.

Animals↗
PubMed1989

Essential fatty acids in plasma phospholipids in schizophrenics.

Blood samples were taken from schizophrenics and control patients in three different centers. The phospholipids were extracted from plasma and their fatty acid composition analyzed. Similar and consistent differences between schizophrenics and controls were observed at all three centers. The n-6 essential fatty acid levels were significantly reduced, whereas n-3 essential fatty acids were elevated.

Adult↗
PubMed1985

Vitamin E, vitamin A and essential fatty acid status of patients hospitalized for anorexia nervosa.

A group of 17 patients hospitalized for anorexia nervosa was assessed for nutritional status with respect to the essential fatty acids and vitamins E and A. Plasma aliquots available from blood drawn upon hospital admission were frozen and later extracted for total lipids. The total lipids were then fractionated by thin layer chromatography to isolate the phospholipids (PL). The fatty acid profile of both total plasma and PLs was determined by gas chromatography. High pressure liquid chromatography was used to quantitate the tocopherol isomers and retinol (vitamins E and A, respectively). The anorexic patients showed below normal weight-for-height, decreased percent body fat, and a high incidence of secondary amenorrhea. Of the four tocopherol isomers measured, only the beta + gamma fraction was significantly lower than the normal value (0.16 +/- .06 mg/dl vs 0.25 +/- 0.51 mg/dl, p less than .001). The essential fatty acids, linoleate and linolenate, were lower in the PL fraction of the anorexic group (linoleate, 19.35 +/- 5.65 vs 24.96 +/- 2.24, p less than .01); linolenate, none detected vs 0.16 +/- 0.13, p less than .05). Other indicators of essential fatty acid status differed from the normal group in the direction of deficiency (total omega 6, 31.44 +/- 7.41 vs 37.42 +/- 3.40, p less than .05; 20:4 omega 6/18:2 omega 6, 0.49 +/- 0.14 vs 40 +/- 0.02, mean +/- standard deviation, p less than .01). Eicosatrienoic acid, however, was not detected in either group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adipose Tissue↗
PubMed1989

Effect on renal function of essential fatty acid supplementation in cystic fibrosis.

Changes in renal hemodynamics, sodium homeostasis, renal acidifying capacity, and aldosterone excretion were studied before and after long-term intravenous essential fatty acid supplementation for a period of 3 years in 11 patients with cystic fibrosis. The mean (+/- SD) glomerular filtration rate was high at the start of the study (133 +/- 18 ml/min/1.73 m2 body surface area) and decreased significantly (p less than 0.05) to within normal values after 1 year of essential fatty acid supplementation. The urinary elimination of an oral sodium load initially was very low (3.6 +/- 2.5 mmol/hr/1.73 m2 body surface area vs control subjects' values of 7.9 +/- 2.0; p less than 0.001) and increased during treatment but was not normalized (p less than 0.05 vs control subjects' values). Free water clearance and distal tubular sodium delivery, which were significantly decreased before treatment (p less than 0.01 and p less than 0.001 vs control subjects' values, respectively) did not increase significantly. The mean urinary aldosterone excretion did not significantly differ from that in control subjects before and after treatment. The acidifying capacity was disturbed, indicating a low renal bicarbonate threshold, and was changed during treatment in only 2 of 10 patients. These data indicate that essential fatty acid deficiency may contribute to the renal disturbances in cystic fibrosis.

Acid-Base Equilibrium↗
PubMed1980

Parenteral safflower oil emulsion (Liposyn 10%): safety and effectiveness in treating or preventing essential fatty acid deficiency in surgical patients.

The safety and effectiveness of a 10% safflower oil emulsion in treating or preventing essential fatty acid deficiency was tested in a prospective study of 15 surgical patients requiring total parenteral nutrition for two to four weeks. Three dosage regimens were evaluated including: Group I: 4% of calories as linoleate daily (five patients), Group II: 4% of calories as linoleate every other day (two patients), and Group III: 8% of calories every other day (eight patients). Patients were monitored for laboratory changes from baseline specifically in those areas where previous fat emulsions have caused serious deviations. No significant changes were noted in hematologic parameters, coagulation studies, cholesterol and triglyceride serum levels. Although there were sporadic mild deviations in liver function changes in several patients, no clinically significant adverse effects could be directly attributed to infusion of the fat emulsion. Three patients had baseline triene/tetraene ratios of 0.4 or greater, indicative of essential fatty/acid deficiency, and these ratios dropped to less than 0.4 within eight days of beginning therapy with the parenteral fat emulsion. The remaining 12 patients maintained a normal triene/tetraene ratio of less than 0.4 throughout the 28 day study period. All three dosage regimens were considered effective for treatment and prevention of essential fatty acid deficiency.

Cholesterol↗
PubMed2003

Beneficial effects of a diet rich in a mixture of n - 6/n - 3 essential fatty acids and of their metabolites on cyclosporine - nephrotoxicity.

In this study we investigated the role of a mixture of n-6/n-3 essential fatty acids, in the cyclosporine model nephrotoxicity. Administration of cyclosporine in rats decreased creatinine clearance and provoked body weight loss, but it did not induce proteinuria and did not alter the urine volume. These changes were associated with decreased urinary ratios of prostaglandin E/thromboxane B and prostaglandin I/thromboxane B excretions. Light microscopic sections showed that 100% of the animals were affected by histological tubular lesions on their kidneys. Administration of cyclosporine to animals fed for 3 months on standard chow containing a mixture of n - 6/n - 3 essential fatty acids, restored creatinine clearance, augmented urine volume and prevented body weight loss. The improvement of renal function was accompanied by increased urinary ratios of prostaglandin E/thromboxane B and prostaglandin I/thromboxane B excretions. Light microscopic sections showed that only 40% of the animals demonstrated histological tubular lesions, of minor importance, to their kidneys. Our results suggest that the metabolites of arachidonic acid can play important role in the development of cyclosporine-nephrotoxicity because they increase the levels of thromboxane A and that the enchanced synthesis of prostaglandins (E) and (I) induced by a mixture of n - 6/n - 3 essential fatty acids, could play a beneficial role in the prevention of this renal dysfunction.

6-Ketoprostaglandin F1 alpha↗