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PubMed1990

Selective removal of retinoids and palmitic acid from microsomes by fatty acid binding protein and cellular retinol binding protein.

Studies were conducted to explore the effect of mouse liver cytosolic proteins enriched in fatty acid binding protein or cellular retinol binding protein on the removal of palmitic acid and retinoids from microsomal membranes. When the soluble proteins were incubated with mouse liver microsomes containing (14C)palmitic acid or (3H)retinoids, it was observed that fatty acid binding protein removed selectively the fatty acid and retinyl ester, whereas the retinol was mainly removed by cellular retinol binding protein.

Animals↗
PubMed1986

[Screening of essential fatty acid deficiency in children. Respective value of the assay of fatty acids in total lipids and lipid fractions of the serum].

This study was carried out in metabolically stable infants aged from one to six months receiving artificial food. The lipid serum fraction presenting changes characteristic of essential fatty acid (EFA) deficiency was determined. A preliminary study (n = 13 samples) showed that analysis of total fatty acids (TFA) and of phospholipids (PL) was more discriminatory than analysis of free fatty acids (FFA), triglycerides (TG) or esterified cholesterol (EC). Comparison of TFA and PL (n = 25 samples) confirmed literature data; in particular, C18: 2 n-6 and C20: 4 n-6 decreased whereas C20: 3 n-9 increased. These changes were clearer and significantly greater (p less than 0.001) for C20: 3 n-9 and C20: 4 n-6 of the PL, but were also very significant for the TFA compared to healthy controls. The C20: n-9/C20: n-6 ratio was identical for all fractions. TFA analysis by gas-liquid chromatography is faster and less costly than analysis of lipid fractions and provides sufficient data for screening of EFA deficiency.

Chemical Fractionation↗
PubMed1986

Validity of the fatty acid composition of subcutaneous fat tissue microbiopsies as an estimate of the long-term average fatty acid composition of the diet of separate individuals.

The relationship between the fatty acid composition of subcutaneous adipose tissue and diet was estimated in 59 Dutch women aged 32-35 years. Food consumption was estimated by taking the means of nineteen 24-hour recalls administered over a period of two and a half years, August 1981-December 1983. Highly significant correlations were found between linoleic acid content of fat tissue and diet (r = 0.70) and also between the linoleic acid-to-saturated fatty acid (linoleic/S) ratio of fat tissue and diet (r = 0.62). This confirms the hypothesis that on an individual level the fatty acid composition of the adipose tissue is a valid index for the habitual dietary fatty acid composition of free-living adults. When using one 24-hour recall instead of the average of 19 recalls, the correlation coefficient between the linoleic/S ratio of the diet and that of the adipose tissue was substantially decreased. This demonstrates the weakening effect of the large day-to-day variation in within-person intake on the correlation between a short-term assessment of the nutrient intake of an individual and a biochemical indicator of long-term nutritional status.

Adipose Tissue↗
PubMed1998

Fatty acid profile and physical properties of milk fat from cows fed calcium salts of fatty acids with varying unsaturation.

Holstein cows (n = 24) averaging 42 d in milk were used in a randomized complete block design during a 4-wk trial. A control total mixed ration (TMR) was compared with TMR supplemented with Ca salts of fatty acids from canola oil, soybean oil, or linseed oil. The three vegetable oils were progressively more unsaturated; the dominant fatty acids were, respectively, cis-delta-9-C18:1, C18:2, and C18:3. Apparent total tract digestibility of dry matter, crude protein, ether extract, and neutral detergent fiber was higher for rations containing Ca salts than for the control ration. Milk yield increased linearly as the unsaturation of the dominant fatty acid in the Ca salts increased. Milk fat percentage was reduced when Ca salts were added to the rations. The addition of Ca salts to the ration decreased the proportions of saturated fatty acids that contained C6 to C16 and increased the proportions of C18:0, cis-delta-C18:1, and trans-delta-11-C18:1 in milk fat. Proportions of C18:2 and C18:3 increased linearly, and cis-delta-9-C18:1 decreased linearly, as the unsaturation of the dominant fatty acid in the Ca salts increased. The proportion of fat that was liquid at 5 degrees C was higher for butter from cows fed diets containing Ca salts, but the proportion of liquid fat at 20 degrees C was not affected. Calcium salts of unsaturated fatty acids added to the diets of dairy cows improved the thermal properties of milk fat.

Animals↗
PubMed2005

Anandamide metabolism by Tetrahymena pyriformis in vitro. Characterization and identification of a 66 kDa fatty acid amidohydrolase.

Fatty acid amidohydrolase, a membrane-bound enzyme found in a variety of mammalian cells, is responsible for the catabolism of neuromodulatory fatty acid amides, including anandamide. In an earlier study we reported that Tetrahymena pyriformis was able to secrete a FAAH-like activity in starvation medium (Karava V., Fasia L., Siafaka-Kapadai A., FEBS Lett. 508 (2001) 327-331). In this study the endocannabinoid anandamide, was found to be metabolized by T. pyriformis homogenate by the action of a FAAH-like enzyme, in a time- and concentration-dependent manner. The main metabolic products of [3H]anandamide hydrolysis were [3H]arachidonic acid and ethanolamine. Amidohydrolase activity was maximal at pH 9-10, it was inhibited by phenylmethylsulfonyl fluoride and arachidonyltrifluoromethyl ketone and was Ca2+ and Mg(2+)-independent. Kinetic experiments demonstrated that the enzyme had an apparent K(m) of 2.5 microM and V(max) of 20.6 nmol/min mg. Subcellular fractionation of T. pyriformis homogenate showed that the activity was present in every subcellular fraction with highest specific activity in the microsomal as well as in non-microsomal membrane fraction. Immunoblot analysis of selected subcellular fractions, using an anti-FAAH polyclonal antibody, revealed the presence of an immunoreactive protein with a molecular mass approximately 66 kDa similar to the molecular mass of the mammalian enzyme. In conclusion, this study demonstrates that a FAAH similar to the mammalian enzyme is present in a unicellular eukaryote, indicating the importance of FAAH activity throughout evolution. It also supports the notion that Tetrahymena species may be a suitable model for metabolic studies on endocannabinoids, as well as for the study of drugs targeted towards FAAH.

Amidohydrolases↗
PubMed1992

Binding of bile acids, organic anions, and fatty acids by bovine intestinal Z protein.

Z protein from bovine small intestinal mucosa was purified and its binding affinities for bile acids, organic anions, and fatty acids were compared with those of bovine hepatic Z protein. Purification of Z protein from intestinal and hepatic cytosol was performed by gel filtration, chromatofocusing, and hydroxyapatite chromatography. Both purified proteins had the same molecular weight (Mr 14,000) and eluted from a chromatofocused gel at about pH 10. Binding studies were performed by the competitive displacement of 8-anilinonaphthalene-1-sulfonic acid and by equilibrium dialysis. Binding affinities for bile acids, organic anions, and fatty acids were very similar between intestinal and hepatic Z proteins. Although the real physiologic role of Z protein remains to be further elucidated, these data indicate that intestinal Z protein participates in the mechanism of intracellular bile acid transfer in enterocytes.

Animals↗
PubMedDate not supplied

Preparation of functional group analogs of unsaturated fatty acids and their effects on the circadian rhythm of a fatty-acid-deficient mutant of Neurospora crassa.

Functional group analogs of oleic, linoleic and linolenic acids were prepared by coverting their double bonds to dibromo, cyclopropyl, epoxy, methoxy, and, in the case of oleic acid, hydroxy groups. These compounds were supplemented to the bd csp cel strain of the mold Neurospora crassa. The cel mutation confers a partial requirement for saturated fatty acids and, also, perturbs the circadian rhythm of spore formation. For example, the period of bd csp cel's rhythm is dramatically lengthened upon supplementation by natural cis-unsaturated fatty acids. Of the analogs tested, only the monoepoxy, monomethoxy, dibromo, and hexabromo stearic acids gave significant period lengthening. Other analogs, which should have comparable abilities to disrupt lipid bilayer packing, gave no rhythm effect. Further, the inactive di- and tri-methoxystearic acid analogs were incorporated to a greater extent than the active mono-methoxystearic acid. The results do not, therefore, support a direct alteration in membrane "fluidity' as the mode of action of the period-lengthening fatty acids.

Chemical Phenomena↗
PubMed1998

Effect of dietary n-3 fatty acids on hypoxia-induced necrotizing enterocolitis in young mice. n-3 fatty acids alter platelet-activating factor and leukotriene B4 production in the intestine.

Necrotizing entercolitis (NEC) is an important neonatal disease with a high mortality rate. Inflammatory mediators, such as mainly platelet-activating factor (PAF), leukotrienes (LT) and tumor necrosis factor play an important role in the genesis of NEC. Diets in omega-3 (n-3) fatty acids appear to have an antiinflammatory effect, which is thought to be due to decreased active prostaglandins and leukotrienes production after incorporation of these fatty acids into cell membrane phospholipids. We investigated the protective effect of fish oil (source of n-3 fatty acids) on hypoxia-induced model of NEC. Young mice were divided into three groups; group 1 mice were fed standard chow (n-3 fatty acids-free), group 2 was fed a chow supplemented by 10% fish oil for 4 weeks. Group 3 mice served as control. We examined the intestinal lesions by light microscopy and measured intestinal tissue PAF and LB4 levels in hypoxia-induced model of NEC. Significantly increased intestinal PAF and LTB4 levels were found in group 1 mice when compared to group 2 and group 3 mice. The histopathology of the intestinal lesions in group 1 animals was characteristic of ischemic injury. In the n-3 fatty acids-supplemented animals these lesions were milder. The present study shows that endogenously released PAF and LTB4 play an important role in mediating hypoxia-induced intestinal necrosis. The present study also suggests that dietary supplementation with n-3 fatty acids suppress intestinal PAF and LTB4 generation in hypoxia-induced bowel necrosis. The intestinal protective effect of n-3 fatty acids in an experimental model of NEC may open new insight into the treatment and prevention of NEC in neonates.

Animals↗
PubMed1987

Peroxisomal fatty acid beta-oxidation in relation to the accumulation of very long chain fatty acids in cultured skin fibroblasts from patients with Zellweger syndrome and other peroxisomal disorders.

The peroxisomal oxidation of the long chain fatty acid palmitate (C16:0) and the very long chain fatty acids lignocerate (C24:0) and cerotate (C26:0) was studied in freshly prepared homogenates of cultured skin fibroblasts from control individuals and patients with peroxisomal disorders. The peroxisomal oxidation of the fatty acids is almost completely dependent on the addition of ATP, coenzyme A (CoA), Mg2+ and NAD+. However, the dependency of the oxidation of palmitate on the concentration of the cofactors differs markedly from that of the oxidation of lignocerate and cerotate. The peroxisomal oxidation of all three fatty acid substrates is markedly deficient in fibroblasts from patients with the Zellweger syndrome, the neonatal form of adrenoleukodystrophy and the infantile form of Refsum disease, in accordance with the deficiency of peroxisomes in these patients. In fibroblasts from patients with X-linked adrenoleukodystrophy the peroxisomal oxidation of lignocerate and cerotate is impaired, but not that of palmitate. Competition experiments indicate that in fibroblasts, as in rat liver, distinct enzyme systems are responsible for the oxidation of palmitate on the one hand and lignocerate and cerotate on the other hand. Fractionation studies indicate that in rat liver activation of cerotate and lignocerate to cerotoyl-CoA and lignoceroyl-CoA, respectively, occurs in two subcellular fractions, the endoplasmic reticulum and the peroxisomes but not in the mitochondria. In homogenates of fibroblasts from patients lacking peroxisomes there is a small (25%) but significant deficiency of the ability to activate very long chain fatty acids. This deficient activity of very long chain fatty acyl-CoA synthetase is also observed in fibroblast homogenates from patients with X-linked adrenoleukodystrophy. We conclude that X-linked adrenoleukodystrophy is caused by a deficiency of peroxisomal very long chain fatty acyl-CoA synthetase.

Facial Bones↗
PubMed2007

Dietary trans 10, cis 12-conjugated linoleic acid reduces the expression of fatty acid oxidation and drug detoxification enzymes in mouse liver.

Mice fed diets containing trans 10, cis 12 (t10, c12)-conjugated linoleic acid (CLA) develop fatty livers and the role of the hepatic fatty acid oxidation enzymes in this development is not well defined. We examined the effects of dietary cis 9, trans 11-CLA (c9, t11-CLA) and t10, c12-CLA on the expression of hepatic genes for fatty acid metabolism. Female mice, 8 weeks old, (six animals per group) were fed either a control diet or diets supplemented with 0.5% c9, t11- or c12-CLA for 8 weeks. DNA microarray analysis showed that t10, c12-CLA increased the expression of 278 hepatic genes and decreased those of 121 genes (>2 fold); c9, t11-CLA increased expression of twenty-two genes and decreased those of nine. Real-time PCR confirmed that t10, c12-CLA reduced by the expression of fatty acid oxidation genes including flavin monooxygenase (FMO)-3 95%, cytochrome P450 (cyt p450) 69%, carnitine palmitoyl transferase 1a 77%, acetyl CoA oxidase (ACOX) 50% and PPARalpha 65%: it increased the expression of fatty acid synthase by 3.5-fold (P<0.05 for all genes, except ACOX P=0.08). It also reduced the enzymatic activity of hepatic microsomal FMO by 40% and the FMO3 specific protein by 67%. c9, t11-CLA reduced FMO3 and cyt P450 expression by 61% (P=0.001) and 38% (P=0.06) and increased steoryl CoA desaturase transcription by 5.9-fold (P=0.07). Both decreased fatty acid oxidation and increased fatty acid synthesis seem to contribute to the CLA-induced fatty liver. Since FMO and cyt P450 are also involved in drug detoxification, suppression of the transcription of these genes by CLA may have other health consequences besides development of fatty liver.

Animal Feed↗
PubMed2001

Two-site ELISA for the quantitative determination of fatty acid synthase.

Fatty acid synthase (FAS) is an enzyme which plays a central role in the de novo biosynthesis of fatty acids. FAS is selectively expressed in certain human cancers and therefore is a putative tumor marker. We developed an enzyme-linked immunosorbent assay (ELISA) for measuring FAS, and investigated its expression and clinical features. In this two-site sandwich ELISA, a polyclonal antibody was used as a capture on Nunc MaxiSorp ELISA/EIA modules and a monoclonal antibody labeled with biotin was used as a signal antibody. The assay was linear with no cross-reactivity with other tumor markers. The within- and between-run CVs were <10%, and the detection limit was 0.15 arbitrary Units/l. Recoveries were 92.4-105.1%. FAS was stable in buffer at 4 degrees C for more than 10 days and stable at 37 degrees C for 2 days. In human serum, FAS levels were significantly higher in patients with breast (1.01+/-0.71 Units/l, mean+/-S.D.), prostate (0.79+/-0.76 Units/l), colon (0.89+/-0.49 Units/l), and ovarian (0.84+/-0.9 Units/l) cancers compared to normal subjects (0.27+/-0.09 Units/l, P<0.01). This assay is sensitive, accurate, and precise and can distinguish between patients with various types of cancer and normal subjects.

Adult↗
PubMed2003

Adipose tissue n-6 fatty acids and acute myocardial infarction in a population consuming a diet high in polyunsaturated fatty acids.

BACKGROUND: The Jewish population of Israel consumes a diet rich in n-6 polyunsaturated fatty acids (PUFAs), principally linoleic acid. The consequences of this diet for ischemic heart disease (IHD) remain unclear. OBJECTIVE: We assessed the association of adipose tissue n-6 fatty acids, which are derived entirely from the diet, with acute myocardial infarction (AMI). DESIGN: A total of 180 cases and 492 IHD-free controls aged 25-64 were included in a population-based case-control study of Jerusalem residents hospitalized with a first AMI. Diet was assessed by the use of a food-frequency questionnaire and adipose tissue fatty acids by gas chromatography of biopsy samples taken from subcutaneous gluteal tissue. The data were analyzed by multivariate logistic regression. RESULTS: Dietary PUFAs (: 10.1% of energy) correlated (r = 0.43, P < 0.001) with adipose tissue linoleic acid, which constituted 25.6% of storage fatty acids. High intakes of linoleic acid were not associated with excess risk of AMI (age- and sex-adjusted odds ratio for the third versus the first tertile: 0.96; 95% CI: 0.62, 1.48; NS). In contrast, arachidonic acid, the long chain n-6 derivative of linoleic acid, was positively associated with AMI (age- and sex-adjusted odds ratio: 2.12; 95% CI: 1.33, 3.36; P = 0.004). With multivariate adjustment, there was no evidence for an adverse association of linoleic acid with AMI, whereas the risk associated with arachidonic acid persisted, albeit attenuated. CONCLUSIONS: A very high linoleic acid intake does not appear to confer increased risk of nonfatal AMI. Nonetheless, the increased risk associated with arachidonic acid, a finding that requires confirmation, tempers an inference that diets rich in n-6 fatty acids are safe vis-à-vis coronary health.

Adipose Tissue↗
PubMed1996

A high cholesterol, (n-3) polyunsaturated fatty acid diet induces hypercholesterolemia more than a high cholesterol (n-6) polyunsaturated fatty acid diet in hamsters.

This study was designed to study the effects of (n-3) polyunsaturated fatty acids (PUFA) on plasma and liver lipids, particularly lipoprotein cholesterol concentrations, in hamsters. Diets rich in (n-3) PUFA (21 g/100 g fatty acid) or (n-6) PUFA (37.4 g/ 100 g fatty acid) with or without 5 g/kg cholesterol (C) supplements were given for 4 wk to male hamsters weighing 70-90 g. The VLDL- and (IDL + LDL)-cholesterol concentrations were 114 and 128% higher in hamsters fed the (n-3) PUFA + C diet than in those fed the (n-6) PUFA + C diet. However, these differences were not observed when cholesterol was not supplemented. Hamsters fed the (n-3) PUFA diet had significantly lower plasma and hepatic triglyceride concentrations than those fed the (n-6) PUFA diet. Concentrations were comparable in hamsters fed (n-6) PUFA + C and (n-3) PUFA + C. Hepatic cholesteryl esters were significantly lower, while hepatic microsomal acyl-CoA:cholesterol acyltransferase activity and VLDL cholesteryl esters were significantly higher in hamsters fed the (n-3) PUFA + C diet than in those fed the (n-6) PUFA + C diet. Our results demonstrate that elevation of VLDL- and (IDL + LDL)-cholesterol in hamsters by (n-3) PUFA, compared with (n-6) PUFA, is dependent on dietary cholesterol supplementation and may be due to decreased catabolism of these lipoproteins.

Acetyl-CoA C-Acyltransferase↗
PubMed1991

Effects of high erucic acid rapeseed oil on fatty acid oxidation in rat liver.

The effects of high erucic acid rapeseed oil (HER) on fatty acid oxidation in rat liver compared with low erucic acid rapeseed oil (LER) were studied. Weanling male SD rats were fed diets containing 20% HER or LER for 1 week or 4 weeks, or 5% HER diet for 4 weeks. The hepatic oxidation capacity of butyric acid or palmitic acid was determined by titrating the propanone produced by their oxidation. The results showed that feeding HER to rats led to an increase in the weight of liver and a decrease in the hepatic oxidation capacity of palmitic acid. Hepatic oxidation of butyric acid was not influenced by the intake of HER. The inhibitory action of HER on the oxidation of long-chain fatty acids probably resulted from the incorporation of erucic acid into mitochondrial membranes, interfering the fatty acyl-CoA transferring system on the membranes, but not from the beta-oxidation enzyme system in mitochondria being directly inhibited.

Animals↗
PubMed1990

Regulation of fatty acid oxidation and triglyceride and phospholipid metabolism by hypolipidemic sulfur-substituted fatty acid analogues.

The mechanisms behind the hypotriglyceridemic effect of 1,10-bis(carboxymethylthio)decane (3-thiadicarboxylic acid) and tetradecylthioacetic acid and the development of fatty liver caused by 3-tetradecylthiopropionic acid (Aarsland et al. 1989. J. Lipid Res. 30: 1711-1718.) were studied in the rat. Repeated administration of S-substituted non-beta-oxidizable fatty acid analogues to normolipidemic rats resulted in a time-dependent decrease in plasma triglycerides, phospholipids, and free fatty acids. This was accompanied by an acute reduction in the liver content of triglycerides and an increase in the hepatic concentration of phospholipids. Mitochondrial fatty acid oxidation was stimulated, whereas lipogenesis was inhibited. The activity of phosphatidate phosphohydrolase decreased while the activity of CTP:phosphocholine cytidylyltransferase increased. These results suggest that the observed triglyceride-lowering effect was due to increased mitochondrial fatty acid oxidation accompanied by a reduction in the availability of the substrate i.e., free fatty acid, along with an enzymatic inhibition (phosphatidate phosphohydrolase). Administration of 3-tetradecylthiopropionic acid led to a drastic increase in the hepatic triglyceride content. Levels of plasma triglyceride phospholipid and free fatty acid also increased. Phosphatidate phosphohydrolase activity was stimulated whereas CTP:phosphocholine cytidylyltransferase was inhibited. Mitochondrial fatty acid oxidation was decreased. These data indicate that the development of fatty liver as an effect of 3-tetradecylpropionic acid is probably due to accelerated triglyceride biosynthesis, which is mediated by an increase in the availability of fatty acid along with stimulation of phosphatidate phosphohydrolase. The results of the present study speak strongly in favor of the hypothesis that phosphatidate phosphohydrolase is a major rate-limiting enzyme in triglyceride biosynthesis. Furthermore, they point out that the biosynthesis of triglycerides and phospholipids might be coordinately regulated. Such regulation is possibly mediated via phosphatidate phosphohydrolase and CTP:phosphocholine cytidylyltransferase. Whether the increase in hepatic phospholipids via increased CDP-pathway accounts for an increase of lipid components for proliferation of peroxisomes (3-thiadicarboxylic acid and tetradecylacetic acid) should be considered.

Animals↗