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PubMed2002

Exercise and insulin increase muscle fatty acid uptake by recruiting putative fatty acid transporters to the sarcolemma.

PURPOSE OF REVIEW: Skeletal muscle metabolic energy, needed to maintain contractile activity, is mainly obtained from glucose and long-chain fatty acids. Recent studies have revealed a remarkable parallel between the regulation of uptake of glucose and fatty acids by muscle, in that each is mediated by sarcolemmal transporters that are recruited from an intracellular storage site. The focus of this review is to describe newly obtained insights on the recruitment of fatty acid transporters and their malfunctioning in diabetes. RECENT FINDINGS: The major fatty acid transporter involved is fatty acid translocase (CD36). Translocation of this protein to the membrane is triggered by muscle contraction and by insulin, and presumably occurs from distinct intracellular pools. This resembles the well documented exercise and insulin-induced recruitment of glucose transporter-4. Whether another transporter, plasma membrane fatty acid-binding protein, is also subject to such recycling is not yet clear. In a rodent model of insulin-dependent (type 1) diabetes, the increased rate of muscle fatty acid uptake could be associated with an increased total amount of fatty acid translocase (CD36). In a model of non-insulin dependent (type 2) diabetes, this increased rate could be associated with a permanent relocalization of fatty acid translocase to the sarcolemma. SUMMARY: These findings indicate a pivotal role for the membrane transporter fatty acid translocase in the exercise and insulin-induced increases of muscle fatty acid uptake and utilization, and suggest that malfunctioning of the cellular recycling of fatty acid translocase is involved in the etiology of insulin resistance and type 2 diabetes.

Animals↗
PubMed1998

The effect of arachidonic acid and free fatty acids on vesicular uptake of glutamate and gamma-aminobutyric acid.

The manner in which arachidonic acid and other free fatty acids influence the vesicular uptake of glutamate and gamma-aminobutyric acid (GABA) has been investigated. The cis-polyunsaturated fatty acid arachidonic acid (20:4), eicosapentanoic acid (20:5) and linolenic acid (18:3) at 150 nmol/mg protein (50 microM) inhibited the vesicular uptake of glutamate and GABA more than 70%. Reduced inhibition of vesicular uptake was seen with the cis-monounsaturated fatty acid oleic acid (18:1) and the trans-mono-unsaturated fatty acid elaidic acid (18:1). The saturated fatty acids stearic acid (16:0) and arachidic acid (20:0) had no significant effect on the uptake. The inhibition of vesicular uptake by arachidonic acid was prevented by the addition of fatty acid free bovine serum albumin. Arachidonic acid inhibited in a dose-dependent manner the generation of the transmembrane pH gradient of the synaptic vesicles. This inhibition was proportional to the inhibition of the vesicular uptake of glutamate and GABA. The saturated fatty acid arachidic acid showed no inhibition of delta pH generation. Arachidonic acid at 200 nmol/mg of protein did not increase the uptake-independent leakage of glutamate and GABA from the vesicles, showing that the effect of arachidonic acid is not caused by an unspecific detergent effect. These results suggest that arachidonic acid and other polyunsaturated fatty acids are acting like proton-ionophores on the vesicular uptake of these neurotransmitters. This finding may have implications for the increased fatty acid concentration during pathological conditions like ischemia and in long term potentiation.

Animals↗
PubMed1993

[Dietary effect of omega-3 polyunsaturated fatty acid supplementation on blood fatty acids, lipid and lipoproteins in patients with ischemic heart disease].

Seventeen patients with a more than 5-month-history of angina pectoris were allocated a diet for 4 weeks. The diet was supplemented with 6.15 g of omega 3-polyunsaturated fatty acids (PUFA) in 125 g canned Far-Eastern sardine. This increased the proportion of eicosapentaenic (EPA) and docosahexaenic acids from 1.28 +/- 0.72 to 9.02 +/- 2.83% and from 2.48 +/- 0.91 to 6.54 +/- 2.01%, respectively; p = 0.0003) in the total serum lipid fraction. The levels of omega 6-PUFA decreased due to linoleic acid (from 24.9 +/- 3.9 to 19.7 +/- 5.2%, p = 0.0014). The EPA/arachidonic acid ratio rose from 0.23 +/- 0.11 to 1.76 +/- 0.58 (p < 0.001). The levels of triglycerides decreased by 36.4% (from 162.3 +/- 55.2 to 103.9 +/- 42.4 mg/dl; p < 0.0005); those of very low density lipoproteins and total cholesterol by 36 and 6.8%, respectively (from 32.5 +/- 11.0 to 20.8 +/- 8.5 mg/dl; p < 0.0005 and from 234.8 +/- 43.2 to 218.4 +/- 39.7 mg/dl; p < 0.05, respectively). The concentrations of high density lipoproteins remained unchanged. Thus, a short-term supplementation of canned Far-Eastern sardine to the diet of patients with CHD caused a substantial changes in blood fatty acid composition and favourable shifts in the levels of lipids and lipoproteins. This allows the Far-Eastern sardine to be regarded as a valuable source of omega 3-PUFA which can be used in the secondary prevention of coronary heart disease.

Adult↗
PubMed1993

Dietary saturated, monounsaturated, n-6 and n-3 fatty acids, and cholesterol influence platelet fatty acids in the exclusively formula-fed piglet.

Platelet lipid composition is important to normal platelet morphology and function, and is influenced by dietary fatty acids and cholesterol. The fatty acid composition and cholesterol content of infant formulas differs from those of human milk, but the possible effects on platelet lipids in young infants is not known. This was studied in piglets fed from birth to 18 d of age with one of eight formulas differing in saturated fatty acid chain length, or content of 18:1, 20:5n-3 plus 22:6n-3, or cholesterol. A reference group of piglets fed sow milk was also studied. Sow milk has a fatty acid composition and cholesterol content similar to that of human milk. Piglets fed formulas high in 18:1 (34.9-40.8% wt fatty acids) and low in 16.0 (< or = 6.5% wt fatty acids) had lower platelet counts and greater platelet size than piglets fed sow milk (40.4% 18:1, 30.7% 16:0). Piglets fed formulas high in 16:0 (27-29.6%) and 18:1 (40-40.6%), or low in both 16:0 (5.9-6.1%) and 18:1 (10.8-11.2%), had similar platelet counts and size to piglets fed sow milk. Platelet phospholipid % 20:4n-6 was lower in all the groups of piglets fed formula than in the group fed sow milk. Addition of fish oil with 20:5n-3 plus 22:6n-3 to the formula further decreased platelet phospholipid 20:4n-6. Addition of cholesterol to the formula increased the platelet phospholipid % 20:4n-6 and platelet volume.

Animals↗
PubMed1997

Evaluation of carbon-11-labelled phenoxy bridged fatty acids for studying myocardial fatty acid metabolism with PET.

A phenylene moiety in the chain of fatty acids was expected to impair metabolic degradation. Three phenoxy-containing [11C]carboxyl-labelled fatty acids were synthesized and evaluated in mice and an in vivo tissue distribution study. Of these three, 1[11C]-3-(p-dodecyloxyphenyl)propionic acid (C12C3) showed the most favourable uptake in the myocardium: 1.2% of the injected dose at 30 min p.i., vs. 0.6% for [11C]palmitate. The metabolic stability of C12C3 and [11C]palmitate was assessed by determining the amount of exhaled [11C]CO2 during a 30-min interval after injection. It was found that the phenoxy moiety in the gamma-position did not prevent the metabolic degradation of C12C3: After 30 min 20.7% of the injected dose was exhaled as [11C]CO2 vs. 12.7% for [11C]palmitate.

Animals↗
PubMed2000

Keloids in rural black South Africans. Part 2: dietary fatty acid intake and total phospholipid fatty acid profile in the blood of keloid patients.

In the second part of this study, emphasis is placed on nutritional intakes (fatty acids and micronutrients) and fatty acid intake and metabolism in the blood, respectively, according to a combined 24 h recall and standardized food frequency questionnaire analyses of keloid prone patients (n=10), compared with normal black South Africans (n=80), and total phospholipid blood (plasma and red blood cell ) analyses of keloid patients (n=20), compared with normal individuals (n=20). Lipid extraction and fractionation by standard procedures, total phospholipid (TPL) separation with thin layer chromatography, and fatty acid methyl ester analyses with gas liquid chromatography techniques were used. Since nutrition may play a role in several disease disorders, the purpose of this study was to confirm or refute a role for essential fatty acids (EFAs) in the hypothesis of keloid formations stated in part 1 of this study. (1)According to the Canadian recommendation (1991), we observed that in keloid patients linoleic acid (LA) and arachidonic acid (AA) dietary intakes, as EFAs of the omega-6-series, are higher than the recommended 7-11 g/d. However, the a-linolenic acid (ALA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) dietary intakes, as EFAs of the omega-3 series, are lower than the recommendation of 1.1-1.5 g/d. This was also the case in the control group, where a higher dietary intake of the omega-6 fatty acids and a slightly lower dietary intake of the omega-3 fatty acids occurred. Thus, we confirm a high dietary intake of LA (as a product of organ meats, diary products and many vegetable oils) and AA (as a product of meats and egg yolks), as well as lower dietary intakes of ALA (as a product of grains, green leafy vegetables, soy oil, rapeseed oil and linseed), and EPA and DHA (as products of marine oils). Lower micronutrient intakes than the recommended dietary allowances were observed in the keloid group that may influence EFA metabolism and/or collagen synthesis. Of cardinal importance may be the lower intake of calcium in the keloid patients that may contribute to abnormal cell signal transduction in fibroblasts and consequent collagen overproduction, and the lower copper intake that may influence the immune system, or perhaps even the high magnesium intake that stimulates metabolic activity. Micronutrient deficiencies also occurred in the diets of the normal black South Africans that served as a control group. In the case of plasma TPLs, deficiency of the omega-3 EFA series (ALA, EPA and DHA) occurred, and this is in accordance with the apparent lower omega-3 EFA intake in the diets of these patients. In the case of the red blood cell TPLs, as a true and reliable source of dietary fatty acid intake and metabolism, sufficient EFAs of the omega-6 series (LA and AA) and the omega-3 series (ALA, EPA and DHA) occurred. For this study group a relative deficiency of nutritional omega-3 EFA intake apparently did occur, but was probably compensated for by blood fatty acid metabolism.

Adolescent↗
PubMed1997

Fatty acid regulation of fatty acid-binding protein expression in the small intestine.

The effects of dietary oil intake and fatty acid infusions on the expression of intestinal and liver fatty acid-binding proteins (I-FABP and L-FABP, respectively) were investigated in the small intestine of mice. A daily force-feeding for 7 days with 0.2 ml sunflower oil specifically increased L-FABP mRNA and protein levels in duodenum and proximal jejunum. This upregulation was mediated in time- and dose-dependent manners by a minute quantity of linoleic acid, the main fatty acid found in sunflower oil. The L-FABP induction was only found with long-chain fatty acids, with the nonmetabolizable, substituted fatty acid alpha-bromopalmitate being far more active. A hormonally mediated effect is unlikely because long-chain fatty acids induced L-FABP mRNA in the Caco-2 cell line cultured in serum-free medium. Therefore, long-chain fatty acids are strong inducers of L-FABP gene expression in the small intestine. In contrast to data found in the rat, I-FABP gene expression appears to be unaffected by a lipid-enriched diet in the mouse.

Animals↗
PubMed1998

Induction of apoptosis by polyunsaturated fatty acids and its relationship to fatty acid inhibition of carnitine palmitoyltransferase I activity in Hep2 cells.

The effects of fatty acids on the induction of apoptosis were studied over a 24 hour period in Hep2 human larynx tumour cells. While oleic and linoleic acids had little effect on the apoptotic index, the polyunsaturated fatty acids alpha-linolenic, gamma-linolenic, arachidonic, eicosapentaenoic and docosahexaenoic acids all induced apoptosis, beginning at approximately 6 hours after fatty acid exposure. By 24 hours after exposure, the apoptotic index had reached as much as 19% in the presence of docosahexaenoic or alpha-linolenic acid. The correlation between degree of unsaturation of the 18-carbon fatty acids and the apoptotic index was r2 = 0.45, 0.89, 0.84 and 0.98 at 6, 8, 12 and 24 hours, respectively. The correlation between mitochondrial carnitine palmitoyltransferase I (CPT I) activity, 6 hours after exposure, and the apoptotic index was r2 = 0.842 and 0.798 at 12 and 24 hours, respectively. The inhibition of CPT I and subsequent fatty acid oxidation by polyunsaturated fatty acids leads to a significant increase in apoptosis, suggesting that CPT I may be involved in the processes of programmed cell death in Hep2 human tumour cells.

Apoptosis↗
PubMed2006

Candida albicans Spt23p controls the expression of the Ole1p Delta9 fatty acid desaturase and regulates unsaturated fatty acid biosynthesis.

In Saccharomyces cerevisiae the endoplasmic reticulum membrane proteins scSpt23p and scMga2p control the formation of unsaturated fatty acids by a mechanism that involves their release from the membrane by ubiquitin-mediated proteolysis. The resulting soluble polypeptides act as transcription activators that specifically control the expression of scOLE1, a gene that encodes scOle1p, a Delta9 fatty acid desaturase that forms cis-monounsaturated fatty acids (9Z-16:1 and 9Z-18:1) from saturated fatty acyl-CoA precursors. ScOle1p is the only long chain fatty acid desaturase in Saccharomyces and its membrane and storage lipids contain only saturated fatty acids and the monounsaturated products of that enzyme. Most other fungi, however, express multiple endoplasmic reticulum desaturases, including enzymes that form both mono- and polyunsaturated fatty acids. These typically include Delta12 and Delta15 enzymes that form the polyunsaturated species, 9Z,12Z-18:2, and 9Z,12Z,15Z-18:3, which are the most abundant fatty acids in membrane and storage lipids. An analysis of genomic DNA sequences shows that Candida albicans has a single homologue of the Saccharomyces scSPT23 and scMGA2 genes that we designate here as caSPT23. This study describes the characterization of the caSPT23 gene product and shows that it can repair the unsaturated fatty acid auxotrophy when it is expressed in a Saccharomyces scspt23Delta;scmga2Delta strain. In addition we show caSPT23 is essential for the expression of one of the two Delta9 desaturase homologues in Candida and potentially other functions associated with fatty acid metabolism.

Amino Acid Sequence↗
PubMed1987

Alpha-linolenic acid deficiency in man: effect of essential fatty acids on fatty acid composition.

Alpha-linolenic acid deficiency (ALAD) is described in five adults receiving long-term gastric tube feeding with a commercially available powdered formula mixed with water and/or skimmed milk. Three patients receiving the same powder mixed with whole milk showed no signs of essential fatty acid deficiency (EFAD). The patients showed scaly dermatitis and skin atrophy. In four patients, supplementing with cod liver oil and soya oil for 4 weeks normalized n-3 acids in plasma and red cells, while n-6 acids remained unchanged or decreased slightly. At the same time, skin changes were normalized. In the fifth patient, supplementing with ethyl linolenate started to normalize skin changes within 5 days, and after 2 weeks had increased the red cell concentration of 22:6n-3 threefold. Simultaneously, 20:4n-6 increased twofold, to above control level. Minimal daily requirement of alpha-linolenic acid and of long-chain n-3 acids is estimated to be 0.2% to 0.4% and 0.1% to 0.2% of calories, respectively.

Adult↗
PubMed1980

Incorporation of hydrogen atoms from deuterated water and stereospecifically deuterium-labeled nicotin amide nucleotides into fatty acids with the Escherichia coli fatty acid synthetase system.

The mechanism of hydrogen incorporation into fatty acids was investigated with intact Escherichia coli cells, a crude enzyme preparation and purified reductases of fatty acid synthetase system. The distributions of deuterium atoms incorporated into fatty acids from 2H2O and stereospecifically deuterium-labeled NADPH or NADH were determined by mass spectrometry. When E. coli was grown in 2H2O, almost every hydrogen atom of cellular fatty acids was incorporated from the medium. When fatty acids were synthesized from acetyl-CoA, malonyl-CoA and NADPH in the presence of a crude enzyme preparation of either E. coli or Bacillus subtilis, almost every hydrogen atom was also incorporated from the medium. In contrast to these results, purified beta-ketoacyl acyl carrier reductase directly transferred the HB hydrogen of NADPH to beta-ketoacyl acyl carrier protein, and purified enoyl acyl carrier protein reductase also transferred the HB hydrogen of NADPH and NADH directly to enoyl acyl carrier protein. In the crude enzyme preparation of E. coli, we found high activities which exchanged the HB hydrogen of NADPH with the deuterium of 2h2o. the conflicting results of the origin of hydrogen atoms of fatty acids mentioned above are explained by the presence of enzymes, which catalyzed the rapid exchange of NADPH with the deterium of 2H2O prior to the reaction of fatty acid synthetase.

Deuterium↗
PubMed1980

Intrauterine fatty acid accretion rates in human brain: implications for fatty acid requirements.

Fatty acid components of infant brain were determined to assess fatty acid requirements for synthesis of structural lipids in brain tissue during the last trimester of development in the fetus. Quantitative fatty acid analysis of cerebellum, frontal and occipital brain lobes indicated rapid accretion of chain elongation and desaturation products during the last trimester of brain growth. Frontal and occipital brain lobes were similar in fatty acid content. Fatty acid accretion rates were determined by regression analysis of tissue fat components at varying gestational ages. Tissue accretion of saturated and omega-9 fatty acids, as well as total fatty acid content, paralleled increases in whole brain weight. Levels of linoleic (C18:2, omega-6) and linolenic (C18:3, omega-3) acids were consistently low in brain during the last trimester of development, while marked substantial accretion of long chain desaturation products, arachidonic (C20:4, omega-6) and docosahexaenoic (C22:6, omega-3) acids occurred. Accretion of individual fatty acids of cerebellum also reflected changes in tissue total fatty acid content, with exception of the levels of C18:3, omega-3 and its chain elongation products present in cerebellum during the last trimester. These developmental changes and estimates of fatty acid incorporation into whole brain and cerebellum are quantitatively relevant to estimation of fatty acid requirements of the low birth weight neonate.

Brain↗
PubMed1991

Gender differences in the response of hepatic fatty acids and cytosolic fatty acid-binding capacity to alcohol consumption in rats.

To investigate possible gender differences in the response of hepatic fatty acids and cytosolic fatty acid-binding capacity to ethanol consumption, both female and male rats (41 days of age) were pair fed liquid diets (with a littermate of the same sex) for 28 days. The diets contained 36% of energy either as ethanol or as additional carbohydrate. After ethanol feeding, the hepatic concentration of fatty acids increased 155% in females (P less than 0.01), whereas there was only a trend for an increase (22%) in males. This was associated with a much smaller increase of cytosolic fatty acid-binding capacity in females (58%) than in males (161%). Whereas the ethanol-induced increase in fatty acid-binding capacity provided an ample excess of binding sites for the fatty acids in males, the increase in females was barely sufficient for the binding of the large increase of fatty acids produced by ethanol in the females. The cytosolic protein responsible for this binding, the liver fatty acid-binding protein of the cytosol (L-FABPc), also promotes esterification of the fatty acids. In keeping with the postulated role of this protein, the ethanol-induced increases in hepatic triacylglycerols, phospholipids, and cholesterol esters were smaller in females than in males. The gender difference in cholesterol esters was associated with parallel changes in acyl-CoA transferase activity. A possible implication of the relatively small and most likely inadequate increase in liver fatty acid-binding capacity and fatty acid esterification during alcohol consumption in the females is that under these circumstances the risk for development of a potentially deleterious accumulation of fatty acids in the liver is increased, thereby contributing to the enhanced vulnerability of females to alcohol-induced hepatotoxicity.

Alcohol Drinking↗
PubMed1982

Fatty acid desaturation and microsomal lipid fatty acid composition in experimental hypothyroidism.

We have studied the influence of experimental hypothyroidism in the rat on the synthesis of unsaturated fatty acids and on liver microsomal lipid fatty acid composition. Hypothyroid rats demonstrated an 80% decrease in delta 9 (stearate) desaturation and a 43% decrease in delta 6 (linoleate) desaturation. Liver microsomal fatty acid composition was altered in the hypothyroid animals with a significantly decreased proportion of arachidonate and increased proportions of linoleate, eicosa-8,11,14-trienoate, eicosapentaenoate and docosahexaenoate. The bulk of these changes occurred in both of the two major phospholipid components, phosphatidylcholine and phosphatidylethanolamine. All of the changes were corrected by treatment of the hypothyroid rat with 25 micrograms of tri-iodothyronine/100 g body wt. twice daily. The diminished delta 9 desaturation did not lead to any changes in fatty acid composition. The increased linoleate and decreased arachidonate levels may be due to the diminished delta 6 desaturase activity, the rate-controlling step in the conversion of linoleate into arachidonate. The increases in the proportions of the other polyunsaturated fatty acid components cannot be explained by changes in the synthesis of unsaturated fatty acids, but are probably due to diminished utilization of these fatty acids.

Animals↗
PubMed2004

Enhanced expression of cytosolic fatty acid binding protein and fatty acid uptake during liver regeneration in rats.

BACKGROUND/AIMS: Cytoplasmic liver fatty acid binding protein (L-FABP) has been suggested to be associated with cellular mitotic activity but the changes in L-FABP mRNA and protein levels during liver regeneration following partial hepatectomy (PHx) are not clear. METHODS: In the present study, we determined the time course of L-FABP mRNA expression and L-FABP levels following 70% PHx using Northern and Western blot, respectively. To elucidate one of the roles for L-FABP in PHx, [3H]-palmitic acid clearance in hepatocytes isolated from 24 h post-PHx and control animals was assessed. RESULTS: L-FABP mRNA increased at 30 min, peaked at approximately 1 h (163 +/- 17%; mean +/- SE, n = 5), and returned to control levels 6 h post-PHx. L-FABP level also increased at 1 h but peaked at 24-h (219 +/- 41%; mean +/- SE, n = 5). Hepatocyte [3H]-palmitic acid clearance increased by 29% at 24-h post-PHx, suggesting an increased intracellular transport (or binding) function by L-FABP. Pre-treatment with dexamethasone statistically reduced L-FABP levels (29%) and suppressed the regenerative process (mitotic activity). CONCLUSIONS: L-FABP mRNA increased sharply in response to PHx but the increase was short lived, while L-FABP level increased at a later stage. Both L-FABP content and fatty acid uptake increased significantly during liver regeneration induced by PHx in rats. It is likely that L-FABP is one of the factors responsible for hepatic regeneration.

Animals↗
PubMed1998

Mechanisms of peroxisome proliferation by perfluorooctanoic acid and endogenous fatty acids.

1. The effects of endogenous fatty acids and perfluorooctanoic acid (PFOA) and its analogs on peroxisomal acyl CoA oxidase (ACO) and microsomal laurate hydroxylase (LH) activities were evaluated in primary cultures of rat hepatocytes and activation of peroxisome proliferator-activated receptor alpha (PPARalpha) in CV-1 cells. The rank order for the stimulation of ACO activity in hepatocytes for selected compounds was PFOA >> octanoic acid>octanedioic acid, perfluorooctanol (inactive). Increases in ACO activity by PFOA, like those of ciprofibrate, were associated with a marked increase in peroxisome number and cytosolic occupancy volume. Maximal effects of ciprofibrate and PFOA on the stimulation of ACO activity were not additive, suggesting that these two compounds share a common pathway of peroxisome proliferation. 2. Saturated monocarboxylic acids of C4 to C18 chain length were inactive, and, among dicarboxylic acids, only small elevations (40-45%) in ACO activity were observed with the long-chain C12 and C16 dioic acids. Of the C18 fatty acids tested, only oleic and linoleic acids, at 1 mM, produced a two- to three-fold elevation in ACO and LH activities. In comparison with endogenous fatty acids, PFOA was more potent and exhibited a different time course and greater magnitude of stimulation of ACO and LH activities in cultured hepatocytes. 3. Addition of mitochondrial beta-oxidation inhibitors (3-mercaptopropionic and 2-bromooctanoic acids) did not alter ACO activity in the presence of octanoic acid or octanedioic acid; nor did they modify the stimulation of ACO activity by PFOA. The carnitine palmitoyltransferase I inhibitor 2-bromopalmitic acid produced a 2.5-fold increase in ACO stimulatory activity and reduced both ciprofibrate- and PFOA-mediated stimulations of ACO activity. 4. Cycloheximide treatment reduced PFOA- and ciprofibrate-induced ACO activities; however, the response to oleic acid was not blocked and increased slightly. 5. In rat and human PPARalpha transactivation assays, the rank order of activation was ciprofibrate > PFOA > oleic acid > or = octanoic acid > octanedioic acid or perfluorooctanol (inactive). PFOA, ciprofibrate and oleic acid were activators of rPPARalpha at concentrations that correlated favorably with the changes in ACO activity in cell culture. Octanoic acid did not increase ACO activity and was a weak activator of PPARalpha. 6. Our findings suggest that fatty acids such as oleic acid (endogenous fatty acids) and PFOA (a stable fatty acid) act through more than one pathway to increase ACO activity in rat hepatocytes. We conclude that the potent effects of PFOA are primarily mediated by a mechanism that includes the activation of liver PPARalpha.

Acyl-CoA Oxidase↗
PubMed1995

Effect of dietary fatty acids on antibody production and fatty acid composition of lymphoid organs in broiler chicks.

This study examined the effect of increasing amounts of dietary polyunsaturated fatty acids on antibody production in vivo and fatty acid composition of plasma and lymphoid tissues in the broiler. Chicks were fed four diets containing 12% added fat made up of different proportions of palm oil and soybean oil and immunized against bovine serum albumin at 14 to 16 d of age. Blood samples were taken every 4 to 5 d for 30 d; then the chicks were killed and liver, spleen, thymus, bursa of Fabricius, and bone marrow were sampled. Fatty acid composition in serum and tissues reflected the composition of the diets, although amounts of saturated fatty acids were tissue-specific. Arachidonic acid concentration was not changed by dietary fatty acid content. Antibody production developed more rapidly, reached a higher level, and was more persistent in the chicks fed lower levels of linoleic acid. A quadratic relationship was found between tissue linoleic acid or total polyunsaturated fatty acid concentrations and antibody production at 11 and 14 d after challenge. No correlation was found with arachidonic acid. It is concluded that dietary fatty acid composition can influence immune response in broilers.

Animals↗