Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “FATTY ACIDS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed2001

Influence of fatty alcohol and other fatty acid derivatives on fatty acid uptake into rat intestinal epithelial cells.

We investigated the influence of various substrates on the uptake of long-chain fatty acid into IEC-6, rat intestinal epithelial cell line. The uptake of [3H]oleic acid into IEC-6 cells was a saturable function of the oleic acid concentration. Long-chain fatty acids significantly inhibited the oleic acid uptake into IEC-6 cells and shorter-chain fatty acids had little or no effect. Various fatty acid esters suppressed the oleic acid uptake into IEC-6. Fatty alcohols also inhibited oleic acid uptake into IEC-6 and the length of the carbon chain played an important role. These results suggest that long-chain fatty acid uptake was inhibited by the substrates which had a structure similar to long-chain fatty acids, especially those with a long carbon chain. At least two molecules, fatty acid translocase and fatty acid transport protein type 4, which are considered to be involved in the long-chain fatty acid transport into the cell, were expressed on IEC-6 cells, supporting the existence of the carrier-mediated system of long-chain fatty acid transport on IEC-6 cells.

Animals↗
PubMed2002

Modulation of essential (n-6):(n-3) fatty acid ratios alters fatty acid status but not bone mass in piglets.

Dietary (n-6) and (n-3) fatty acids have been implicated as important regulators of bone metabolism. The main objective of this research was to define the response of whole-body growth, fatty acid status and bone mass to a reduced dietary (n-6):(n-3) fatty acid ratio. A secondary objective was to determine whether there is an amount of fat x fatty acid ratio interaction for these outcomes. Piglets (n = 32) were randomized to 1 of 4 diets: group 1: [30 g fat/L + (n-6):(n-3) ratio 4.5:1]; group 2: [30 g fat/L + (n-6):(n-3) ratio 9.0:1]; group 3: [60 g fat/L + (n-6):(n-3) ratio 4.5:1]; and group 4: [60 g fat/L + (n-6):(n-3) ratio 9.0:1]. After 21 d, outcomes assessed included growth, fatty acid status and bone mass and metabolism. Growth and bone mass did not differ among the four groups nor did arachidonic acid (AA as g/100 g fatty acids) in plasma, adipose and brain. Piglets fed diets 1 and 3 with the lower (n-6):(n-3) ratio had lower liver AA (P < 0.001). Those fed diets 1 and 2 containing 30 g fat/L had lower docosahexaenoic acid (DHA as g/100 g fatty acids) in liver (P < 0.001), plasma (P = 0.019) and adipose tissue (P = 0.045). However, piglets fed diets 1 and 3 had higher (P < 0.001) brain DHA than those fed diets with a higher (n-6):(n-3) ratio. Higher plasma DHA was associated with less bone resorption (r = -0.44, P = 0.01). Therefore, elevation of dietary (n-3) fatty acids supports growth and fatty acid status while not compromising bone mass. The results may be of relevance to the nutritional management of preterm infants whose DHA status is often too low and bone resorption too high.

Adipose Tissue↗
PubMed2005

Expression of liver-type fatty-acid-binding protein, fatty acid synthase and vascular endothelial growth factor in human lung carcinoma.

OBJECTIVE: A key enzyme of fatty acid synthesis, fatty acid synthase (FAS), is expressed in human cancers, including squamous-cell carcinoma of the lung, and long-chain fatty acids are intracellularly transported and/or taken up from blood by fatty-acid-binding proteins (FABPs). Since the liver-type (L-) FABP, a member of the FABPs, is detected in a subset of gastric adenocarcinomas, the expression of FAS, L-FABP and vascular endothelial growth factor (VEGF) was investigated in human lung carcinomas to elucidate the mechanisms of production and transportation of fatty acid(s) in cancer. METHODS: Expression of L-FABP, FAS and VEGF in 199 surgically resected lung carcinomas was examined immunohistochemically. Possible associations of the expression of each protein with major clinicopathological factors were analyzed. RESULTS: L-FABP was detected in 60% (120 of 199) of the lung carcinoma cases; detection was increased in large-cell carcinoma (80%) and adenosquamous carcinoma (83%), but low in squamous-cell carcinoma (47%) and in small-cell carcinoma (57%). Overall expression of FAS was 67.3% (134 of 199 cases) and that of VEGF was 86.8% (158 of 199 cases), respectively. Expression of L-FABP was not correlated with the FAS status, but there was a tendency to co-expression of L-FABP and VEGF. There was no association between L-FABP, FAS or VEGF expression and clinicopathological data. CONCLUSIONS: L-FABP, FAS and VEGF are highly expressed in human lung cancer, and expression of L-FABP is associated with that of VEGF but not that of FAS, suggesting that L-FABP might be involved in the uptake of fatty acid(s) from the bloodstream.

Adult↗
PubMed1997

Elevated expression of fatty acid synthase and fatty acid synthetic activity in colorectal neoplasia.

Expression of the primary enzyme catalyzing the synthesis of fatty acids, ie, fatty acid synthase (FAS), and ex vivo fatty acid synthetic activity were examined in colorectal epithelium and neoplasms, including the relationship to tumor progression and prognosis. Immunohistochemistry for FAS showed only faint staining of native colorectal mucosa, but increased expression was found in all sporadic adenomas (n = 18), adenomas associated with familial adenomatous polyposis (n = 7), hyperplastic polyps (n = 3), dysplasias arising in ulcerative colitis (n = 17), and colorectal carcinomas (n = 130) including 11 with contiguous adenomas. The intensity of staining was strong in 53% of carcinomas, intermediate in 38%, and weak in 9%. Activity of the fatty acid synthetic pathway measured by labeling of six surgical specimens with [U-14C]acetate was 2- to 7-fold higher in colorectal carcinomas than adjacent native mucosa (P = 0.006) and 6- to 16-fold higher than serosal fat (P = 0.01). Activity correlated with immunohistochemical expression (Spearman's rank correlation coefficient = 0.85; P < 0.001). There was no statistically significant association between patient survival and FAS staining intensity of carcinomas. Our study shows that FAS is expressed in all colorectal neoplasms and there is a concomitant increase in fatty acid synthesis. FAS may therefore represent a potential therapeutic target.

Adenoma↗
PubMed2000

Regulation of hepatic delta-6 desaturase expression and its role in the polyunsaturated fatty acid inhibition of fatty acid synthase gene expression in mice.

Dietary polyunsaturated fatty acids (PUFA) of the (n-6) and (n-3) families uniquely suppress the expression of lipogenic genes while concomitantly inducing the expression of genes encoding proteins of fatty acid oxidation. Although considerable progress has been made toward understanding the nuclear events affected by PUFA, the intracellular mediator responsible for the regulation of hepatic lipogenic gene expression remains unclear. On the basis of earlier fatty acid composition studies, we hypothesized that the Delta-6 desaturase pathway was essential for the production of the fatty acid regulator of gene expression. To address this hypothesis, male BALB/c mice (n = 8/group) were fed for 5 d a high glucose, fat-free diet (FF) or the FF plus 50 g/kg 18:2(n-6) with and without eicosa-5, 8,11,14-tetraynoic acid (ETYA) (200 mg/kg diet), a putative inhibitor of the Delta-6 desaturase pathway. ETYA had no effect on food intake or weight gain, but it completely prevented 18:2(n-6) from suppressing the hepatic abundance of fatty acid synthase mRNA. ETYA ingestion was associated with a decrease in the hepatic content of 20:4(n-6) and an increase in the amount of 18:2(n-6). The fatty acid composition changes elicited by ETYA were accompanied by a decrease in the enzymatic activity of Delta-6 desaturase. Interestingly, the hepatic abundance of Delta-6 desaturase mRNA was actually induced by ETYA one- to twofold. When the product of Delta-6 desaturase, i.e., 18:3(n-6), was added to the ETYA plus 18:2(n-6) diet, the hepatic content of 20:4(n-6) was normalized. In addition, 18:3(n-6) consumption reduced the level of hepatic Delta-6 desaturase mRNA by 50% and completely prevented the increase in fatty acid synthase mRNA that was associated with ETYA ingestion. Apparently, Delta-6 desaturation is an essential step for the PUFA regulation of the fatty acid synthase gene transcription. Finally, the suppression of Delta-6 desaturase by PUFA and its induction by ETYA suggest that the Delta-6 desaturase gene may be regulated by two different lipid-dependent mechanisms.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1995

Determination of plasma non-esterified fatty acids and triglyceride fatty acids by gas chromatography of their methyl esters after isolation by column chromatography on silica gel.

Non-esterified fatty acids (NEFA) and triglycerides were isolated from human plasma by column chromatography on silica gel. Eight principal fatty acids of each of these lipid classes were determined by gas chromatography of their methyl ester derivatives and quantified relative to multipoint standard curves. Within-day relative standard deviations for plasma non-esterified fatty acid and triglyceride fatty acid determinations were 2.4 and 3.2%, respectively. Day-to-day relative standard deviations for plasma non-esterified fatty acid and triglyceride fatty acid determinations were 1.4 and 1.1%, respectively. The total plasma concentration and the relative proportions of the eight non-esterified fatty acids determined by this method were significantly different from results obtained according to two generally accepted methods for direct plasma non-esterified fatty acid determination without a specific isolation step. These comparisons suggested that considerable fatty acid ester lipid hydrolysis occurred during these direct determination procedures, and that this hydrolysis resulted in 3-fold overestimation of plasma NEFA content by those methods. Measured levels of arachidonic acid are substantially overestimated by these direct determination methods in which non-esterified fatty acids are not isolated before derivatization.

Chromatography, Gas↗
PubMed1991

Labeling of adipocyte membranes by sulfo-N-succinimidyl derivatives of long-chain fatty acids: inhibition of fatty acid transport.

Sulfo-N-succinimidyl derivatives of the long-chain fatty acids, oleic and myristic, were synthesized and covalently reacted with isolated rat adipocytes. The plasma membrane proteins labeled by these compounds and the effect of labeling on the transport of long-chain fatty acids were investigated. Sulfo-N-succinimidyl oleate (SSO) and myristate (SSM) inhibited the transport of fatty acids (by about 70%). Inhibition of fatty acid transport was not a result of alterations in cell integrity, as intracellular water volume was not changed. It did not reflect effects on fatty acid metabolism, since it was observed under conditions where greater than 90% of the fatty acid taken up was recovered in the free form. The inhibitory effect was specific to the fatty acid transport system, as the transport of glucose and the permeation of retinoic acid, a substance with structural similarities to long-chain fatty acids, were unaffected. Sulfosuccinimidyl oleate reacted exclusively with a plasma membrane protein with an apparent size of 85 kDa while sulfosuccinimidyl myristate also labeled a 75-kDa protein. These proteins were among the ones labeled by diisothiocyanodisulfonic acid (DIDS) which also inhibits fatty acid transport irreversibly. The data suggest that the 85-kDa protein, which is the only one labeled by all three inhibitors is involved in facilitating membrane permeation of long-chain fatty acids.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1967

Characterization of clostridia by gas chromatography. I. Differentiation of species by cellular fatty acids.

Fatty acids of 41 strains representing 13 species of Clostridium were extracted directly from whole cells and examined as methyl esters by gas-liquid chromatography. Both visual and quantitative comparisons of the resulting chromatograms for the presence and relative amounts of large major peaks allowed rapid differentiation of C. perfringens, C. sporogenes, and C. bifermentans from each other and from 10 other species. Each of the three former species possessed a different characteristic fatty acid methyl ester profile that was exhibited by all strains tested within the respective species. Culture age and growth media influenced the relative proportions of certain of the acids, but such differences did not limit species differentiation.

Chromatography, Gas↗
PubMed2004

Mechanisms of regulation of gene expression by fatty acids.

Fatty acids (FA) regulate the expression of genes involved in lipid and energy metabolism. In particular, two transcription factors, sterol regulatory element binding protein-1c (SREBP-1c) and peroxisome proliferator activated receptor alpha (PPARalpha), have emerged as key mediators of gene regulation by FA. SREBP-1c induces a set of lipogenic enzymes in liver. Polyunsaturated fatty acids (PUFA), but not saturated or monounsaturated FA, suppress the induction of lipogenic genes by inhibiting the expression and processing of SREBP-1c. This unique effect of PUFA suggests that SREBP-1c may regulate the synthesis of unsaturated FA for incorporation into glycerolipids and cholesteryl esters. PPARalpha plays an essential role in metabolic adaptation to fasting by inducing the genes for mitochondrial and peroxisomal FA oxidation as well as those for ketogenesis in mitochondria. FA released from adipose tissue during fasting are considered as ligands of PPARalpha. Dietary PUFA, except for 18:2 n-6, are likely to induce FA oxidation enzymes via PPARalpha as a "feed-forward " mechanism. PPARalpha is also required for regulating the synthesis of highly unsaturated FA, indicating pleiotropic functions of PPARalpha in the regulation of lipid metabolic pathways. It is yet to be determined whether FA regulate other transcription factors such as liver-X receptor, hepatocyte nuclear factor 4, and carbohydrate response element binding protein.

Animals↗
PubMed1992

Does a threshold for the effect of dietary omega-3 fatty acids on the fatty acid composition of nuclear envelope phospholipids exist?

Existence of a dietary maximal level or threshold for incorporation of omega 3 fatty acids into membrane phospholipids is of interest as it may further define understanding of the dietary requirement for omega 3 fatty acids. To test whether feeding increasing levels of dietary omega 3 fatty acids continues to increase membrane omega 3 fatty acid content, weanling rats were fed a nutritionally adequate semipurified diet which provided increasing amounts of C20 and C22 omega 3 fatty acids, such as 20:5 omega 3 and 22:6 omega 3. Dietary 20:5 omega 3 and 22:6 omega 3 were provided by substituting a purified shark oil concentrate of high 22:6 omega 3 content for safflower oil high in 18:2 omega 6. After four weeks of feeding, nuclear envelopes from four animals in each diet group were prepared, lipid was extracted and phospholipids separated. Arachidonic acid content in membrane phosphatidylcholine, phosphatidylethanolamine, phosphatidylinositol and phosphatidylserine was significantly reduced by feeding increased dietary levels of omega 3 fatty acids. Decline of 20:4 omega 6 level in phospholipid tended to stabilize when the dietary content of total omega 3 fatty acids reached 4-5% of total fatty acids. Above this level, dietary omega 3 fatty acids did not result in a further decrease in membrane content of 20:4 omega 6. Increase in membrane phospholipid content of 20:5 omega 3 occurred as the dietary intake of omega 3 fatty acids increased from 1.1% to 5% of total fatty acids.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2003

Effects of dietary conjugated linoleic acid on fatty acid composition and cholesterol content of hen egg yolks.

The main objectives of the present study were to determine the effect of dietary conjugated linoleic acid (CLA) isomers on the fatty acid composition and cholesterol content of egg-yolk lipids. Forty-five 25-week-old laying hens were randomly distributed into five groups of nine hens each and maintained in individual laying cages, throughout 12 weeks of the experiment. They were assigned to the five treatments that consisted of commercial layer diets containing 0, 5, 10, 15 or 20 g pure CLA/kg. Feed intake of hens varied little and insignificantly. Egg mass was uniformly lower (P<0.05) in the hens fed the CLA-enriched diets. Feed conversion efficiency, when expressed per kg eggs, was impaired (P<0.05), although without obvious relation to the dietary CLA concentration. Feeding the CLA-enriched diets resulted in gradually increasing deposition of CLA isomers (P<0.01) in egg-yolk lipids. Saturated fatty acids were increased (P<0.01) and monounsaturated fatty acids decreased (P<0.01). Polyunsaturated fatty acids (PUFA), when expressed as non-CLA PUFA, were also significantly decreased (P<0.01). The most striking effects (P<0.01) were observed for palmitic (16 : 0) and stearic (18 : 0) acids, which increased from 23.6 to 34 % and from 7.8 to 18 %, respectively. On the other hand, oleic acid (18 : 1n-9) decreased from 45.8 to 24.3 %. Among non-CLA PUFA, linoleic (18 : 2n-6) and alpha-linolenic (18 : 3n-3) acids were strongly (P<0.01) decreased, from 14.2 to 7.7 % and from 1.3 to 0.3 %, respectively. The same was true for arachidonic (20:4n-6) and docosahexaenoic (22 : 6n-3) acids. The cholesterol content of egg yolks, when expressed in mg/g yolk, was not affected by the dietary CLA concentrations. In conclusion, unless the adverse effects of CLA feeding to laying hens on the fatty acid profile of egg yolks are eliminated, the CLA-enriched eggs cannot be considered functional food products.

Animal Feed↗
PubMed1977

Characterization of liver cholic acid coenzyme A ligase activity. Evidence that separate microsomal enzymes are responsible for cholic acid and fatty acid activation.

Investigations on the cholic acid CoA ligase activity of rat liver microsomes were made possible by the development of a rapid, sensitive radiochemical assay based on the conversion of [3H]choloyl-CoA. More than 70% of the rat liver cholic acid CoA ligase activity was associated with the microsomal subcellular fraction. The dependencies of cholic acid CoA ligase activity on pH, ATP, CoA, Triton WR-1339, acetone, ethanol, magnesium, and salts were investigated. The hypothesis that the long chain fatty acid CoA ligase activity and the cholic acid CoA ligase activity are catalyzed by a single microsomal enzyme was investigated. The ATP, CoA, and cholic (palmitic) acid kinetics neither supported nor negated the hypothesis. Cholic acid was not an inhibitor of the fatty acid CoA ligase and palmitic acid was not a competitive inhibitor of the cholic acid CoA ligase. The cholic acid CoA ligase activity utilized dATP as a substrate more effectively than did the fatty acid CoA ligase activity. The cholic acid and fatty acid CoA ligase activities appeared to have different pH dependencies, differed in thermolability at 41 degrees, and were differentially inactivated by phospholipase C. Moreover, fatty acid CoA ligase activity was present in microsomal fractions from all rat organs tested while cholic acid CoA ligase activity was detected only in liver microsomes. The data suggest that separate microsomal enzymes are responsible for the cholic acid and the fatty acid CoA ligase activities in liver.

Adenosine Triphosphate↗
PubMed1993

A high omega 3 fatty acid diet alters fatty acid composition of heart, liver, kidney, adipose tissue and skeletal muscle in swine.

The fatty acid profiles and total lipid contents of two skeletal muscles, adipose tissue, heart, liver and kidney of swine fed a diet rich in omega 3 (n-3) fatty acids (i.e., 5% fish oil) was investigated. These values were compared to those determined for animals which were fed an equal caloric diet low in n-3 fatty acids (i.e., 5% coconut oil). All supplementations were given over a 13-week period. The lipids were extracted with chloroform-methanol, trans-esterified and the relative fatty acid methyl-esters concentrations were determined using capillary gas chromatography. The fish oil diet significantly enhanced the relative amounts of n-3 fatty acids (i.e., eicosapentaenoic acid and docosahexaenoic acid) in all tissues examined. In the heart, liver and kidney, the increases in n-3 fatty acids were compensated by decreases primarily in arachidonic acid, but in the other tissues the contents of lauric and myristic acids were also reduced. In general, the n-3 fatty acid contents were 40-165% higher in the animals fed the fish oil. Supplementation of n-3 fatty acids in swine induced a significant incorporation of these fatty acids throughout the body, however the extent of this incorporation differed between tissues perhaps due to tissue-specific metabolic pathways.

Adipose Tissue↗
PubMed2004

Characterization of bile acids and fatty acids from ox bile in oil paintings by gas chromatography-mass spectrometry.

Characterization of ox bile, traditionally used in painting, is of interest in the fields of archaeometry and conservation and restoration of works of art. Bile acids, fatty acids (F), and cholesterol found in ox bile have been identified using a derivatization method that combines the formation of ethyl esters from the carboxylic groups and the trimethylsilyl ethers from hydroxyl groups. This method of analysis is consistent with these others proposed by the authors to analyze drying oils, proteins, and diterpenic resins usually used as binders and varnishes by the painters. Bile acids from binary samples such as animal glue/ox bile, casein/ox bile and Arabic gum/ox bile have been successfully analyzed using the proposed method. Finally, a method of analysis of mixtures of drying oil and ox bile has been also proposed attempting to quantitatively characterize samples in which ox bile was added to the drying oil for increasing the surfactant properties.

Animals↗
PubMed1985

Effects of 2[5(4-chlorphenyl)pentyl]oxirane-2-carboxylate on fatty acid synthesis and fatty acid oxidation in isolated rat hepatocytes.

The effects of the hypoketonaemic and hypoglycaemic compound 2[5(4-chlorophenyl)pentyl]oxirane-2-carboxylate (POCA) on fatty acid synthesis and fatty acid oxidation in rat hepatocytes were examined. Two microM-POCA caused a small stimulation of fatty acid synthesis which might be due to an increased flux through pyruvate dehydrogenase. Ten to one hundred microM-POCA inhibited (40-70%) fatty acid synthesis. At low concentrations (less than or equal to 5 microM) POCA was a more powerful inhibitor of fatty acid oxidation than of synthesis, but at higher concentrations (10-100 microM) the inhibition of synthesis and oxidation was similar. One hundred microM POCA-CoA inhibited acetyl-CoA carboxylase by about 22% and 100 microM-palmitoyl-CoA by about 33%. Since POCA was a more potent inhibitor of fatty acid synthesis than palmitate, but POCA-CoA did not inhibit acetyl-CoA carboxylase more strongly than palmitoyl-CoA, it is suggested that POCA-CoA may inhibit fatty acid synthase directly.

Acetyl-CoA Carboxylase↗
PubMed1994

Dietary omega-3 and polyunsaturated fatty acids modify fatty acyl composition and insulin binding in skeletal-muscle sarcolemma.

Feeding animals with diets high in saturated fat induces insulin resistance, and replacing saturated fat isocalorically with poly-unsaturated fat, especially long-chain omega-3 fatty acids, will prevent the development of insulin resistance in skeletal-muscle tissue. To investigate the mechanism, rats were fed on high-fat (20%, w/w) semipurified diets for 6 weeks. Diets containing ratios of polyunsaturated/saturated (P/S) fatty acid of 0.25 (low-P/S diet) and 1.0 (high-P/S diet) were used to study the effect of the level of saturated fat. To study the effects of omega-3 fatty acids, diets with a low-P/S ratio containing either 0 (low-omega-3 diet) or 3.3% (high-omega-3 diet) long-chain omega-3 fatty acids from fish oil were fed. Plasma membrane from skeletal muscle was purified. The content of fatty acids in sarcolemmal phospholipid was significantly related to the dietary composition. Insulin binding to intact sarcolemmal vesicles prepared from rats fed on diets high in omega-3 fatty acids increased 14-fold compared with animals fed on the low-omega-3 diet (P < 0.0001). Feeding rats on a diet with a high P/S ratio increased sarcolemmal insulin binding by 2.3-fold (P < 0.05). Increased insulin binding was due to increased receptor number at the low-affinity high-capacity binding site. Dietary effects on insulin binding were eliminated when studies were carried out on detergent-solubilized membranes, indicating the importance of the phospholipid fatty acyl composition for insulin binding. The results suggest that dietary omega-3 and polyunsaturated fatty acids increase insulin binding to sarcolemma by changing the fatty acyl composition of phospholipid surrounding the insulin receptor, and this might be the mechanism by which dietary fatty acids modify insulin action.

Animals↗
PubMed1989

Inborn errors of amino acid and fatty acid metabolism with hypoglycemia as a major clinical manifestation.

During the last decade it has become increasingly clear that severe hypoglycemia may be caused by specific enzymatic defects of amino acid and fatty acid metabolism. Several reports have presented hypoglycemic syndromes with reduced fatty acid transport or oxidation, decreased ketogenesis, or abnormalities of the Krebs cycle and electron transport chain. It is of particular interest that several enzymatic defects here discussed may present as Reye's syndrome. An intriguing fact is a highly variable clinical presentation, even in the presence of well-defined enzyme deficiencies. Some patients are desperately ill in the newborn period, whereas in other cases there are symptoms only during catabolic phases later in childhood. The presence of hypoglycemia may be related to low levels of acetyl CoA, with consequently reduced gluconeogenesis; alternatively the glucose-sparing effect of ketones is lost in states of reduced ketone body production. Treatment with pharmacological doses of vitamins may be attempted, depending upon the established or suspected diagnoses. With manifest hypoglycemia i.v. glucose infusion is the treatment of choice. By such means convulsions, and brain damage may be prevented.

Amino Acid Metabolism, Inborn Errors↗
PubMed1975

The effect of essential fatty acid deficiency upon fatty acid uptake by the brain.

Young adult rats, either control or essential fatty acid deficient, were administered either [3-H] oleic acid or [3-H] arachidonic acid by stomach tube. In addition, a group of control rats was given [3-H] palmitic acid. The rats were killed at various times therafter, and the radioactivity of the lipids of brain and plasma was examined. In confirmation of previous work, the blood lipid label was found to rise rapidly and then fall, wheras the activity of brain lipids increased slowly and did not show a decline through the 24-h period studied. Analysis of the brain uptake data according to first-order kinetics confirmed the impressions gained from visual inspection of the data. The initial rate of uptake of arachidonic acid was about 4.5 times that of oleic acid in control animals and in deficient animals. Essential fatty acid deficiency, however, did not induce an altered rate of uptake for either oleic acid or arachidonic acid. The rate of uptake of palmitic acid by control rats was not significantly different from that of oleic acid. Even though the initial rates of incorporation of oleic and arachidonic acids were not changed during essential fatty acid deficiency, the final levels of radioactivity obtained in brain lipids were higher in deficient rats with both fatty acids. The plateau value obtained with oleic acid was 1.5 times higher in deficient animals, while the plateau value for arachidonic acid was 1.7 times higher. An experiment in which deficient animals were allowed access to a control diet for 12 or 24 h prior to the labeling experiment suggested that the higher levels of radioactivity found in brain lipids of deficient animals was not due to an isotope dilution effect. Such animals still displayed the labeling pattern of deficient animals with arachidonic acid, while the results with oleic acid varied somewhat. Our results suggest that essential fatty acid deficiency does not alter the ability of the brain to take up the fatty acids studied. However, the fatty acids, especially arachidonic, are retained in the brain to a greater extent in the deficient animals.

Animals↗