Acids In Liver Phospholipids Research Articles

Protein-Energy Malnutrition during Gestation and Lactation in Rats Affects Growth Rate, Brain Development and Essential Fatty Acid Metabolism

The influence of feeding a low protein diet to rat dams during gestation and lactation on lipid metabolism in pups was studied. Wistar rats were fed 5, 10, 15 and 25% dietary protein during gestation and lactation. Pup growth was monitored until weaning, and brain weight, protein concentration, proteolipid concentration and total lipid phosphorus concentration of brain were analyzed. The levels of fatty acids in dam milk as well as in pup liver phospholipids and brain prosphatidylcholine and phosphatidylethanolamine were determined. The progressive deprivation of maternal dietary protein produced a reduction in the total saturated fatty acid concentration of dam milk and an increment in the concentration of nonmetabolized linoleic acid. Pup body and brain weights as well as proteolipid, protein and total lipid phosphorus concentrations in brain were reduced in proportion to the degree of dietary protein deficiency. The products:precursor ratio of (n-6) fatty acids in liver phospholipids revealed an impairment in the elongation-desaturation pathway due to maternal protein deficiency. Both (n-6) and (n-3) polyunsaturated fatty acids within brain phosphatidylethanolamine were decreased by reduced maternal dietary protein intake, whereas only the linoleic acid-derived products were similarly affected in the corresponding phosphatidylcholine fraction. These results demonstrate the widespread and profound deleterious effects of low protein levels of maternal diet on the growth rate, brain development and fatty acid metabolism of rat pups.

НОРМАЛІЗАЦІЯ ФІТОПРЕПАРАТОМ «КВЕРТУЛІН» ОБМІНУ ЕСЕНЦІАЛЬНИХ ЖИРНИХ КИСЛОТ ФОФСОЛІПІДІВ ПЕЧІНКИ ЩУРІВ, ЯКІ ОТРИМУВАЛИ ПАЛЬМОВУ ОЛІЮ НА ТЛІ ДИСБІОЗУ

Keywords: liver, phospholipids, essential fatty acids, palm oil, dysbiosis, herbal medicine. Aim. To study the effect of the phytopreparation kvertulin on the processes of biosynthesis of PUFA of liver phospholipids in rats treated with palm oil against the background of dysbiosis. Methods. Rats consumed a fat-free diet (group 1), a diet with 15 % palm oil (group 2), a diet with 15 % palm oil on the background of experimental dysbiosis (group 3) and a diet with 15 % palm oil on background of dysbiosis + kvertulin. The duration of the experiment is 40 days. The content of fatty acids in liver phospholipids was determined by gas chromatography. The ratio of the PUFA content was used to calculate the “activity” of ω-3-desaturase, the intensity of synthesis of arachidonic acid, and the intensity of synthesis of docosahexaenoic acid. Results: In rats of the 3rd group, which received palm oil against the background of dysbiosis, there was a decrease in the content of ω-3 PUFA, an increase in the ratio of ω-6 / ω-3 PUFA, and a decrease in the “activity” of ω-3-desaturase. In rats of the 4th group, which received kvertulin, the content of PUFA was completely restored and the “activity” of enzymes of their biosynthesis was normalized. Conclusion. The use of the phytopreparation kvertulin normalizes the endogenous biosynthesis of PUFA of liver phospholipids in rats consuming palm oil against the background of dysbiosis.

Rapid changes in liver lipid composition and pancreatic islet K+ handling and secretory behaviour provoked by the intravenous administration of a medium-chain triglyceride:fish oil emulsion to long-chain polyunsaturated ω3 fatty acid-depleted rats

Second generation rats depleted in long-chain polyunsaturated omega3 fatty acids are currently used as an animal model for the insufficient dietary supply of such fatty acids often prevailing in Western populations. The present study deals mainly with the effects of a novel medium-chain triglyceride: fish oil emulsion (MCT:FO), as compared to a control medium-chain triglyceride:olive oil emulsion (MCT: OO), administered as an intravenous bolus to the omega3-depleted rats 60-120 min before sacrifice upon selected biochemical and biophysical variables. The major findings consisted of a severe decrease of the omega3 fatty acid content of liver lipids in non-injected omega3-depleted rats and its partial correction after injection of the MCT:FO emulsion. The omega3-depleted rats also displayed liver steatosis, increased incorporation of long-chain polyunsaturated omega6 fatty acids in liver phospholipids and increased activity of liver Delta9-desaturase. As judged from the effects of ouabain upon 86Rb net uptake by isolated pancreatic islets, the activity of Na+,K+-ATPase was virtually abolished in the omega3-depleted rats. The latter defect was corrected by prior intravenous injection of the MCT:FO emulsion, this coinciding with suppression of the excessive secretory response to a number of insulin secretagogues otherwise observed in the islets of omega3-depleted rats injected or not with the MCT:OO emulsion.

Elaidic Acid and Oleic Acid Have Opposite Effects on Serum Glucose, Insulin and Immunoglobulin Levels and Eicosanoid Production in Streptozotocin-Induced Diabetic Rats

The present study was designed to evaluate the physiological effect of trans fatty acid in the diabetic condition. After feeding the mixture of oleic (cis) or elaidic (trans) acids with safflower oil (3 : 7, wt/wt) at the dietary level of 10% for 2 weeks, rats were treated with streptozotocin and reared on the same diets for an additional week. The dietary level of elaidic acid was 6.4 energy %, which corresponded to the level that causes an increase in plasma low-density lipoprotein cholesterol and a decrease in high-density lipoprotein cholesterol in humans. The following differences were observed in rats fed trans acid in comparison with those fed cis acid; (a) significant reduction of water consumption and serum glucose, and an elevation of serum insulin, (b) a reducing trend of serum and liver lipids, (c) a reducing trend of the proportion of stearic and arachidonic acids in liver phospholipids and (d) a significant reduction of the concentration of serum immunoglobulin G (IgG) and an increase in IgE. Thus, the results indicate that elaidic acid may not further aggravate metabolic disorders caused under the diabetic condition more than the cis counterpart even when consumed at a relatively high level, with the exception of the response of serum immunoglobulins.

Effect of linseed oil supplementation on concentrations of (n‐3) polyunsaturated fatty acids in liver phospholipids of rats fed diets containing either an oil rich in conjugated linoleic acids, sunflower oil or high‐oleic acid sunflower oil

This study investigated the metabolism of alpha-linolenic acid and the formation of eicosanoids in rats fed diets with three different dietary fats (30 g/kg diet): either a conjugated linoleic acid (CLA) preparation with a high concentration of cis-9, trans-11 CLA (32.2 g/100 g) and trans-10, cis-12 CLA (33.3 g/100 g) and a low concentration of linoleic acid (0.5 g/100 g), sunflower oil (SFO) with a high concentration of linoleic acid or high-oleic acid sunflower oil (HO-SFO) with a high concentration of oleic acid. Basal diets with those oils were fed for 4 weeks. In the fifth week, the same diets supplemented with 50 g of linseed oil/kg as a source of alpha-linolenic acid were fed. To study the effect of the oils on the metabolism of alpha-linolenic acid, the amounts of individual (n-3) polyunsaturated fatty acids (PUFA) in liver phospholipids (phosphatidyl choline and phosphatidyl ethanolamine) were determined; to study the effect on eicosanoid formation, the concentrations of various two-series eicosanoids in liver and plasma, the activity of the secretory phospholipase A2 and the relative mRNA concentrations of cyclooxygenases-1 and 2 in the liver were measured. Rats fed the CLA diets had the highest concentrations of long chain (n-3) PUFA deriving from delta6, delta5 and 14-desaturation of alpha-linolenic acid in liver phospholipids; rats fed the SFO diet had the lowest concentrations of those fatty acids. The concentration of arachidonic acid in liver phospholipids and the concentrations of eicosanoids in liver and plasma were lowest in rats fed the CLA diet and highest in the rats fed the SFO diet. Moreover, rats fed the CLA diet had a higher gene expression of delta6-desaturase in the liver than the other two groups of rats. The results show that feeding the CLA oil reduced the formation of arachidonic acid and eicosanoids but enhanced the formation of long chain (n-3) PUFA and their incorporation into tissue lipids when compared with feeding SFO or HO-SFO.

Enteral nutrition with stearidonic acid increases incorporation of antiinflammatory N-3 fatty acids in liver phospholipids in the rat

We have shown that an enteral nutrition formula containing eicosa-pentaenoic acid (20:5n-3; EPA) provided beneficial antiinflammatory effects in critically ill patients with acute lung injury. The use of diets enriched with stearidonic acid (18:4n-3; SDA) may provide a novel means to increase EPA content in tissue phospholipids and to provide the health benefits typically associated with n-3 fatty acids from fish oil. There is little known about the effects of increased consumption of SDA on tissue phospholipid fatty acid composition. We examined whether diets supplemented with SDA can be used as a precursor to increase EPA content in liver phospholipids and to determine the effectiveness of SDA in increasing tissue EPA content as compared with dietary EPA in rats. Male Long--Evans rats ( n = 10) were randomly divided into three dietary groups and fed a modified US-17 diet providing 200 kcal/kg/day and containing either 2% oleic acid (OA, 18:1 n-9) ( n = 4), 1% EPA /1% OA ( n = 3), or 1% SDA/1% OA ( n = 3) for 2 weeks. Dietary fatty acid composition was controlled by substituting the ethyl esters of EPA and SDA for OA; thus changes in phospholipid fatty acid composition would be the result of dietary changes of these fatty acids. The fatty acid compositions (mol %) of liver phospholipids were determined by gas chromatography. There was a small reduction, although not significant, in AA content with EPA and SDA as compared with OA. SDA resulted in an increase in EPA content in liver phospholipids that was approximately 50% of that for EPA. There was a smaller increase in tissue DPA content with SDA than EPA as compared with OA. There was no significant increase in DHA content with either EPA or SDA as compared with OA. These results indicate that dietary SDA can be used to increase EPA content in liver phospholipids and the relative effectiveness of SDA conversion to EPA and incorporation into tissue phospholipids was equivalent to one-half of dietary EPA. TABLE—ABSTRACT P77 Fatty acid OA EPA SDA 20:4 n-6 (AA) 28.3 ± 1.02 a 25.1 ± 0.42 a 26.6 ± 0.30 a 20:5 n-3 (EPA) 0.02 ± 0.06 a 1.21 ± 0.43 b 0.66 ± 0.04 a,b 22:5 n-3 (DPA) 0.16 ± 0.04 a 1.65 ± 0.33 b 1.01 ± 0.04 c 22:6 n-3 (DHA) 6.49 ± 0.26 a 6.39 ± 0.004 a 6.67 ± 0.43 a Note. Values with different superscripts are significantly different ( P ≤ 0.05).

Liver cancer is induced by a subnecrogenic dose of DENA when associated with fasting/refeeding: role of glutathione-transferase and lipid peroxidation

In previous studies, we reported that fasting/refeeding has a role in sustaining the initiation of liver cancer by a subnecrogenic (noninitiating) dose of diethylnitrosamine (DENA). This research investigated whether the metabolic alterations imposed by fasting/refeeding provide an imbalance between the generation of carcinogenic molecules and the scavenger defense mechanisms in rat liver. Metabolism of DENA, levels of reduced glutathione (GSH) and GSH transferase (GST) activity, as well as basal and stimulated malondialdehyde (MDA) production, were examined. Rats fasted for 4 days showed a decrease in the liver levels of GSH, GST activity, monounsaturated fatty acids and % of labeled nuclei. After 1 day of refeeding, at which point DENA was administered, the levels of GSH recovered, GST activity remained below control values, basal and stimulated MDA production and content of total polyunsaturated fatty acids in liver phospholipids decreased. One day after DENA treatment, MDA production further decreased, although the % of labeled nuclei increased. No significant changes in the content of arachidonic acid, the main target of peroxidation, were observed at any time. The results indicated that the induction of the hepatocellular carcinoma was associated with a depression of GST activity and lipid peroxidation when rats were given 20 mg/kg of DENA after 1 day of refeeding after 4-day fasting.

Activities of liver microsomal fatty acid desaturases in zinc-deficient rats force-fed diets with a coconut oil/safflower oil mixture of linseed oil.

The present study was conducted to investigate the effect of zinc deficiency on fatty acid desaturation in rats fed two different types of dietary fat, a mixture of coconut oil and safflower oil (7:1, w/w, "coconut oil diet") or linseed oil ("linseed oil diet"). In order to ensure an adequate food intake, all rats were force-fed by gastric tube. Zinc deficiency caused statistical significant reduction of delta 9-desaturase activity in liver microsomes of rats fed coconut oil diet and tendencial reduction (p < 0.15) in rats fed linseed oil diet compared with control rats fed diets with the same type of fat. In agreement with this effect, zinc deficiency in the rats fed both types of dietary fat increased the ratio between total saturated and total monounsaturated fatty in liver phospholipids and liver microsomes. Zinc deficient rats on the coconut oil diet had unchanged delta 6-desaturase activity with linoleic acid as substrate and lowered activity with alpha-linolenic acid as substrate. In contrast, zinc deficient rats on the linseed oil diet had increased delta 6-desaturase activity with linoleic acid as substrate and unchanged activity with alpha-linolenic acid. Because linoleic acid is the main substrate for delta 6-desaturase in the rats fed coconut oil diet, and alpha-linolenic acid is the main substrate in the rats fed linseed oil diet, it is concluded that in vivo delta 6-desaturation was not changed by zinc deficiency in the rats fed both types of dietary fat. Activity of delta 5-desaturase was also not changed by zinc deficiency in the rats fed both dietary fats. Levels of fatty acids in liver phospholipids and microsomes derived by delta 4-, delta 5-, and delta 6-desaturation were not consistently changed by zinc deficiency in the rats fed both types of dietary fat. Thus, the enzyme studies and also fatty acid composition data of liver phospholipids and microsomes indicate that zinc deficiency does not considerably disturb desaturation of linoleic and alpha-linolenic acid. Therefore, it is suggested that similarities between deficiencies of zinc and essential fatty acids described in literature are not due to disturbed desaturation of linoleic acid in zinc deficiency. The present study also indicates that zinc deficiency enhances incorporation of eicosapentaenoic acid into phosphatidylcholine of rats fed diets with large amounts of n-3 polyunsaturated fatty acids.

Growth and Liver Polar Fatty Acid Composition of Year-1 Channel Catfish Fed Various Lipid Sources at Two Water Temperatures

Abstract Young channel catfish (Ictalurus punctatus) with an initial weight of 0.9 ± 0.03 g were fed semipurified diets containing 7% lipids as beef tallow, corn oil, linseed oil, menhaden oil, or a mixture (1:1:1) of menhaden oil, beef tallow, and corn oil at two water temperatures, 17 ± 1°C and 28 ± 0.5°C, for 9 weeks. At the higher temperature, fish fed the menhaden oil and the mixed-oil diets had greater weight gains (P < 0.05) than fish fed the other diets. Weight gains for fish fed beef tallow, corn oil, or linseed oil did not significantly differ (P > 0.05). At the lower water temperature, weight gain was much less, and the only significant difference among treatments was between the fish fed menhaden oil or mixed oil and those fed beef tallow, which gained no weight. The concentration of polyene fatty acids in liver phospholipids was higher at the low temperature than at the high temperature (P < 0.05). The primary n-3 highly unsaturated fatty acid (HUFA) in liver phospholipids of fish fed menhaden oil or the mixed oils was 22:6 n-3, docosahexaenoic acid (DHA). Fish fed corn oil had primarily 20:4 n-6, arachidonic acid (AA), in their phospholipids, and those fed linseed oil had a small amount of 20:5 n-3, eicosapentaeonic acid (EPA), but no DHA in their liver phospholipids. This study indicates that the presence of fish oil, a source of n-3 HUFA, in the diet enhances growth of young channel catfish at optimum and suboptimum temperatures.

Unusual isomeric polyunsaturated fatty acids in liver phospholipids of rats fed hydrogenated oil.

Linoleic acid (18:2 omega 6) and linolenic acid (18:3 omega 3) are precursors of two series of essential fatty acids (EFA) formed by alternate desaturations and elongations. In EFA deficiency (EFAD), oleic acid (18:1 omega 9) and palmitoleic acid (16:1 omega 7) undergo the same reactions to form polyunsaturated fatty acids (PUFA) of other structures. Partially hydrogenated soybean oil (PHSO) contains isomeric 18:1 acids that can be converted to unusual isomers of 18:2 by liver microsomes. To test whether 18:2, 20:3, and 20:4 of unusual structure occur in phospholipids as a consequence of EFAD or ingestion of PHSO, rats were fed corn oil, an EFA-deficient diet, or PHSO to provide isomeric 18:1 acids. At 2.5 months the phospholipids were isolated from livers and converted to methyl esters, and the 18:2, 20:2, 20:3, and 20:4 fractions were isolated. The 18:2 and 20:2 fractions were ozonized, and, by using a computer solution of simultaneous equations, the structures and proportions of each isomer were calculated. The 20:3 and 20:4 fractions were analyzed by ozonolysis and capillary gas chromatography. When corn oil was fed, the major isomer in each group was 9,12-18:2, 11,14-20:2, 8,11,14-20:3, and 5,8,11,14-20:4. Patterns in EFAD- and PHSO-fed groups were more diverse, with large proportions of unusual isomers. Feeding EFA-deficient diet and PHSO induced measurable amounts of unusual PUFA at each step of the cascade, and these PUFA may compete in metabolism of normal PUFA and are substrates for oxidative formation of autacoids of unknown structures and function.

Effects of Biotin Deficiency on Polyunsaturated Fatty Acid Metabolism in Rats

The effects of biotin and protein-calorie deficiency on metabolism of liver phospholipids in rats were determined. Weanling male Long-Evans rats were fed ad libitum a biotin-deficient (0.4 µg biotin/g diet) or a biotin-adequate (2.4 µg biotin/g diet) diet for 49 days. A pair-fed group was fed biotin-adequate diet but restricted to the amount consumed by biotin-deficient rats. The effects of these diets on food intake, weight gain, biotin content of serum and fatty acid composition of liver phospholipid were determined. Growth and food intake were significantly depressed in biotin-deficient and pair-fed rats. Biotin concentration in serum was significantly reduced in biotin-deficient and in pair-fed rats. Biotin deficiency caused significantly increased concentrations of 15:0, 17:0 and total odd-chain fatty acids in liver phospholipids. Combined biotin and protein-calorie deficiency and protein-calorie deficiency alone caused significantly increased concentrations of 18:2ω6 in liver phospholipids. Biotin deficiency caused significant reduction in liver phospholipid 20:3ω6. Reduced arachidonic acid (20:4ω6) level was due to combined biotin protein-calorie deficiency. Protein-calorie deficiency alone was primarily responsible for reduced levels of 22:5ω6. Biotin deficiency alone caused significant increases in liver phospholipids 18:3ω3 and 22:6ω3.

Changes in the content of n-6 fatty acids in liver phospholipids in rats as a consequence of partially hydrogenated dietary oils

The effects of unhydrogenated and partially-hydrogenated marine and rapeseed oils on the relative content of n-6 fatty acids in rat liver phospholipids were studied by gas-liquid chromatography. The type of dietary oil strongly affected the pattern of n-6 fatty acids in the liver phospholipids even after a relatively short feeding period (3 weeks). With diets deficient in linoleic acid, accumulation of the 20:3 n-9 fatty acid was observed in the animals receiving partially hydrogenated oils, but not in the animals receiving the unhydrogenated marine oil which contained relatively high amounts of polyunsaturated fatty acids of the n-3 family. The results presented are in line with reports in the literature that dietary trans fatty acids may inhibit the desaturation-elongation enzyme systems of rat liver. The observed effects did not appear to be directly correlated to the dietary content of very-long-chain monounsaturated fatty acids.

Influence of partially hydrogenated vegetable and marine oils on lipid metabolism in rat liver and heart

Partially hydrogenated marine oils containing 18:1-, 20:1- and 22:1-isomers and partially hydrogenated peanut oil containing 18:1-isomers were fed as 24-28 wt% of the diet with or without supplement of linoleic acid. Reference groups were fed peanut, soybean, or rapeseed oils with low or high erucic acid content. Dietary monoene isomers reduced the conversion of linoleic acid into arachidonic acid and the deposition of the latter in liver and heart phosphatidylcholine. This effect was more pronounced for the partially hydrogenated marine oils than for the partially hydrogenated peanut oil. The content of trans fatty acids in liver phospholipids was similar in groups fed partially hydrogenated fats. The distribution of various phospholipids in heart and liver was unaffected by the dietary fat. The decrease in deposition of arachidonic acid in rats fed partially hydrogenated marine oils was shown in vitro to be a consequence of lower delta 6-desaturase activity rather than an increase in the peroxisomal beta-oxidation of arachidonic acid. The lower amounts of arachidonic acid deposited may be a result of competition in the delta 6-desaturation not only from the C22- and C20-monoenoic fatty acids originally present in the partially hydrogenated marine oil, but also from C18- and C16-monoenes produced by peroxisomal beta-oxidation of the long-chain fatty acids.

Influence of diet on conversion of 14C1-linolenic acid to docosahexaenoic acid in the rat.

14C1-Linolenic acid was incorporated into lipids of hearts, livers, and carcasses of male rats. We studied the influence of diet composition on extent and distribution of radioactivity. A CHOW diet, a purified, essential fatty acid (EFA)-deficient diet, a purified control diet, and EFA-deficient diets with four fatty acid supplements were used. Supplements of 18:2n-6, 20:4n-6, 15:3n-3, and 22:6n-3 were given as single doses. Radioactivities in liver phosphatidyl ethanolamines (PE), phosphatidyl cholines, and neutral lipids were measured. The distribution of radioactivity among the fatty acids in liver phospholipids was determined. Rats on CHOW diet incorporated far less radioactivity than any other group into lipids of hearts and livers. Most of the activity in livers was recovered as 20:5n-3 and 22:6n-3 in all rats. In EFA-deficient rats, the radioactivity in 22:6n-3 of liver PE was still increasing 36 hr after 14C1-linolenic acid had been administered. The n-6 supplements (18:2n-6 and 20:4n-6) seemed to reduce the coversion of 20:4n-3 to 20:5n-3 (desaturation), whereas the n-3 supplements (18:3n-3 and 22:6n-3) reduced the conversion of 20:5n-3 to 22:5n-3 (elongation). Formation of 22:6n-3 may be controlled by 22:6n-3 itself at the elongation of 20:5n-3 to 22:5n-3.

The ( n−6) Pentaene:( n−3) Hexane fatty acid ratio as an index of linolenic acid deficiency

The administration of semisynthetic diets with different relative linoleic and linolenic acid contents to growing rats results in changes of the relative percentages of 22:5( n−6) and 22:6( n−3) fatty acids in liver phospholipids. The 22:5(n−6) 22:6(n−3) fatty acid ratio rises when diets with a high linoleic/linolenic acid ratio, showing a time-course trend similar to that of n−9 trienes/ n−6 tetraenes observed in essential fatty acid deficiency. The ( n−6) pentaene/( n−3) hexaene ratio is proposed as an index of relative linolenic acid deficiency.

THE METABOLISM OF FATTY ACIDS IN THE RAT. VI. ARACHIDONIC ACID.

AbstractGöransson, G. The metabolism of fatty acids in the rat. VI. Arachidonic acid. Acta physiol. scand. 1965. 64. 1–5. ‐H3‐labeled arachidonic acid and C14‐labeled palmitic acid were simultaneously injected into male rats. Arachidonic acid was preferentially incorporated into liver phospholipids as might be expected from the preponderance of this fatty acid in liver phospholipids as compared to glycerides. Initially, the labeled arachidonic acid and the labeled palmitic acid were oxidized at similar rates but at later times more arachidonic acid than palmitic acid was recovered from the whole animal. This may be explained by the preferential incorporation of arachidonic acid into phospholipid in combination with the low turnover rate of the phospholipids, especially those containing essential fatty acids. The pattern of label in the blood glycerides closely resembled that in the corresponding liver fraction.