Fatty acid composition of selected organs of gerbils maintained on a fat-deficient or fat-supplemented diet

The fatty acid composition of liver, heart, and testes was determined in gerbils maintained on a fat-deficient or fatsupplemented diet since the age of twenty-eight days and in gerbil pups, the mothers of which were placed on the respective diets on the day of delivery. Pups born to these mothers were killed at 11 to 19 days at which time increased concentrations of 16∶1, 18∶1, and 20∶3ω9 and decreased concentrations of 18∶2 and 20∶4 (and 22∶5ω6 in testes) were apparent in organs of fat-deficient compared to fat-supplemented gerbils. Similar but more marked changes occurred in organs of gerbils placed on the fat-deficient diet at twenty-eight days of age and examined at intervals of time up to two months later. In these animals, minimal changes were seen also in fatty acids of the brain. The concentration of 22∶6ω3 was resistant to change with the fat-deficient diet. Deficient gerbils had hair loss, decreased quantities of spermatids and spermatozoa in the testis, and most but not all had decreased body weight compared to the fat-supplemented controls. Extremely high concentrations of oleic acid were present in carcass fatty acids of deficient compared to supplemented gerbils, indicating an extremely dynamic fatty acid metabolism in these animals.     

Daily variations of the biosynthesis and composition of fatty acids in rats fed on complete and fat-free diets

This report describes the daily changes in fatty acid composition and fatty acid desaturation in rats feeding on a complete diet and a fat-free diet successively. Rats on a complete diet showed a good homeostasis in the percentage of fatty acid in plasma, with a possible palmitic acid rhythm, but the fat-free diet initiated an essential fatty acid-deficient pattern in a few hours. The light-dark period in animals feeding on a complete diet motivates a feeding rhythm that causes changes in linoleic and arachidonic acids in the whole liver and microsomes that are related to Δ6 and Δ5 desaturase activities. The patterns of Δ6 and Δ5 desaturase changes were different. Linoleic acid intake during the dark periods (complete diet feeding) caused a decrease of Δ6 desaturase activity and the activation of Δ5 desaturation that led to an increase of arachidonic acid biosynthesis. The feeding of a fat-free diet eliminated the rhythm observed in linoleic and arachidonic acid composition in the liver and changed the desaturase rhythms. The Δ9 desaturase activity in the liver also showed a daily rhythm in the complete-diet period that disappeared with the change to a fat-free diet, while the activity increased markedly. A negative correlation existed between the percentage of linoleic acid in the liver and the Δ9 desaturase activity. However, no correlation was found between Δ9 desaturase activity and the percentage of 16∶1 and 18∶1 in the complete-diet period.     

Relationship between mouse liver Δ9 desaturase activity and plasma lipids

This study was undertaken to investigate the total plasma fatty acid composition and the relationship between plasma triacylglycerol (TG) levels and liver Δ9 desaturase activity in mice fed n−3 and/or n−6 fatty acid or hydrogenated coconut oil (HCO) (maximum 25 mg/g) supplemented diets. Generally, plasma TG levels and Δ9 desaturase activity were inversely correlated with the ratio of the sum of long chain n−3 fatty acids to 18∶2n−6 and to the ratio of the sum of long chain n−3 fatty acids to 18∶n−3, but they were positively correlated with the ratio of products and substrates (18∶1/18∶0) of the enzyme in plasma total lipids. The n−3 fatty acid (mainly 20∶5n−3) enriched diet, when compared to the HCO diet at 21 d, caused a significant reduction in plasma TG levels but not in Δ9 desaturase activity. However, a marked reduction in plasma TG content (50–60%) and Δ9 desaturase activity (55–70%) was observed when both 20∶5n−3 and 18∶3n−6 were supplemented in the diet. The plasma TG levels and Δ9 desaturase activity rose again when the animals were fed the HCO diet or chow. The results suggest that low dose supplementation of a mixture of n−3 (mainly 20∶5n−3) and n−6 (18∶3n−6) fatty acids modified both plasma TG content and liver Δ9 desaturase activity, in parallel.     

Effects of zinc deficiency and castration on fatty acid composition and desaturation in rats

The effects of zinc deficiency and testosterone on fatty acid composition of plasma lipids and microsomes of liver, intestine and testes were studied. The activities of fatty acid desaturase (Δ6 and Δ5) in rat liver and testes were also measured. A significant decrease in the level of arachidonic acid was observed in plasma of normal rats fed the zinc-deficient diet. Castration significantly decreased arachidonic acid but increased 20∶3 fatty acid, which is negligible in normal rats. Testosterone and zinc administration restored arachidonic acid to normal values. Zinc deficiency does not significantly change the fatty acid profile in liver, but castration decreased both arachidonic and 22∶6 fatty acid. Intestinal mucosal microsomes showed that the predominant fatty acid in this tissue, palmitic acid, is independent of zinc status, whereas polyunsaturated fatty acids 18∶2 and 20∶4 were decreased by zinc-deficient diet or castration. Zinc deficiency sharply decreased 22∶5 fatty acid and to some extent, other polyunsaturated fatty acids in testis microsomes. These changes in fatty acids are in agreement with increased Δ9 desaturation and decreased Δ5 desaturase activity. In testes, both Δ6 and Δ5 desaturase activities are decreased in zinc deficiency. It appears that zinc influences the conversion of linoleic to arachidonic acid, whereas testosterone influences Δ6 desaturase activity. The data suggest that zinc deficiency may be one of the important factors in the causation of polyunsaturated fatty acid deficiency, which in turn, may induce serum hypertriglyceridemia.     

Effects of oleic,arachidonic and 5,8,11,14-nonadecatetraenoic acids on lipid secretion and ketogenesis in perfused rat liver

The effects of perfused oleic (18∶1n−9), arachidonic (20∶4n−6) and 5,8,11,14-nonadecatetraenoic (19∶4n−5) acids on triglyceride and cholesterol secretion and ketone body production were studied in isolated rat liver. As compared to oleic and 19∶4n−5 acids, both ketone body production and triglyceride secretion were significantly lowered when arachidonic acid was perfused. The concentration of triglyceride in the post-perfused liver was lower upon perfusion with arachidonic acid than upon perfusion with oleic acid or 19∶4n−5 acid. Cholesterol secretion in the liver perfused with arachidonic acid or 19∶4n−5 acid was significantly higher than with oleic acid. The concentration of cholesterol in the post-perfused liver was slightly but significantly higher with 19∶4n−5 acid than with the other fatty acids. The results suggest that 19∶4n−5 acid when compared with arachidonic acid affects lipid metabolism in liver differently.     

Effects of parenteral nutrition with high doses of linoleate on the developing human liver and brain

The developmental changes in the fatty acid composition of ethanolamine phosphoglycerides (EPG) and choline phosphoglycerides (CPG) were studied in the liver and brain of 18 newborn infants with gestational ages ranging from 20 to 44 wk. A small group of five newborns receiving total parenteral nutrition (TPN) with high doses of linoleic acid (18∶2ω6) was also studied and compared to controls of the same gestational age to look for effects on the developmental fatty acid patterns of liver and brain EPG and CPG. TPN with Intralipid 20% was given for 4–12 days, the total fat intake being 14.7–90 g (mean ±S.D.=47.1±29.8 g). The main developmental changes in the liver and brain of the control group were an increase in 22∶6ω3 (docosahexaenoic acid) at the end of gestation and a linear decrease in 20∶4ω6 (arachidonic acid) and 18∶1ω9 (oleic acid) in EPG and CPG. A very good correlation in the percent values of these fatty acids in the brain and liver tissues was obtained. Very significant changes in the fatty acid composition of liver EPG and CPG could be found in the infants receiving TPN with Intralipidmainly an increase in 18∶2ω6, a decrease in the linoleate elongation/desaturation to longer members of the series and a decrease in the 22∶6ω3 levels of liver EPG and CPG. In the brain, only an increase in the 18∶2ω6 value of CPG, not accompanied by any increase in the longer ω6 fatty acids, could be detected. Possible adverse effects of high doses of 18∶2ω6 on the tissue levels of long chain polyunsaturated fatty acids (PUFA), especially of 22∶6ω3, are discussed.     

Desaturase activities in rat model of insulin resistance induced by a sucrose-rich diet

A sucrose-rich diet, as compared with a similar starch diet, induces a time-dependent typical noninsulin-dependent diabetes syndrome characterized by insulin resistance in rats. Within the first 3 wk, there was glucose intolerance associated with hyperinsulinemia, hypertriglyceridemia, and high plasma FFA. In this study, we examined the effect of the sucrose-rich diet vs. the starch diet during short-(3 wk) and long-term treatment (6 mon) on hepatic Δ9, Δ6, and Δ5 desaturases. These enzymes modulate monounsaturated FA and PUFA biosynthesis, respectively. Sucrose feeding (3 wk) caused an initial hyperinsulinemia that was normalized within 6 mon. In the early period (3 wk), stearoyl-CoA desaturase-1 (SCD-1) mRNA and activity were decreased, whereas Δ6 desaturase mRNA abundance and Δ6 and Δ5 desaturase activities remained unchanged. After 6 mon of sucrose feeding, activities of the Δ9, Δ6, and Δ5 desaturases were each increased. The SCD-1 and Δ6 desaturase mRNA were also correspondingly higher. These increases were consistent with an increase in oleic acid, the 20∶4/18∶2 ratio, and 22∶4n−6 and 22∶5n−6 acids in liver and muscle lipids. On the other hand, the percentage of 22∶6n−3 acid was decreased. In conclusion, a sucrose-rich diet after 6 mon induces an increase in rat liver SCD-1 and Δ6 desaturase mRNA and enzymatic activities that are opposite to the changes reported in insulin-dependent diabetes mellitus. It appears that neither blood insulin levels nor insulin resistance is a factor affecting the Δ9, Δ6, and Δ5 desaturase changes in mRNA and activity found with the sucrose-rich diet.     

Effects of dietary triolein and sunflower oil on insulin release and lipid metabolism in zucker rats

Obese and lean male Zucker rats were fed ad libitum on diets containing either 50 (L) or 200 (H) g/kg diet of either triolein (T) or sunflowerseed oil (S). The specific activity of the hepatic microsomal Δ9 desaturase enzyme was depressed in both lean and obese rats fed the HS diet compared with the other three diets. The fatty acid composition of liver and subcutaneous white adipose tissue lipids were consistent with a lower Δ9 desaturation activity in rats fed the H diets, particularly for the HS diet. In both genotypes, microsomal Δ9 desaturase activity and the ratio of 16∶1/(16∶0+16∶1) fatty acids in liver lipids were inversely related to the proportion of 18∶2 in liver lipid. Plasma insulin concentrations and rates of glucose-stimulated insulin release in vivo were higher in obese rats compared with lean rats, and plasma insulin levels were higher in rats fed S compared with T. There was no relationship between Δ9 desaturase activity and either plasma insulin concentration or rates of insulin release in vitro. These findings suggest that hepatic Δ9 desaturase activity of Zucker rats is responsive to changes in the proportion of 18∶2 in liver lipids but is not affected by changes in insulin secretion.     

Interactive effects of prenatal ethanol and N−3 fatty acid supplementation on brain development in mice

This study assesses the combined effects on brain and behavioral development of ethanol administration and supplementation of the maternal diet with long chain n−3 polyunsaturated fatty acids. From day 7 to 17 of gestation, pregnant mice were fed equivalent daily amounts of isocaloric liquid diets; 20% of the energy was provided by either ethanol or maltose-dextrin, and a further 20% by either safflower oil (rich in linoleic acid, 18∶2n−6), or a combination of safflower oil with a fish oil concentrate (rich in eicosapentaenoic acid, 20∶5n−3, and docosahexaenoic acid, 22∶6n−3). On day 18 the liquid diets were replaced by lab chow; a fifth group was maintained on lab chow throughout the experiment. Measures on the pups included brain weight and the fatty acid composition of the brain phospholipids on days 22 and 32 post-conception (birth=day 19), as well as behavioral development. Maternal weight gain during gestation was decreased by ethanol relative to maltose-dextrin, and increased by fish relative to safflower oil. On day 32, the brain weight of ethanoltreated animals fed fish oil was greater than their safflower oil controls, whereas the reverse was true in the two maltose-dextrin groups; a similar trend was apparent on day 22. The brain phospholipid content of the longer chain fatty acids (20∶4n−6, 22∶4n−6, 22∶5n−6, 20∶5n−3, 22∶5n−3, 22∶6n−3) on day 22 reflected that of the prenatal diet, with the proportion of n−3 compounds being higher and that of n−6 floer in the fish oil than safflower oil groups. Prenatal dietary effects were absent by day 32, with the exception of lower 22∶5n−6 in fish oil groups. Dietary supplementation with n−3 fatty acids increased the ratio of 20∶3n−6 to 20∶4n−6, which is consistent with a blockade of the activity of Δ-5 desaturase. On day 22 the incorporation of dietary long chain n−3 fatty acids into the brain phosphatidylcholine fraction was enhanced in the ethanol-treated animals; by day 32 the animals treated prenatally with ethanol also showed increased levels of long chain n−6 compounds. Behavioral development was retarded by ethanol, but there was no effect of the dietary oils. These results support the hypothesis that effects of ethanol on the developing brain may be modified by the availability of an exogenous supply of long chain fatty acids.     

A diet containing myristoleic plus palmitoleic acids elevates plasma cholesterol in young growing swine

The objective of this study was to test the effect of a novel fatty acid mixture, enriched with myristoleic and palmitoleic acids, on plasma lipoprotein cholesterol concentrations. Weanling pigs were assigned to one of six groups and each group received a diet differing in fatty acid composition. Diets were fed for 35 days and contained 10 g added cornstarch/100 g (to provide baseline data) or 10 g added fatty acids/100 g. For those diets containing added fatty acids, extracted lipids contained 36% myristoleic plus palmitoleic acid combined (14∶1/16∶1 diet), 52% palmitic acid (16∶0 diet), 51% stearic acid (18∶0 diet), 47% oleic acid (18∶1 diet), or 38% linoleic acid (18∶2 diet). Witht the exception of the cornstarch diet, all diets contained approximately 30% myristic acid. There were no significant differences in weight gain across treatment groups (P=0.22). All diets caused a significant increase in triglycerides and in total, low density lipoprotein, high density lipoprotein, and very low density lipoprotein cholesterol. The increase in total plasma cholesterol from pretreatment values was greatest in pigs fed the 14∶1/16∶1 and 18∶1 diets. However, the increase in low density lipoprotein cholesterol from the pretreatment concentration was greatest in the 14∶1/16∶1-fed pigs. Increases in very low density lipoprotein cholesterol above pretreatment concentrations were lowest in 16∶0-fed pigs and greatest in 18∶1-fed pigs. Dietary fatty acids elicited changes in plasma fatty acids which generally were reflective of the diets, although the 18∶0 diet did not alter plasma fatty acid concentrations and the 16∶0 diet increased plasma 16∶0 only at the end of the study. These results demonstrated that the combination of myristoleic plus palmitoleic acids increased plasma cholesterol in young pigs, suggesting that fatty acid chain length, rather than degree of unsaturation, is primarily responsible for the effects of fatty acids on circulating lipoprotein cholesterol concentrations.     

Effect of dexamethasone on the fatty acid composition of total liver microsomal lipids and phosphatidylcholine molecular species

Dexamethasone depresses Δ6 and Δ5 and increases Δ9 desaturase and synthase activities. Therefore, we investigated the effect on the fatty acid composition of microsomal liver lipids and phosphatidylcholine (PtdCho) molecular species. After 15 d of treatment we found a notable decrease in arachidonic acid, a small decrease in stearic acid, and increases of linoleic, oleic, palmitoleic, and palmitic acids in liver microsomal total lipids and PtdCho. The study of the distribution of the PtdCho molecular species indicated that 18∶0/20∶4n−6, 16∶0/20∶4n−6, and 16∶0/18∶2n−6 predominated in the control animals. Dexamethasone, as expected because of its depressing effect on arachidonic acid synthesis and activation of oleic and palmitic acid synthesis, evoked a very significant decrease in 18∶0/20∶4n−6 PtdCho (P<0.001) and an important increase in 16∶0/18∶2n−6. The invariability of 16∶0/20∶4n−6 PtdCho could be related to the antagonistic effect of arachidonic and palmitic acid synthesis. PtdCho species containing oleic acid were not significant. The bulk fluidity and dynamic properties of the microsomal lipid bilayer measured by fluorometry using the probes 1,6-diphenyl-1,3,5-hexatriene and 4-trimethylammonium-phenyl-6-phenyl-1,3,5-hexatriene showed no significant modification, probably owing to a compensatory effect of the different molecular species, but changes of particular domains not detected by this technique are possible. However, the extremely sensitive Laurdan detected increased lipid packing in the less-fluid domains of the polar-nonpolar interphase of the bilayer, possibly evoked by the change of molecular species and cholesterol/phospholipid ratio. The most important effect found is the decrease of arachidonic acid pools in liver phospholipids as one of the corresponding causes of dexamethasone-dependent pharmacological effects.     

Severe fatty liver in rats fed a fat-free ethanol diet,and its prevention by small amounts of dietary arachidonate

Rats were fed ethanol and a fat-free diet for 30 days to determine whether dietary fat is needed for the development of fatty liver. The severity of fatty liver was similar to that of rats fed an isocaloric diet with 35% fat. Small amounts (29 mg/day) of dietary arachidonic acid prevented alcoholic fatty liver. Rats fed either the alcohol (AF) or control (CF) fat-free diets developed essential fatty acid deficiency (EFAD) as measured by the triene/tetraene ratio of liver and plasma lipids. Rats fed arachidonic acid (AA, alcohol and CA, control diets) did not develop EFAD. Although EFAD alone did not cause the development of fatty liver, the combination of dietary ethanol and EFAD did. The ratios of 16∶1/16∶0 and 18∶1/18∶0 in liver lipids indicated that desaturase enzymes were less active and lipogenesis was reduced in rats fed the AA diet compared to those fed the AF diet. In contrast, stimulated lipogenesis appears to have been the cause of fatty liver in rats fed the AF diet. Presented at the XII International Congress of Nutrition, San Diego, CA, August 1981. Abbreviations: Diets are indicated as fat-free with ethanol (AF), fat-free without ethanol (CF), or similar diets with 0.9% of the calories as arachidonic acid with (AA) or without (CA) ethanol. The composition of these diets is discribed in the text and Table 1.     

Long chain fatty acid deficits in brain myelin sphingolipids of undernourished rat pups

A restricted maternal dietary intake (40% of ad libitum intake) is known to cause myelin deficit that is accompanied by decreased amounts of individual phospholipids and sphingolipids in brain myelin of suckling rats. This communication reports the effects of the same nutritional stress on the fatty acid composition of brain myelin lipids. In myelin of 19-day-old normally fed rats, palmitate (16∶0), stearate (18∶0) and oleate (18∶1) accounted for 80–90% of all fatty acids in phosphatidylcholine, phosphatidylethanolamine and phosphatidylserine. Maternal dietary restriction resulted in deficits of total fatty acid content, but did not affect the proportional distribution of individual fatty acids among phospholipids. By contrast, longer chain (22- and 24-carbon) fatty acids accounted for more than half the fatty acid content of myelin cerebroside and sulfatide from the 19-day-old control rat pups. In undernourished rats of that age, proportions of lignocerate (24∶0) and nervonate (24∶1) in cerebroside and sulfatide were 40–50% lower than those in control rats. This, together with higher proportions of 16∶0, 18∶0 and 18∶1 and a higher ratio of C₁₆−C₂₀ to C₂₂−C₂₄ in under-nourished than in control rats, suggests an impairment in fatty acid chain elongation. Ten days of nutritional rehabilitation failed to restore the fatty acid imbalances; however, after an additional 5 days of ad libitum feeding, the experimental and control values were similar. The undernutrition results in hypomyelination, which is characterized by a proportional decrease in lignoceric and nervonic acids of sphingolipids.     

Dietary cholesterol modulates Δ6 and Δ9 desaturase mRNAs and enzymatic activity in rats fed a low-EFA diet

The effects of a 1% addition of cholesterol to a diet low in EFA on FA desaturases were examined. The administration of cholesterol markedly increased the esterified cholesterol content in microsomes and total liver lipids from the first day, whereas the proportion of free cholesterol remained unaltered throughout the treatment. An excellent homeostasis in the free cholesterol content was apparently evoked by the acyl-CoA cholesterol acyltransferase. The cholesterol esters were mainly oleate, palmitate, and stearate, and the addition of cholesterol increased the relative proportions of cholesterol palmitoleate and oleate. The addition of cholesterol to a low-EFA diet induced, as in animals fed a high-FFA diet, a marked increase in liver stearoyl-CoA desaturase-1 mRNA and enzyme activity. This increased activity apparently evoked a similar enhancement of palmitoleic and oleic acids in total and microsomal liver lipids. The cholesterol-rich diet depressed the liver Δ6 and Δ5 desaturase activity. However, the abundance of Δ6 desaturase mRNA was not modified throughout the treatment. This indicates that the depressive effect is evoked at a step beyond that controlled by the mRNA level. The depression of both enzymatic activities was consistent with the decrease in the percentages of arachidonic acid and DHA in total and microsomal liver lipids. Taken together, these results indicate that through its modulating effect on the desaturases, dietary cholesterol may lead an animal or humaan fed low-EFA diet to a true deficiency by the decreased synthesis of the highly polyunsaturated acids derived from linoleic and α-linolenic acids.     

Desaturation of fatty acids inTrypanosoma cruzi

Uptake and metabolism of saturated (16∶0, 18∶0) and unsaturated [18∶1(n−9), 18∶2(n−6), 18∶3(n−3)] fatty acids by cultured epimastigotes ofTrypanosoma cruzi were studied. Between 17.5 and 33.5% of the total radioactivity of [1-¹⁴C]labeled fatty acids initially added to the culture medium was incorporated into the lipids ofT. cruzi and mostly choline and ethanolamine phospholipids. As demonstrated by argentation thin layer chromatography, gas liquid chromatography and ozonolysis of the fatty acids synthesized, exogenous palmitic acid was elongated to stearic acid, and the latter was desaturated to oleic acid and 18∶2 fatty acid. The 18∶2 fatty acid was tentatively identified as linoleic acid with the first bond in the Δ9 position and the second bond toward the terminal methyl end. Exogenous stearic acid was also desaturated to oleic and 18∶2 fatty acid, while oleic acid was only converted into 18∶2. All of the saturated and unsaturated fatty acids investigated were also converted to a small extent (2–4%) into polyunsaturated fatty acids. No radioactive aldehyde methyl ester fragments of less than nine carbon atoms were detected after ozonolysis of any of the fatty acids studied. These results demonstrate the existence of Δ9 and either Δ12 or Δ15 desaturases, or both, inT. cruzi and suggest that Δ6 desaturase or other desaturases of the animal type are likely absent in cultured forms of this organism.     

Effect of specific dietary fatty acids on lipogenesis in the livers and mammary glands of lactating mice

The effects of linoleic, linolenic and columbinic acids fed as 4% of a high carbohydrate (50% glucose) diet on the activities and the amounts of several enzymes associated with fatty acid synthesis in livers and mammary glands of lactating mice were compared with those for stearic and oleic acids. Fatty acid synthesis, measured in vivo, was significantly lower in livers of mice ingesting all 3 polyunsaturated fatty acids (PUFA), whereas in mammary glands synthesis was lower only in mice receiving columbinic acid. The activities of fatty acid synthetase (FAS) and acetyl CoA carboxylase were significantly reduced in liver by all 3 PUFA, as were activities of glucose-6-phosphate dehydrogenase, malic enzyme (ME) and citrate cleavage enzyme (CCE), also associated with lipogenesis. In mammary gland, on the other hand, the activities of these enzymes were unaffected by dietary PUFA. The tissue contents of FAS, ME and CCE, measured by rocket immunoelectrophoresis, were found to be significantly reduced in liver by linoleate, linolenate and columbinate but were not significantly altered in mammary gland. The decrease in hepatic lipogenesis observed was principally due to a decrease in the amounts of these enzymes induced by the dietary PUFA but the inhibition in mammary gland caused by columbinate could not be accounted for by a reduction in enzyme contents and therefore may be due to allosteric effects which occur when fatty acid synthesis is measured with³H₂O. The fatty acid composition in liver and mammary gland of dams and in liver and kidney of pups completely reflected dietary fatty acids. Columbinate made up ca. 20% of the total fatty acids in both tissues of the columbinic acid-fed mice and ca. 15% in the pup tissues. This suggests that columbinate is incorporated into milk lipids of dams and is easily absorbed by pups. The elevated ratios of 16/16∶1 and 18/18∶1 in liver and mammary gland of dams and liver and kidney of the pups from dams fed linoleate, linolenate and columbinate suggest that each of these polyunsaturated fatty acids in the diet can inhibit the activity of Δ9 desaturase.     

Effect of diet on triglyceride structure and composition of egg yolk lipids

Hens were fed a practical diet supplemented and unsupplemented with 5% menhaden oil and a synthetic fat-free diet for a period of 90 days. Egg yolks from hens fed each of the three diets were analyzed for fatty acid composition and positional distribution of the fatty acids by successive chromatographic techniques. The triglycerides were resolved into fractions containing, 0, 1, 2 and 3+ double bonds per molecule. Each of these types was quantitated and analyzed for fatty acid distribution. The positional distribution was determined with the aid of pancreatic lipase hydrolysis. The feeding of the practical diet supplemented with 5% menhaden oil produced an increase in the 14∶0 acid in the intact triglycerides, 2-monoglycerides and 1,3-diglycerides with the majority of this acid being bound in the 1,3 positions. In the monounsaturated triglycerides the 16∶0 acid was linked predominantly at the 1,3 positions. The feeding of the fat-free diet produced a decrease in the 16∶1 acid content of the egg yolk lipids in the monounsaturated series, in the intact triglycerides, the 2-monoglycerides and the 1,3-diglycerides. The 18∶0 acid was linked more often at the 1,3 positions than at the 2 position, and was not affected by the diet consumed by the hens. Hens fed the fat-free diet produced more monounsaturated and diunsaturated triglycerides than those fed the other diets. Linoleic acid exhibited the greatest degree of preference for the 2 position, which was followed in turn by oleic acid. All other major acyl components were found to be preferentially esterified at the 1,3 positions. The difference observed in the fatty acid composition of egg yolk neutral and polar lipids was attributable to the fatty acid content of the diet. In the case of the oleic and linoleic acids, there was less variation in the saturated fatty acid content, which could be traced to the type of diet fed.     

Effects of feeding Lunaria oil rich in nervonic and erucic acids on the fatty acid compositions of sphingomyelins from erythrocytes, liver, and brain of the quaking mouse mutant

Feeding an oil from Lunaria biennis rich in 22∶1n−9 and 24∶1n−9 to homozygous quaking (qk.qk) mice caused a large increase in the percentage of 24∶1n−9 and corresponding decreases in the percentage of 24∶0 and 22∶0 in sphingomyelins from liver, erythrocytes, and milk. Brain sphingomyelin from 2-wk-old qk.qk pups born to qk.qk mothers maintained on the Lunaria oil had essentially normal percentage of 24∶1n−9 and 18∶0, in contrast to pups born to mothers maintained on a control oil rich in 18∶1n−9 whose brain sphingomyelin had a markedly reduced percentage of 24∶1n−9 and an increased percentage of 18∶0. After 2 wk and up to and beyond weaning, the qk.qk pups from Lunaria-fed mothers weaned on to the Lunaria diet had a markedly decreased percentage of 24∶1n−9 in their brain sphingomyelin, accompanied by an increased percentage of 18∶0, as compared to heterozygous quaking mice. However, the percentage of 24∶1n−9 in brain sphingomyelin in qk.qk pups weaned on to the Lunaria diet continued throughout this period (2–8 wk postbirth) to be significantly higher than in qk.qk pups weaned on to the control diet. We conclude that dietary 24∶1n−9 influences the fatty acid composition of brain sphingomyelin in qk.qk mice, but only via the mother in pre- or early postnatal animals. We further consider that the dietary effects may be elicited mainly in the sphingomyelin of nonmyelinated brain cells, and that the nervonic acid in myelin sphingomyelin may be formed mainly by chain elongation in oligodendrocytes from shorter chain fatty acid precursors.     

Hypothyroidism and thyroxin substitution affect the n−3 fatty acid composition of rat liver mitochondria

The effects of hypothyroidism and of daily treatment for up to 21 days with thyroxin (T4, 0.5 μg/100 g body weight) on the fatty acid composition of total lipid, phosphatidylethanolamine, and phosphatidylcholine of rat liver mitochondria were studied. The fatty acid compositions of hypothyroid and euthyroid (control) rats of similar age were compared. The n−6 and n−3 polyunsaturated fatty acids (PUFA) were affected differently by the hypothyroid state. The levels of linoleic (18∶2n−6), γ-linolenic (18∶3n−6) and dihomo-γ-linolenic acids (20∶3n−6) were higher in hypothyroid rats than in controls, while the level of arachidonic acid (20∶4n−6) was lower, which suggests an impairment of the elongase and desaturase activities. The n−3 polyunsaturated fatty acids, eicosapentaenoic (EPA, 20∶5n−3) and docosapentaenoic (22∶5n−3) acids, were higher in hypothyroid rats, whereas the linolenic acid (18∶3n−3) content remained constant. The level of docosahexaenoic acid (DHA, 22∶6n−3) was dramatically decreased in hypothyroid rats, while the levels of C₂₂ n−6 fatty acids were unchanged. The differences were probably due to the competition between n−3 and n−6 PUFA for desaturases, elongases and acyltransferases. When hypothyroid rats were treated with thyroxin, the changes induced by hypothyroidism in the proportions of n−6 fatty acids were rapidly reversed, while the changes in the n−3 fatty acids were only partially reversed. After 21 days of thyroxin treatments, the DHA content was only half as high in hypothyroid rats than in euthyroid rats. These results suggest that the conversion of 18∶2n−6 to 20∶4n−6 is suppressed in the hypothyroid state which favors the transformation of 18∶3n−3 to 20∶5n−3. The marked decrease in DHA content indicates an impairment of the enzymes involved in the DHA metabolism, possibly the n−3 Δ4 desaturase or the acyltransferases. The increased levels of EPA and 22∶5n−3 is consistent with the inhibition of the n−3 pathway at the Δ4 desaturase step. Observed modifications in the fatty acid composition may significantly alter eicosanoid synthesis and membrane functions in hypothyroidism.     

Effect of dietary fats on desaturase activities and the biosynthesis of fatty acids in rat-liver microsomes

Four groups of rats were fed diets containing 15% (w/w) high-oleic safflower oil (SFO, rich incis-18∶1 acids), a mixture of 80% partially hydrogenated soybean oil plus 20% corn oil (H+CO, rich intrans-18∶1 acids), lard (L, rich in saturated fatty acids) and corn oil (Co, rich in 18∶2ω6). Fatty acid composition of liver microsomes and activities of the Δ⁵, Δ⁶ and Δ⁹ desaturases were determined. Microsomal Δ⁶ desaturase activity and arachidonic acid were lower in the H+CO group compared with SFO of L. No difference was found in the Δ⁵ or Δ⁶ desaturase activity of CO and SFO groups. Thus, the oleic-acid level of the SFO diet had no effect on the metabolism of 18∶2ω6. Fluorescent polarization studies, usingtrans-parinaric acid as a probe, showed no differences between the physical states of phospholipid vesicles made from lipids isolated from each group. We concluded that thetrans-18∶1 acids in partially hydrogenated soybean oil have a more inhibitory effect than saturated acids on EFA metabolism, even in the presence of adequate amounts of essential fatty acid.