Glyceride metabolism in the myopathic hamster

Analysis of plasma lipids of 30- and 185-day-old BIO 82.62 myopathic hamsters and age-matched normal controls revealed a decrease in only the concentration of cholesteryl esters of 185-day-old diseased animals. Measurement of lipoprotein lipase (LPL) activity in heart, muscle, and adipose tissue showed no difference between the activity of the enzyme in the heart and muscle of the cardiomyopathic hamsters and that of the age-matched controls. In adipose tissue, however, LPL activity was depressed in the diseased animals in both age groups. No difference was found in the activity of hormone sensitive lipase. Incorporation of sn[U-¹⁴C] glycerol-3-phosphate into total lipids was found to be depressed in homogenates of heart, muscle, and adipose tissue but unchanged in liver homogenates of diseased animals. It was concluded that the decrease in the capacity to synthesize glycerides, rather than limiting substrate concentrations, could be the cause of the decrease in the lipid content in some tissues of the cardiomyopathic hamster.     

Lipid content and fatty acid composition of heart and muscle of the BIO 82.62 cardiomyopathic hamster

Microscopic and analytical studies of the lipids in the heart and muscle of the BIO 82.62 myopathic hamsters and agematched normal animals at the average ages of 33, 67, and 108 days were performed. Microscopic examinations did not show increased lipid depositions in the hearts of the diseased animals as was found in the BIO 14.6 strain. No consistent differences in the lipid content of the cardiomyopathic hamsters (BIO 82.62) and age-matched controls were observed in the three age groups except in the cholesterol content of muscle. Cholesterol increased significantly (P<0.01) in the 67 and 108 day old animals. This increase elevated the cholesterol/phospholipid ratio. Analysis of the fatty acid composition of triglycerides showed that the cardiomyopathic hamsters store more saturated fatty acids in both heart and muscle than do their normal counterparts. The abundance of more saturated fatty acids may imply that either the desaturation mechanism is altered in the diseased animals or that unsaturated fatty acids are preferentially utilized in other processes.     

Δ9 desaturase activity in bovine subcutaneous adipose tissue of different fatty acid compositiondesaturase activity in bovine subcutaneous adipose tissue of different fatty acid composition

Two experiments were conducted to investigate the relationship between Δ⁹ desaturase (stearoyl-coenzyme A desaturase) activity and fatty acid composition in subcutaneous adipose tissue from cattle of different backgrounds. In Experiment 1, subcutaneous adipose tissue samples were taken from carcasses of pasture-fed cattle and feedlot cattle fed for 100, 200, or 300 d. Adipose tissue from pasture-fed cattle had significantly lower total saturated fatty acids and higher total unsaturated fatty acids than feedlot cattle. Desaturase activity correspondingly was 60–85% higher in pasture-fed cattle than in feedlot cattle. There was no difference in the fatty acid composition or desaturase activity among samples from the 100-, 200-, and 300-d feedlot cattle. In Experiment 2, adipose tissue samples were collected from carcasses of feedlot cattle fed for 180 d with either a standard feedlot ration (control group), or a ration containing rumen-protected cottonseed oil (CSO) for the last 70–80 d. Adipose tissue from the CSO-fed cattle was more saturated than that from the control group, having significantly more 18∶0 and less 16∶1 and 18∶1. Correspondingly, adipose tissue from the CSO group had significantly lower desaturase activity. The elevated 18∶2 in adipose tissue from the CSO group confirmed that unsaturated fatty acids (including cyclopropenoid fatty acids) were protected from biohydrogenation. Further studies are needed to determine whether the repression of desaturase activity results from direct inhibition by cyclopropenoic acids or by higher dietary contents of 18∶2.     

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.     

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 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.     

Changes in the fatty acid composition of rat lung lipids during development and following age-dependent lipid peroxidation

Analyses of the fatty acid content and composition of various lung lipids were conducted in rats 1 day, 5 days, and 12 days after birth and in adult animals in order to define more clearly the specific lipid peroxidizing system found in neonatal rat lungs. Lipid peroxidation occurs in the 900×g supernatant fraction of rat lung homogenates in an age-dependent manner independent of the addition of any factor and is maximal at 5 days of age. No lipid peroxidation is evident in similar preparations of either newborn or adult lung tissue. As the animals develop, arachidonic and docosahexaenoic acids, fatty acids which are both highly susceptible to lipid peroxidation in the presence of a suitable catalyst, decrease gradually when measured as the percentage of the total fatty acids in the triglyceride fraction of the lung. The total quantity of triglycerides, however, is significantly lower in lungs from 1-day-old rats than at any other age. The fatty acid composition and total quantity of both lung phospholipids and lung free fatty acids do not show similar changes. Following in vitro incubation of the 900×g supernatant fraction of peroxidizing lung homogenates, an appreciable decrease in the amount of arachidonic and docosa-hexaenoic acid could be detected in lung triglycerides. Less extensive decreases were observed in the phospholipid fraction. No changes in these components were observed in newborn or adult animals. The addition of triarachidonin to the 900×g supernatant fraction of lung homogenates resulted in increased malondialdehyde release at all ages tested while added arachidonic acid increased the formation of malondialdehyde only in 5- and 12-day-old rat lung preparations. The addition of triolein, cholesterol arachidonate, and diarachidonyl phosphatidylcholine had no effect on malondialdehyde formation at any age. The age-dependent lipid peroxidation observed after in vitro incubation of rat lung homogenate preparations, therefore, may result from the relatively high concentration of triglycerides containing polyunsaturated fatty acids present in the neonatal tissue. As the susceptible polyunsaturated fatty acids of lung triglycerides are replaced by less unsaturated species, this activity may diminish concomitantly. Recipient of Public Heath Service Research Career Development Award 5-K04-HD00068 from the National Institute of Child Health and Human Development.     

The influence of dietary fat on the lipogenic activity and fatty acid composition of rat white adipose tissue

The in vivo fatty acid synthesis rate, selected enzyme activities and fatty acid composition of rat white adipose tissue from animals fed semisynthetic diets of differing fat type and content were studied. All animals were starved for 48 hr and then refed a fat-free (FF) diet for 48 hr. They were then divided into three groups. One group was continued on the FF diet for 48 hr. Another group was fed a diet containing 44% of calories from corn oil (CO). The final group was fed a diet containing 44% of calories from completely hydrogenated soybean oil (HSO). The animals on the FF diet had a marked increase in adipose tissue fatty acid synthesis during the 96-hr feeding peroid (as measured by³H incorporation into adipose fatty acids). Addition of either CO or HSO to the diets did not significantly inhibit fatty acid synthesis in dorsal or epididymal adipose tissue. The activities of the enzymes' fatty acid synthetase, ATP-citrate lyase and glucose-6-phosphate dehydrogenase increased on the FF diet and generally were not inhibited significantly by the addition of either fat to the diets. Linoleic acid was the major polyunsaturated fatty acid (ca. 22%) in adipose tissue. Monounsaturated fatty acids (palmitoleic, oleic,cis-vaccenic) made up ca 38% of the total adipose fatty acids, while saturated fatty acids accounted for about 32% (myristic, palmitic and stearic). White adipose tissue in mature male rats was a major depot for n−3 fatty acids. There were differences in the fatty acid composition of epididymal and dorsal adipose tissue, particularly in their content of long chain, polyunsaturated fatty acids with epididymal tissue containing more of these compounds than dorsal fat. The fatty acid composition of the white adipose tissue did not change significantly during fasting or 96 hr of refeeding the FF diets. The addition of HSO to the diet for 48 hr had little influence on the adipose tissue fatty acid composition, but the addition of CO to the diet caused a 7% increase in the dorsal adipose tissue linoleate content (as percentage of total dorsal adipose tissue fatty acids) within 48 hr compared to animals fed the stock diet and those starved for 48 hr. The fatty acid synthesis data indicated that adipose tissue in the rat can continue to be a source of de novo fatty acid synthesis in animals consuming high-fat diets.     

Growth Hormone Enhances Arachidonic Acid Metabolites in a Growth Hormone Transgenic Mouse

In a transgenic growth hormone (GH) mouse model, highly elevated GH increases overall growth and decreases adipose depots while low or moderate circulating GH enhances adipose deposition with differential effects on body growth. Using this model, the effects of low, moderate, and high chronic GH on fatty acid composition were determined for adipose and hepatic tissue and the metabolites of 20:4n-6 (arachidonic acid) were characterized to identify metabolic targets of action of elevated GH. The products of Δ-9 desaturase in hepatic, but not adipose, tissue were reduced in response to elevated GH. Proportional to the level of circulating GH, the products of Δ-5 and Δ-6 were increased in both adipose and hepatic tissue for the omega-6 lipids (e.g., 20:4n-6), while only the hepatic tissues showed an increase for omega-3 lipids (e.g., 22:6n-3). The eicosanoids, PGE₂ and 12-HETE, were elevated with high GH but circulating thromboxane was not. Hepatic PTGS1 and 2 (COX1 and COX 2), SOD1, and FADS2 (Δ-6 desaturase) mRNAs were increased with elevated GH while FAS mRNA was reduced; SCD1 (stearoyl-coenzyme A desaturase) and SCD2 mRNA did not significantly differ. The present study showed that GH influences the net flux through various aspects of lipid metabolism and especially the desaturase metabolic processes. The combination of altered metabolism and tissue specificity suggest that the regulation of membrane composition and its effects on signaling pathways, including the production and actions of eicosanoids, can be mediated by the GH regulatory axis.     

Fatty acid composition of triglycerides from adipose tissue transplanted between obese and lean mice

The subcutaneous adipose tissue of genetically obese mice (ob/ob) differs from that of lean litter-mates not only by virtue of its larger cells but also in its fatty acid composition; it contains a higher proportion of palmitoleic acid and a lower proportion of linoleic acid. To determine whether these differences in fatty acid composition were inherent in fat cells, subcutaneous adipose tissue from obese and lean mice was transplanted under the kidney capsules of lean and obese host mice and the fatty acid composition of the neutral lipids of the graft and of the host perirenal and subcutaneous fat was determined 1 or 2 months later. The fatty acid composition of grafts from lean donors in obese mice resembled that of the perirenal adipose tissue of the obese hosts after 1 month, with a lower proportion of linoleic acid and a higher proportion of palmitoleic acid than in lean mice. Grafts from obese mice in lean mice had fatty acid compositions which were either unchanged, partially changed or which completely resembled that of the host. The use of grafts prelabeled by feeding the donor margaric acid indicated that total lack of fatty acid turnover, rather than selective metabolic processes, was responsible for the failure of some grafts from obese mice in lean mice to acquire the fatty acid composition of the perirenal adipose tissue of the host.     

Altered fatty acid desaturation and microsomal fatty acid composition in the streptozotocin diabetic rat

Streptozotocin diabetes in the rat diminishes the synthesis of both monounsaturated and polyunsaturated fatty acids. Rat liver microsomal fatty acid composition and fatty acid desaturation were studied in the streptozotocin diabetic rat. The major alterations in fatty acid composition found in the diabetic rat were decreased proportions of palmitoleic, oleic and arachidonic acids and an increased proportion of linoleic and docosahexaeneoic acids. These findings, other than the increased docosahexaeneoic acid, probably result from the diminished liver microscomal δ9 and δ6 desaturase activities found in these animals. These changes are not due to the diminished weight gain of the diabetic animals since restricting food intake of control animals to achieve a similar weight gain failed to reproduce either the changes in fatty acid composition or the decrease in fatty acid desaturation. The increased food intake of the diabetic animal may contribute to the altered proportions of linleic and arachidonic acids since limiting food intake in diabetic animals to that of normal controls diminished the magnitude of these changes. Insulin therapy for 2 days not only reverses and overcorrects the diminished desaturase activities, but likewise reverses and overcorrects the altered fatty acid composition, with the exception of the diminished arachidonic aicd levels which are further decreased following insulin therapy. These findings strongly suggest that most of the changes in fatty acid composition in the diabetic rat are indeed caused by the diminished fatty acid desaturase activities.     

Variations of fatty acid composition of erythrocyte and plasma lipids in the rat during the first period of life

The changes occurring in the fatty acid composition of the erythrocyte lipids during the first weeks of life were studied in the rat. The major changes consisted of a progressive decrease in oleic acid and a progressive increase in linoleic acid. A lower but significant increase in arachidonic acid was also observed. These changes are not related to variations in erythrocyte age; rather, they appear to be related to the age of the animal. Since somewhat similar changes were observed in the fatty acid composition of the major lipid classes of plasma during the first weeks of life, the possibility that these variations could account for the changes in the fatty acid composition of erythrocyte lipids was considered. Some support to this possibility was found in the results of experiments in which erythrocytes taken from 15-day-old rats were incubated with plasma taken from newborn rats. The changes in the fatty acid composition of erythrocytes and plasma lipids do not appear to be dependent on dietary lipids, since they occur during the suckling period, i.e., before the rats begin to ingest the pelleted diet which presents a fatty acid pattern completely different to that of the dams' milk.     

Influence of medium-chain triglycerides on lipid metabolism in the rat

Lipid metabolism was studied in rats fed diets containing corn oil, coconut oil, or medium-chain triglyceride (MCT), a glyceride mixture containing fatty acids of 8 and 10 carbons in length. The ingestion of MCT-supplemented, cholesterolfree diets depressed plasma and liver total lipids and cholesterol as compared with corn oil-supplemented diets. In rats fed cholesterol-containing diets, plasma cholesterol levels were not influenced by dietary MCT, but liver cholesterol levels were significantly lower than in animals fed corn oil. In vitro cholesterol synthesis from acetate-1-¹⁴C was lower in liver slices of rats that consumed MCT than in similar preparations from corn oil-fed rats. Studies of fatty acid carboxyl labeling from acetate-1-¹⁴C and the conversion of palmitate-1-¹⁴C to C₁₈ acids by liver slices showed that chain-lengthening activity is greater in the liver tissue of rats fed MCT than in the liver of animals fed corn oil. The hepatic fatty acid desaturation mechanisms, evaluated by measuring the conversion of stearate-2-¹⁴C to oleate, was also enhanced by feeding MCT. Adipose tissue of rats fed MCT converts acetate-1-¹⁴C to fatty acids at a much faster rate than does tissue from animals fed corn oil. Evidence is presented to show that the enhanced incorporation of acetate into fatty acids by the adipose tissue of rats fed MCT represents de novo synthesis of fatty acids and not chain-lengthening activity. Data are also presented on the fatty acid composition of plasma, liver, and adipose tissue lipids of rats fed the different fats under study.     

Effect of PUFA at sn‐2 position in dietary triacylglycerols on the fatty acid composition of adipose tissues in non‐ruminant farm animals

The influence of the distribution of polyunsaturated fatty acids on the glycerol backbone of dietary triacylglycerols on the fatty acid profile of adipose tissue and muscle phospholipids was investigated in growing‐finishing pigs (48) and broiler chicken (84). The animals were fattened on barley/soybean meal diets supplemented with a blend of soybean oil and beef tallow, either in the ratio 3:1 w/w (high‐PUFA) or 1:3 w/w (low‐ PUFA). Part of the high‐ and low‐PUFA blends was chemically interesterified to randomly distribute all fatty acids over the three positions of the glycerol. Thus, two sets of diets of identical overall fatty acid composition, but differing in the distribution of fatty acids in the triacylglycerols, were fed. Growth performance and carcass composition were neither affected by fatty acid composition nor by randomisation of dietary fats in either animal species. Apparent digestibility of energy was slightly lower in pigs fed the low‐PUFA blends. Fatty acid profile of subcutaneous fat of pigs and broilers as well as of internal body fat (lamina subserosa) and muscle phospholipids of pigs varied according to the dietary fatty acid composition but was not affected by randomisation of dietary fats. These findings are explained in terms of the hydrolysis of TAG during transport of lipids from enterocytes to adipose tissue cells and the continuous lipolysis and re‐esterification of fatty acids that take place in adipose tissue cells.     

A critical review of methods used to estimate linoleic acid Δ6‐desaturation ex vivo and in vivo

Δ6‐desaturase is located in a pivotal position in the metabolism of essential fatty acids (EFA). Various methods have been used to estimate Δ6‐desaturase activity, including the assessment of: (i) tissue fatty acid compositions (and associated product/precursor ratios), (ii) Δ6‐desaturase activities ex vivo, and (iii) isotopically labelled linoleic acid metabolism in vivo. This review critically examines these methods and considers their appropriateness and reliability in assessing linoleic acid metabolism in diabetes and cardiovascular disease. In general, there was a good agreement between the three methods and the effect of experimental diabetes on linoleic acid metabolism. In humans, however, the effect of diabetes on tissue fatty acid composition was inconsistent, and there was a paucity of data on linoleic acid metabolism ex vivo and in vivo. The inconsistency in human fatty acid compositional data may relate to variable and uncontrolled intakes of linoleic acid and its n‐6 metabolites, but also to a less extreme insulin deficiency as studied in animals. Risk markers for cardiovascular disease generally reduced rat liver Δ6‐desaturase activity ex vivo. This was not, however, reflected in tissue fatty acid compositions in these controlled studies. Linoleic acid metabolism, as determined by tissue fatty acid composition in humans, is reduced in cardiovascular disease; however, the omnivorous dietary patterns and decreased linoleic acid intakes make this conclusion potentially unreliable. Few stable‐isotope studies have been conducted on the effect of cardiovascular risk markers on linoleic acid metabolism, and there is a requirement for this type of work to be standardised to facilitate inter‐study comparisons. These studies may eventually help optimise EFA intake in health and disease conditions.     

Changes in tissue polyunsaturated fatty acids with age, in spontaneously hypertensive rats

The relationship between the biosynthesis of long-chain fatty acids and their distribution in the key organs of hypertension is of considerable interest because of their role in the production of vasoactive eicosanoids and their effects on membrane properties. The present study analyzed the fatty acid compositions of the total lipids in the kidney, aorta, heart, and hepatocytes of 1-, 3-, and 6-mon-old spontaneously hypertensive rats (SHR) and their normotensive controls, Wistar Kyoto rats (WKY) by capillary gas chromatography. The major changes concerned the polyunsaturated fatty acids (PUFA). The percentage of arachidonic acid (AA) was significantly greater in the 1-mon-old SHR kidney than in the WKY kidney, but it was lower at 3 and 6 mon. The percentage of eicosapentaenoic acid was very low in the SHR kidney. The results for the aorta were similar, with marked decreases in 18:2n−6 and 18:3n−3 in SHR aged 1 and 6 mon. Despite a higher proportion of 18:2n−6 and AA at 6 mon, there was no major change in the SHR heart lipids. The fatty acid spectrum in the liver provides additional evidence for the previously reported inhibition of desaturase activities in SHR. Thus, this study shows that the PUFA composition is modified differently in different tissues in SHR, and this may be related to the pathogenesis of hypertension in these animals.     

Effect of simvastatin on desaturase activities in liver from lean and obese zucker rats

The effect of simvastatin, a hypocholesterolemic drug, on the biosynthesis of arachidonic acid was studied in obese and lean Zucker rats. After administration of 2 mg/kg body weight/d for 13 d, Δ6 and Δ5 desaturase activities were measured in liver microsomes at two substrate concentrations. In untreated rats, the Δ6 desaturation rate was similar in the obese and lean rats when measured at saturating substrate levels, whereas Δ5 desaturation was lower in the obese animals. Treatment with simvastatin did not change Δ6 desaturation in either phenotype but increased Δ5 desaturation in obese rats to reach the unchanged rate observed in lean animals. The changes were not reflected in the fatty acid composition of liver microsomal phospholipids when expressed as μg fatty acid/g of liver.     

Hepatoma,host liver,and normal rat liver neutral lipids as affected by diet

Groups of normal and hepatoma (7288CTC) bearing rats were maintained on normal chow and fat-free diets for 4 weeks. Normal liver, host liver, and hepatoma neutral lipids were examined in detail and compared. Water content, unaffected by diet was: hepatoma, 82 percent; host liver, 71 percent; and normal liver, 67 percent. The fat-free diet had no effect upon the hepatoma neutral lipids but elevated the triglyceride level in normal and host liver, shifted the triglyceride carbon number distribution to lower mol wt, and elevated the percentage of monoenoic acids in triglycerides and cholesteryl esters. Host triglyceride concentrations were ca. half, and cholesterol levels were reduced moderately relative to normal liver values. Hepatoma cholesterol levels were higher and triglyceride concentrations lower than normal and host liver values. Hepatoma triglycerides differed dramatically from liver and were characterized by increased concentrations of high mol wt species and a fivefold increase in the percentage of C-20 and C-22 fatty acids. The percentage of C-20 and C-22 fatty acids in hepatoma cholesteryl esters also increased ca. fivefold relative to liver. The data indicate that the systems that regulate triglyceride and cholesteryl ester fatty acid composition in liver do not control the compositions of these lipid classes in this hepatoma. The unchanged high level of essential fatty acids in the hepatoma lipids from the fat-free fed animals demonstrates the hepatoma's ability to absorb and conserve specific fatty acids.     

Effect of subacute toxic levels of dietary cyclopropenoid fatty acids upon membrane function and fatty acid composition in the rat

The effect of subacute toxicity levels of dietary cyclopropenoid fatty acids upon several physiological parameters was determined in the rat. Diets containing 2% corn oil, 2%Sterculia foetida oil or 2% hydrogenatedSterculia foetida oil were fed.Sterculia foetida oil (50% cyclopropenoid fatty acids) fed rats exhibited retarded growth, elevated organ to body wt ratios, increased saturation of tissue lipid, and abnormal histopathology when compared to corn oil and hydrogenatedSterculia foetida oil fed rats. Growth was retarded 50%, liver/body wt doubled, and the percentage of saturated fatty acids in adipose tissue increased 2.5-fold forSterculia foetida oil vs. corn oil comparisons. Three membrane systems were examined in corn oil andSterculia foetida oil fed rats. Erythrocyte hemolysis rate in 0.3 M glycerol was increased by 30%; induction of mitochondrial swelling by reduced glutathione was inhibited completely and microsomal codeine demethylase activity was depressed nearly 50% inSterculia foetida oil fed rats. The ability of cyclopropenoid fatty acids to inhibit fatty acyl desaturase and influence tissue and membrane lipid composition is discussed. Most of the detrimental effects observed in cyclopropenoid fatty acids fed rats may be associated with alteration of normal lipid metabolism and membrane function.     

Regulation of polyunsaturated fatty acid metabolism in tissue phospholipids of obese (fa/fa) and lean (fa/−) Zucker rats. 1. Effect of dietary lipids on cardiac tissue

The present investigation addressed three questions: (i) Does the obese syndrome alter the fatty acid composition of cardiac tissue and membrane phospholipids in obese (fa/fa) rats? (ii) Are changes, if they occur, similar to those reported for tissues of the genetically obese (ob/ob) mouse? (iii) Can cardiac tissue phospholipids and their component fatty acids be modified by dietary lipids and if so does this occur to the same extent in both fa/fa and lean (Fa/?) rats? Proportions of polyunsaturated fatty acids (PUFA) in cardiac total phospholipids of fa/fa rats differed significantly from those of Fa/? rats and from those reported for ob/ob mice. Increased 18∶2n?6 and decreased 20∶4n?6 and 22∶6n?3 in fa/fa rats indicated impaired PUFA metabolism, possibly reduced Δ6 and/or Δ5 desaturase activity, compared with Fa/? rats. No differences in hepatic Δ6 and Δ5 desaturase activity between fa/fa and Fa/? were found but enhanced activity of Δ9 desaturase activity in fa/fa as compared to Fa/? was evident. Inclusion of sunflower oil (SO) or triolein (TO) at 5% and 20% by weight in the diet elicited marked changes in the fatty acyl composition of cardiac phospholipids in both fa/fa and Fa/? rats when compared with animals fed the control Oxoid diet alone. Supplementation with triolein was most effective, reducing 18∶2n?6 and increasing 20∶4n?6 proportions in fa/fa rats so that they resembled those in Fa/? rats fed the control Oxoid diet. The type of fat rather than the amount of its dietary intake appears to be the main determinant of the observed changes in phospholipid composition. Pair feeding hyperphagic fa/fa rats to the lower intakes of Fa/? rats did not abolish the characteristic differences in the proportions of PUFA in cardiac phospholipids between the two phenotypes. The effect of triolein on cardiac phospholipid fatty acid composition in the present studies is intriguing and may be relevant in understanding the beneficial role of dietary olive oil in ameliorating cardiovascular disease in man.