Reduction in medium chain acids and monoenoic acids in livers and plasma of rats fed eicosa-5,8,11,14-tetraynoic acid

Male Sprague-Dawley rats were fed for 8 weeks a corn oil (CO) diet or a hydrogenated coconut oil (HCNO) diet. These diets were fed in the absence or presence of eicosa-5,8,11,14-tetraynoic acid (TYA). The inclusion of TYA in the HCNO diet reduced the levels of 12∶0 and 14∶0 in the total fatty acids of livers and plasma. With either diet, the presence of TYA caused an alteration in the fatty acid composition of these tissues so as to reduce the values of the ratios: 16∶1/16∶0, 18∶1/18∶0, and 20∶4/18∶2. These results suggest that dietary TYA can influence the hepatic metabolism of medium chain fatty acids and that it may inhibit the desaturase enzyme involved in the synthesis of not only 20∶4 but also of monoenoic fatty acids.     

Effect of eicosatetraynoic acid on liver and plasma lipids

Groups of rats were fed a fat-free diet supplemented with 0.5% safflower oil (control) or the control diet containing 0.5% of 5,8,11,14-eicosatetraynoic acid (TYA). Blood was collected weekly and plasma lipids analyzed. After 4 weeks, the animals were killed and the liver lipids were analyzed in detail. The acetylenic fatty acid perturbed plasma neutral lipid and phospholipid class concentrations and reduced growth rates. Liver triglyceride concentrations were reduced dramatically in the TYA fed animals, suggesting interference with complex lipid synthesis. Plasma and liver triglycerides were shifted to higher molecular weight species suggesting that TYA affected fatty acid metabolism. The phospholipids showed an accumulation of 18∶2 and a fall in 20∶4 percentages indicating an inhibition in the conversion of linoleate to arachidonate. All major lipid classes exhibited an increase in 18∶1 levels. Analysis of the octadecenoate positional isomers indicated the proportion of oleate increased substantually in all lipid classes whereas vaccenate proportions had fallen dramatically. All of the data collectively suggest that TYA inhibits the elongation of unsaturated fatty acids. A group of rats bearing hepatoma 7288CTC were also fed the TYA diet. Host liver lipids were affected by TYA similar to normal TYA fed animals, but the effects on hepatoma lipids were marginal.     

Dietary fats rich in saturated fatty acids (12∶0, 14∶0, and 16∶0) enhance gallstone formation relative to monounsaturated fat (18∶1) in cholesterol-fed hamsters

To test the possibility that dietary palmitic acid (16∶0) may be lithogenic, different fats were blended to exchange 18∶1 in olive oil with either 16∶0 in palm stearin, 12∶0+14∶0 in coconut oil, or 14∶0+16∶0 in butterfat. Dietary 18∶2 was held constant at 1.2% energy (en) (with extra safflower oil as needed) in these four purified diets containing low fat (11% of total energy) and 0.4% cholesterol. A fifth, high-fat diet provided 40% of the total energy as the 16∶0-rich blend. All hamsters fed the low-fat, 16∶0-rich blend for six weeks developed cholesterol gallstones (8/8). Although the gallstone incidence was lower for the 12∶0+14∶0-rich diet (5/8), the severity of stone formation in affected hamsters was equal to that in the low-fat, 16∶0-rich group. Mucin accumulation in gallbladder bile was often associated with cholesterol gallstones in diets containing 16∶0, but was minimal in 18∶1-rich and 12∶0+14∶0-rich groups. Neither the lithogenic index (all>1.0), plasma lipids, nor liver cholesterol was a selective predictor of stone formation. The high-fat, 16∶0-rich diet actually decreased cholesterol stone incidence (3/8) and severity, but yielded a high incidence of pigment stones (5/8). Thus, saturated fat and 16∶0per se were not responsible for the exaggerated lithogenesis. Because the antilithogenic 18∶1-rich diet also normalized the 18∶2 intake (1.2% en) relative to previous butter diets (0.3% en), the potential importance of essential fatty acids (EFA) deficiency in the model was tested in a second study by feeding graded amounts of 18∶2 (0.3, 0.6, 0.9, and 1.2% en) as safflower oil in four low-fat, butter-rich diets (11% en as fat) without alleviating gallstone incidence or severity. These studies indicate that substitution of 18∶1 for saturated fatty acids in low-fat diets reduces gallstone formation without affecting the lithogenic index. Furthermore, intake of 18∶2 at or below the EFA requirement does not appear to be a major factor in this model.     

Stimulation of hepatic lipogenesis by eicosa-5,8,11,14-tetraynoic acid in mice fed a high linoleate diet

Liver slices, from mice fasted for one day and then refed for three days either a 15% corn oil diet or a 15% corn oil diet containing eicosa-5,8,11,14-tetraynoic acid (TYA), were incubated with [1-¹⁴C] acetate or [³H]H₂O to determine lipogenic capacity. Dietary TYA produced a twofold stimulation in fatty acid and cholesterol synthesis. TYA also caused an increase in the relative proportion of linoleate (C_18∶2) and a decrease in that of arachidonate (C_20∶4) in liver. Thus, (a) despite high levels of C_18∶2, hepatic lipogenesis can be increased, and (b) even short term feeding of TYA can alter the hepatic fatty acid composition presumably by inhibition of arachidonate synthesis from linoleate.     

Comparative study of the blood pressure effects of four different vegetable fats on young,spontaneously hypertensive rats

Following the suckling period, four groups of male four-week-old spontaneously hypertensive rats (SHR) were fed semisynthetic diets with 14% (by weight) of either sunflower seed oil [46% 18∶2(n−6); linoleic acid (LA)-rich], linseed oil [62.5% 18∶3(n−3)+12.9% 18∶2(n−6); α-linolenic acid (LNA)-rich], evening primrose oil [9.2% 18∶3(n−6)+71% 18∶2(n−6); γ-linolenic acid (LNA)-rich] or hydrogenated palm kernel fat [1.5% 18∶2(n−6); polyunsaturated fatty acid (PUFA)-deficient], respectively, up to an age of 18 wk. All diets enriched with PUFA provoked an attenuation of hypertension development. The effect was lowest in the LA-rich group and highest in the γ-LNA-rich group. Differences in fatty acid composition of renal phospholipids between groups reflect the fatty acids present in the respective dietary fats. Renomedullary production of PGF_2α was significantly reduced in α-LNA-rich and slightly diminished in γ-LNA-rich fed rats. Aortic formation of 6-keto-PGF_1α and TXB₂ was increased in animals fed the γ-LNA-rich diet. Thus, the attenuation of hypertension development cannot be explained only by changes in prostanoid formation. Other mechanisms possibly involved should be pursued.     

Reduction of essential fatty acid deficiency in rats fed a low iron fat free diet

Young male rats were fed ad libitum for 8 weeks a low iron fat-free (FF-Fe) diet or a fat-free diet supplemented with iron (FF+Fe). The relative levels of 16∶1 to 16∶0 and 18∶1 to 18∶0 in the total fatty acids of liver and other tissues (plasma, erythrocytes and intestinal mucosa) were considerably decreased because of a lack of dietary iron. In rats fed the FF-Fe diet, the levels of essential fatty acids (18∶2ω6+20∶4ω6) in tissues were 2-to 3-fold greater than in the corresponding tissues of rats fed the FF+Fe diet. Eicosatrienoic acid (20∶3ω9) levels in tissue lipids from rats fed the FF+Fe diet were high (8–16%), whereas they were low (2–5%) in the case of animals fed the FF-Fe diet. The proportion of 20∶4 in total fatty acids of tissues was 2-to 3-fold greater in rats fed the FF-Fe diet than when they were fed the FF+Fe diet. Therefore, the relative levels of 20∶3ω9/20∶4ω6 varied from 1-2.9 in tissue lipids of rats fed the FF+Fe diet, while it varied only from 0.2–0.3 in animals fed the FF-Fe diet. These results suggest that a lack of dietary iron may reduce the synthesis of 16∶1, 18∶1, 20∶3 and 20∶4 and the metabolism of 20∶4.     

Triglyceride composition of bovine milk fat with elevated levels of linoleic acid

The effect of increasing the linoleic acid (18∶2) content of milk fat on the composition and structure of the triglycerides (TG) was investigated. Protected sunflower seed supplement was added to the diet of a cow grazing on pasture, and the structure and composition of the milk fat compared with the milk fat from its monozygous twin which had been fed a control diet. The relative proportions of TG fractions of high, medium, and low molecular weight in the milk fat with elevated levels of 18∶2 (15.5% 18∶2) were 43.0, 19.5, and 37.5 moles %, respectively, compared with 36.1, 19.7, and 44.2 moles %, respectively, in the milk fat from the cow fed the control diet. Separation of these three TG fractions of each milk fat into TG classes with different levels of unsaturation showed that the milk fat with elevated levels of 18∶2 contained higher proportions of diene, triene, and tetraene TG and correspondingly lower proportions of saturated and, to a lesser extent, monoene TG. The saturated and monoene TG from the two milk fats had similar fatty acid compositions. However, the diene TG of the 18∶2-rich milk fat included high proportions of the combination of 18∶2 with two saturated fatty acids (FA) which are minor constituents of normal milk fats. Likewise, the triene TG reflected the presence of 18∶2 in combination with 18∶1 and a saturated FA.     

Effects of various dietary fats on cardiolipin acyl composition during ontogeny of mice

Cardiolipin (CL) is a unique mitochondrial phospholipid, containing up to 85 wt% 18∶2n−6 in mammals. The influence of maternal dietary fatty acids on the acyl composition of offspring CL has not been examined previously. Adult female mice were thus fed diets rich in 18∶1n−9 (olive oil), 18∶2n−6 (safflower oil), 18∶3n−3 (linseed oil) or 20∶5n−3 and 22∶6n−3 (fish oil/safflower, 9∶1, w/w), for a five month period, encompassing two breeding cycles. Offspring from the second breeding cycle were then fed these diets. The acyl composition of CL, phosphatidylcholine and phosphatidylethanolamine from liver and heart was evaluated from mice killed 3, 18 and 42 days after parturition. The primary nutrient sources at these three time points were transplacental nutrients, breast milk and the diet, respectively. Maternal diet was found to influence the acyl composition of CLvia both placental transfer of fatty acids and breast milk. Fish oil feeding resulted in replacement of a substantial portion of 18∶2n−6 with 22∶6n−3; after 42 days, the area% of 18∶2n−6 in heart CL was reduced from 62% in safflower oil fed mice to 12%. In comparison to fish oil feeding, linseed oil feeding resulted in a much lower accumulation of 22∶6n−3. Olive oil feeding resulted in substantial replacement of 18∶2n−6 with 18∶1n−9 (18∶2n−6 was reduced from 62% to 31%). Physiologically, these findings are relevant because changes in CL acyl composition may influence the activity of associated inner mitochondrial membrane enzymes. This work was presented in part as an Honored Student Award paper at the 82nd Annual AOCS Meeting, Chicago, IL, May 1991.     

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.     

Differential effects of dietary linoleic and α-linolenic acid on lipid metabolism in rat tissues

Comparative effects of feeding dietary linoleic (safflower oil) and α-linolenic (linseed oil) acids on the cholesterol content and fatty acid composition of plasma, liver, heart and epididymal fat pads of rats were examined. Animals fed hydrogenated beef tallow were used as isocaloric controls. Plasma cholesterol concentration was lower and the cholesterol level in liver increased in animals fed the safflower oil diet. Feeding the linseed oil diet was more effective in lowering plasma cholesterol content and did not result in cholesterol accumulation in the liver. The cholesterol concentration in heart and the epididymal fat pad was not affected by the type of dietary fatty acid fed. Arachidonic acid content of plasma lipids was significantly elevated in animals fed the safflower oil diet and remained unchanged by feeding the linseed oil diet, when compared with the isocaloric control animals fed hydrogenated beef tallow. Arachidonic acid content of liver and heart lipids was lower in animals fed diets containing safflower oil or linseed oil. Replacement of 50% of the safflower oil in the diet with linseed oil increased α-linolenic, docosapentaenoic and docosahexaenoic acids in plasma, liver, heart and epididymal fat pad lipids. These results suggest that dietary 18∶2ω6 shifts cholesterol from plasma to liver pools followed by redistribution of 20∶4ω6 from tissue to plasma pools. This redistribution pattern was not apparent when 18∶3ω3 was included in the diet.     

Dietary saturated fat level alters the competition between α-linolenic and linoleic acid

Male weanling rats were fed semi-synthetic diets high in saturated fat (beef tallow) vs high in linoleic acid (safflower oil) with or without high levels of α-linolenic acid (linseed oil) for a period of 28 days. The effect of feeding these diets on cholesterol content and fatty acid composition of serum and liver lipids was examined. Feeding linseed oil with beef tallow or safflower oil had no significant effect on serum levels of cholesterol. Serum cholesterol concentration was higher in animals fed the safflower oil diet than in animals fed the beef tallow diet without linseed oil. Feeding linseed oil lowered the cholesterol content in liver tissue for all dietary treatments tested. Consumption of linseed oil reduced the arachidonic acid content with concomitant increase in linoleic acid in serum and liver lipid fractions only when fed in combination with beef tallow, but not when fed with safflower oil. Similarly, ω3 fatty acids (18∶3ω3, 20∶5ω3, 22∶5ω3, 22∶6ω3) replaced ω6 fatty acids (20∶4ω6, 22∶4ω6) in serum and liver lipid fractions to a greater extent when linseed oil was fed with beef tallow than with safflower oil. The results suggest that the dietary ratio of linoleic acid to saturated fatty acids or of 18∶3ω3 to 18∶2ω6 may be important to determine the cholesterol and arachidonic acid lowering effect of dietary α-linolenic acid.     

Influence of dietary fat composition on intestinal absorption in the rat

Omega-3 fatty acids influence the function of the intestinal brush border membrane. For example, the omega-3 fatty acid eicosapentaenoic acid (20∶5ω3) has an antiabsorptive effect on jejunal uptake of glucose. This study was undertaken to determine whether the effect of feeding α-linolenic acid (18∶3ω3) or EPA plus docosahexaenoic acid (22∶6ω3) on intestinal absorption of nutrients was influenced by the major source of dietary lipid, hydrogenated beef tallow or safflower oil. Thein vitro intestinal uptake of glucose, fatty acids and cholesterol was examined in rats fed isocaloric diets for 2 weeks: beef tallow, beef tallow + linolenic acid, beef tallow + eicosapentaenoic acid/docosahexaenoic acid, safflower oil, safflower oil + linolenic acid, or safflower oil + eicosapentaenic acid/docosahexaenoic acid. Eicosapentaenoic acid/docosahexaenoic acid reduced jejunal uptake of 10 and 20 mM glucose only when fed with beef tallow, and not when fed with safflower oil. Linolenic acid had no effect on glucose uptake, regardless of whether it was fed with beef tallow or safflower oil. The jejunal uptake a long-chain fatty acids (18∶0, 18∶2ω6, 18∶3ω3, 20∶4ω6, 20∶5ω3 and 22∶6ω3) and cholesterol was lower in salfflower oil than with beef tallow. When eicosapentaenoic acid/docosahexaenoic acid was given with beef tallow (but not with safflower oil), there was lower uptake of 18∶0, 20∶5ω3 and cholesterol. The demonstration of the inhibitory effect of linolenic acid or eicosapentaenoic acid/docosahexaenoic acid on cholesterol uptake required the feeding of a saturated fatty acid diet (beef tallow). These changes in uptake were not explained by differences in the animals’ food intake, body weight gain or intestinal weight. Feeding safflower oil was associated with an approximately 25% increase in the jejunal and ileal mucosal surface area, but this increase was prevented by combining linolenic acid or eicosapentaenoic acid/docosahexaenoic acid with safflower oil. Different inhibitory patterns were observed when mixtures of fatty acids were present together in the incubation medium, rather than in the diet: for example, when 18∶0 was in the incubation medium with 20∶4ω6, the uptake of 20∶4ω6 was reduced, whereas the uptake was unaffected by 18∶2ω6 or 20∶5ω3. Thus, (1) the inhibitory effect of eicosapentaenoic acid/docosahexaenoic acid on jejunal uptake of glucose, fatty acids and cholesterol was influenced by the major dietary lipid, saturated (beef tallow) or polyunsaturated fatty acid (safflower oil); and (2) different omega-3 fatty acids (linolenic acid versus eicosapentaenoic acid/docosahexaenoic acid) have a variable influence on the intestinal absorption of nutrients.     

Dietary linoleic acid and the fatty acid profiles in rats fed partially hydrogenated marine oils

The influence of the linoleic acid levels of diets containing partially hydrogenated marine, oils (HMO) rich in isomeric 16∶1, 18∶1, 20∶1 and 22∶1 fatty acids on the fatty acid profiles of lipids from rat liver, heart and adipose tissue was examined. Five groups of rats were fed diets containing 20 wt% fat−16% HMO+4% vegetable oils. In these diets, the linoleic acid contents varied between 1.9% and 14.5% of the dietary fatty acids, whereas the contents oftrans fatty acids were 33% in all groups. A sixth group was fed a partially hydrogenated soybean oil (HSOY) diet containing 8% linoleic acid plus 32%trans fatty acids, mainly 18∶1, and a seventh group, 20% palm oil (PALM), with 10% linoleic acid and notrans fatty acids. As the level of linoleic acid in the HMO diets increased from 1.9% to 8.2%, the contents of (n−6) polyunsaturated fatty acids (PUFA) in the phospholipids increased correspondingly. At this dietary level of linoleic acid, a plateau in (n−6) PUFA was reached that was not affected by further increase in dietary 18∶2(n−6) up to 14.5%. Compared with the HSOY- or PALM-fed rats, the plateau value of 20∶4(n−6) were considerably lower and the contents of 18∶2(n−6) higher in liver phosphatidylcholines (PC) and heart PC. Heart phosphatidylethanolamines (PE) on the contrary, had elevated contents of 20∶4(n−6), but decreased 22∶5(n−6) compared with the PALM group. All groups fed HMO had similar contents oftrans fatty acids, mainly 16∶1 and 18∶1, in their phospholipids, irrespective of the dietary 18∶2 levels, and these contents were lower than in the HSOY group. High levels of linoleic acid consistently found in triglycerides of liver, heart and adipose tissue of rats fed HMO indicated that feeding HMO resulted in a reduction of the conversion of linoleic acid into long chain PUFA that could not be overcome by increasing the dietary level of linoleic acid.     

The effect of dietary fats on the plasma lipid composition of sheep

This study reports on the plasma lipid compositions of sheep fed either a control diet (C), a control diet supplemented with tallow (A) or polyunsaturated fatty acid (B) that had been protected against hydrolysis and hydrogenation in the rumen, or a control diet supplemented with maize oil (D). Diet B considerably increased the 18∶2 content of all the major plasma lipid fractions. Although the feeding of diet D also resulted in an increase in the 18∶2 contents within the cholesteryl ester, unesterified fatty acid, and phospholipid fractions the increases were considerably less than those observed with diet B; the levels of 18∶2 within the triglyceride fraction remained similar to that for the sheep which received the control diet. The effect of feeding diet A was confined solely to the triglyceride fraction where the concentrations of 16∶0 and 18∶1 were increased. The lipoproteins of the plasma were separated into very low density lipoproteins (d<1.006), low density lipoproteins (1.006<d<1.063), and high density lipoproteins (1.063<d<1.21), and the distribution of the major lipids between these lipoprotein fractions was investigated. Diet B increased considerably the proportion of triglyceride found in association with the very low density fraction and the concentrations of 18∶2 within all the lipoprotein fractions; these increases in the concentrations of 18∶2 were not confined to any particular lipid fraction of the lipoproteins. In contrast, the increases in the concentrations of 18∶2 produced as a result of feeding diet D were confined to the low and high density lipoproteins. The effect of feeding diet A was confined to fatty acid changes within the triglycerides of the low and very low density lipoproteins.     

Effects of dietary primrose oil on mammary tumorigenesis induced by 7,12-dimethylbenz(a) anthracene

The mammary tumor-promoting effect of a high-fat diet containing 20% evening primrose oil (PO) was compared to that of a 20% corn oil (CO) diet. Mammary tumors were induced in female Sprague-Dawley rats using 10 mg (Study 1) and 5 mg (Study 2) 7,12-dimethylbenz(a)anthracene (DMBA). The 10 mg dose of DMBA gave a total mammary tumor incidence of 47% in rats fed the PO diet and 80% for those fed the CO diet. When only adenocarcinomas were counted, the malignant mammary tumor incidences were 41% in rats fed the PO diet and 73% in rats fed the CO diet. In a second study using 5 mg DMBA to induce mammary tumors, total tumor incidences were 50% for PO-fed rats and 63% for those receiving a CO diet. Again, when only adenocarcinomas were counted, tumor incidences were 27% for PO- and 63% for CO-dieted rats. Analysis of plasma fatty acid profiles indicated that animals fed a 20% PO diet showed significant increases in 18∶3 and 20∶4 fatty acids and significant decreases in 16∶0 and 18∶1 compared to animals fed a 20% CO diet. These results indicate that the mammary tumor promoting effect of a diet containing 20% fat can be diminished by substituting PO for CO. Moreover, the promoting effect on mammary cancer by a high-fat diet could be depressed by feeding a source of γ-linolenic acid (GLA).     

Lymphatic recovery of exogenous oleic acid in rats on long chain or specific structured triacylglycerol diets

Specific structured triacylglycerols, MLM (M=medium-chain fatty acid, L=long-chain fatty acid), rapidly deliver energy and long-chain fatty acids to the body and are used for longer periods in human enteral feeding. In the present study rats were fed diets of 10 wt% MLM or LLL (L=oleic acid [18∶1n−9], M=caprylic acid [8∶0]) for 2 wk. Then lymph was collected 24 h following administration of a single bolus of ¹³C-labeled MLM or LLL. The total lymphatic recovery of exogenous 18∶1n−9 24 h after administration of a single bolus of MLM or LLL was similar in rats on the LLL diet (43% and 45%, respectively). However, the recovery of exogenous 18∶1n−9 was higher after a single bolus of MLM compared with a bolus of LLL in rats on the MLM diet (40% and 24%, respectively, P=0.009). The recovery of lymphatic 18∶1n−9 of the LLL bolus tended to depend on the diet triacylglycerol structure and composition (P=0.07). This study demonstrated that with a diet containing specific structured triacylglycerol, the lymphatic recovery of 18∶1n−9 after a single bolus of fat was dependent on the triacylglycerol structure of the bolus. This indicates that the lymphatic recovery of long-chain fatty acids from a single meal depends on the overall long-chain fatty acid composition of the habitual diet. This could have implications for enteral feeding for longer periods.     

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.     

n−3 Fatty acid requirements of the newborn

Whether docosahexaenoic acid (22∶6n−3) is an essential nutrient for term or preterm infants, or if not, the quantity of dietary linolenic acid (18∶3n−3) needed to support sufficient synthesis of 22∶6n−3 for assimilation in the central nervous system is unknown. Infants fed formulas have lower plasma and red blood cell (RBC) levels of 22∶6n−3 than breast fed infants. No relationship between the intake of 18∶3n−3 in formula (0.8 or 4.5% of fatty acids, 18∶2n−6/18∶3n−3 ratio 35∶1 or 7∶1, respectively) and the infant's RBC 22∶6n−3 was found. Premature infants (<33 wk gestation) also showed a decrease in RBC 22∶6n−3 during feeding with formula containing 18∶3n−3 as the only n−3 fatty acid. However, a marked decrease in plasma and RBC 22∶6n−3 occurred between premature birth and the start of full enteral feeding at 1–2 wk of age. This was not reversed by breast milk or formula feeding. Piglets, which are appropriate for studies of infant lipid metabolism, had decreased brain synaptic plasma membrane, retina and liver 22∶6n−3 and increased 22∶5n−6 when fed formula with 0.8% fatty acids (0.3% of kcal) as 18∶3n−3. Formula with 4.0% fatty acids (1.7% of kcal) as 18∶3n−3 resulted in similar accretion of 22∶6n−3 in the organs compared to milk fed animals. The studies suggest the dietary requirement for 18∶3n−3 in term animals in energy balance exceeds 0.3% diet kcal. Studies in the premature infants suggest 18∶3n−3 may be oxidized rather than desaturated to 22∶6n−3 if energy requirements are not met, and that due to early lipid restriction and later rapid growth, premature infants may have higher dietary n−3 requirements than term infants. Based on a paper presented at the Symposium on Milk Lipids held at the AOCS Annual Meeting, Baltimore, MD, April 1990.     

Effects of dietary n−3 polyunsaturated fatty acids on phospholipid composition and calcium transport in mouse cardiac sarcoplasmic reticulum

The effects of dietary n−3 and n−6 polyunsaturated fatty acids on the fatty acid composition of phospholipid, Ca⁺⁺· Mg⁺⁺ ATPase and Ca⁺⁺ transport activities of mouse sarcoplasmic reticulum were investigated. Mice were fed a 2 weight percent fat diet containing either 0.5 weight percent ethyl esters of 18∶3n−3, 20∶5n−3 or 22∶6n−3 as a source of n−3 polyusaturated fatty acid or 0.5 weight percent safflower oil as a cource of n−6 polyunsaturated fatty acid for 10 days. Olive oil (2 weight percent) was used as a control diet. Although feeding n−6 polyunsaturated fatty acid induced very little modifications of the phospholipid sarcoplasmic reticulum fatty acid composition, feeding n−3 polyunsaturated fatty acid altered it markedly. Inclusion of 18∶−3, 20∶5n−3 or 22∶6n−3 in the diet caused an accumulation of 22∶6n−3, which replaced 20∶4n−6 and 18∶2n−6 in phospholipid sarcoplasmic reticulum. The saturated fatty acids were significantly increased with a concurrent reduction of 18∶1n−9. These changes in the fatty acid composition resulted in a decrease in the values of the n−6/n−3 polyunsaturated fatty acid ratio and a decrease in the ratio of 20 carbon to 22 carbon fatty acids esterified in the phospholipid sarcoplasmic reticulum. This was associated with a decrease in Ca⁺⁺ uptake by n−3 polyunsaturated fatty acid enriched sarcoplasmic reticulum vesicles as compared with n−6 fatty acid and control diet sarcoplasmic reticulum vesicles. However, neither the affinity for Ca⁺⁺ nor the maximal velocity of ATP hydrolysis activity of Ca⁺⁺·MG⁺⁺ ATPase were altered by the different diets. The data suggest that the incorporation of 22∶6n−3 and/or the decrease of 20∶4n−6 plus 18∶2n−6 in the phospholipid sarcoplasmic reticulum may affect the membrane lipid bilayer structure and make it more permeable to Ca⁺⁺.     

Positional distribution on n−3 fatty acids in triacylglycerols from rat adipose tissue during fish oil feeding

The present study was designed to investigate the metabolism of the n−3 olyunsaturated fatty acids (PUFA) in adipose tissue and its dependence upon dietary factors. Changes in the positional distribution of the fatty acids in triacylglycerols from retroperitoneal adipose tissue were studied as a function of time on rats fed for 4 wk a diet enriched with fish oil. The stereospecific analysis of triacylglycerols was based on random formation ofrac-1,2-diacylglycerols by Grignard degradation. This was followed by synthesis ofrac-phosphatidic acids and treatment with phospholipase A₂. In the triacylglycerols of the fish oil diet, 57% of the total n−3 fatty acids were in position 3,i.e., two-thirds of 22∶5n−3 and 22∶5n−3 were esterified insn-3 position, whereas 22∶6n−3 was equally distributed in positions 2 and 3. After 4 wk of feeding fish oil, the fatty acid composition of adipose tissue triacylglycerols reached a steady state. Half of the n−3 fatty acids were found in position 3, namely 75% of 22∶5n−3, 50% of 20∶5n−3 and 18∶4n−3 and 45% of 22∶6n−3, the latter being equally distributed in positions 2 and 3. This pattern of distribution resembled that found in triacylglycerols of the fish oil diet, except for a higher proportion of 20∶5n−3 in adipose tissue in position 1 at the expense of position 3. Throughout the 4-wk period of fish oil feeding, the distribution pattern of minor n−3 fatty acids (18∶4n−3 and 22∶5n−3) in adipose tissue triacylglycerols remained unchanged. On the other hand, at the onset of fish oil feeding, 20∶5n−3 and 22∶6n−3 became concentrated in position 3, but thereafter 20∶5n−3 was progressively incorporated into position 1 and 22∶6n−3 into position 2. We thus conclude that n−3 fatty acids are differentially esterified in triacylglycerols of white adipose tissue. Despite the complex sequence of hydrolysis and acylation steps involved, the positional distribution of n−3 fatty acids was found to be similar in both the fish oil diet and the stored fat, in contrast to what was observed for nonessential fatty acids.