Dietary (n-3) fatty acids affect rat heart, liver and aorta protective enzyme activities and lipid peroxidation

In a 16-wk study, weanling Wistar rats (32 males and 32 females) were fed a modified AIN-76 diet containing 20% fat with various (n-3) fatty acids. All dietary fats provided the same amount of saturates, monounsaturates, and total essential fatty acids [(n-6) + (n-3)]. The control diet contained lard/corn oil (L/CO). The other diets contained (n-3) fatty acids from linseed oil (LSO), from linseed oil + menhaden oil (LSO + MO) or from menhaden oil (MO). The (n-3) diets reduced total and HDL-cholesterol, particularly in rats fed the MO diet. Platelet thromboxane levels were equally depressed by the LSO and MO diets. Dietary (n-3) fatty acids significantly elevated docosahexaenoic acid in livers and hearts of male and female rats, with females reaching higher levels. This increase was accompanied by reduced arachidonic acid, except for hearts of females in which the major decrease was in linoleic acid. Overall, enzyme activities in the MO-fed group were decreased to the following levels (relative to the activity in the control group): heart Mn superoxide dismutase (SOD), 28%; liver CuZnSOD, 82%; aorta CuZnSOD, 32%. Greater reductions in these enzyme activities were seen in the female rats fed the MO diet compared with male rats. Lipid peroxidation, assessed by urinary, heart and liver thiobarbituric acid reactants, was increased by dietary (n-3) fatty acids (MO greater than LSO + MO greater than LSO greater than L/CO) and was higher in females than in males. These results indicate that enhanced lipid peroxidation occurs with the increased oxidative stress of elevated tissue (n-3) fatty acids accompanied by reduced SOD activity.     

Menhaden oil decreases high-fat diet-induced markers of hepatic damage, steatosis, inflammation, and fibrosis in obese Ldlr-/- mice

The frequency of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) has increased in parallel with obesity in the United States. NASH is progressive and characterized by hepatic damage, inflammation, fibrosis, and oxidative stress. Because C20-22 (n-3) PUFA are established regulators of lipid metabolism and inflammation, we tested the hypothesis that C20-22 (n-3) PUFA in menhaden oil (MO) prevent high-fat (HF) diet-induced fatty liver disease in mice. Wild-type (WT) and Ldlr(-/-) C57BL/6J mice were fed the following diets for 12 wk: nonpurified (NP), HF with lard (60% of energy from fat), HF-high-cholesterol with olive oil (HFHC-OO; 54.4% of energy from fat, 0.5% cholesterol), or HFHC-OO supplemented with MO (HFHC-MO). When compared with the NP diet, the HF and HFHC-OO diets induced hepatosteatosis and hepatic damage [elevated plasma alanine aminotransferase (ALT) and aspartate aminotransferases] and elevated hepatic expression of markers of inflammation (monocyte chemoattractant protein-1), fibrosis (procollagen 1α1), and oxidative stress (heme oxygenase-1) (P ≤ 0.05). Hepatic damage (i.e., ALT) correlated (r = 0.74, P < 0.05) with quantitatively higher (>140%, P < 0.05) hepatic cholesterol in Ldlr(-/-) mice fed the HFHC-OO diet than WT mice fed the HF or HFHC-OO diets. Plasma and hepatic markers of liver damage, steatosis, inflammation, and fibrosis, but not oxidative stress, were lower in WT and Ldlr(-/-) mice fed the HFHC-MO diet compared with the HFHC-OO diet (P < 0.05). In conclusion, MO [C20-22 (n-3) PUFA at 2% of energy] decreases many, but not all, HF diet-induced markers of fatty liver disease in mice.     

Dietary n-3 polyunsaturated fatty acids alter lipid composition and decrease prostaglandin synthesis in rat spleen

Three groups of rats were fed a semisynthetic diet containing 10% olive oil, 10% corn oil, or 10% menhaden oil for three weeks. Olive oil was used as a control and corn and menhaden oils as sources of n-6 and n-3 fatty acids, respectively. The spleen phospholipids were enriched with eicosapentaenoic (20:5 n-3) and docosahexaenoic acids (22:6 n-3) in rats on menhaden oil diets. The enrichment of these n-3 fatty acids was accompanied by a decrease in the arachidonic acid content (20:4 n-6) of spleen phospholipids. The syntheses of prostaglandin E₂ (PGE₂), 6-keto prostaglandin F_1α (6 keto PGF_1α) and thromboxane B₂ (TXB₂) from endogenous substrates in n-3 fatty acid enriched spleens were decreased by 50, 57 and 80% respectively. These studies indicate that dietary n-3 fatty acids can effectively displace arachidonic acid from phospholipids and decrease prostaglandin synthesis in rat spleen.     

Regulation of hepatic microsomal cytochrome P450IIE1 level by dietary lipids and carbohydrates in rats

The present work tests the hypothesis that high fat/low carbohydrate diets elevate the level of liver microsomal cytochrome P450IIE1. Male Sprague-Dawley rats were fed liquid diets containing varied ratios of corn oil/carbohydrate for 4 d. Rats fed diets with higher fat/carbohydrate ratios produced higher serum acetone levels and higher hepatic microsomal P450IIE1 content and N-nitrosodimethylamine demethylase activity than those fed diets with lower fat/carbohydrate ratios. This dietary fat/carbohydrate effect on P450IIE1 also was observed with modified semipurified AIN-76A diets. In addition, both the quantity and the extent of unsaturation of dietary lipids affected P450IIE1 regulation. At moderate fat levels (5 and 20% diet), rats fed corn oil and menhaden oil diets produced higher P450IIE1 activity than those fed lard and olive oil diets. Rats fed a diet containing 20% corn oil or an amount of linoleic acid equivalent to the 20% corn oil diet showed twofold to threefold increases in the level of P450IIE1 over those fed a fat-free diet. Rats fed a 25% corn oil diet showed twofold higher enflurane metabolism in vivo than those fed a 0.5% corn oil diet. The present results suggest that the constitutive P450 enzyme level is regulated by dietary fat/carbohydrate ratios.     

Disparate effects of dietary fatty acids on activity of 5'-nucleotidase of rat liver plasma membrane

The effects of incorporation of dietary n-3 polyunsaturated fatty acids (PUFA) into rat liver plasma membrane on the activity of 5'-nucleotidase (EC 3.1.3.5) was studied. The membrane phospholipids from rats fed a diet containing 10% by weight menhaden oil (MO) for 3 wk contained more n-3 PUFA and less n-6 PUFA in phospholipids classes, i.e., 24% and 65% less linoleic and arachidonic acid in phosphatidylcholine, than in rats fed 10% coconut oil (CNO) diets. The specific activity of 5'-nucleotidase in n-3 PUFA-enriched hepatic plasma membranes was 1.6- to 2-fold higher than that in rats fed CNO or corn oil (CO). Lineweaver-Burk plots for 5'-nucleotidase in liver plasma membranes isolated from rats fed MO and CNO showed no significant differences in Km values but the Vmax was increased by 67% in MO-fed rats. Arrhenius plots showed a break point in 5'-nucleotidase activity at 28.3 degrees C and 30.8 degrees C in plasma membranes from MO- and CNO-fed rats, respectively. The implications of this in the generation of adenosine and its possible impact on physiological functions are discussed.     

Suppression of altered hepatic foci development by a high fish oil diet compared with a high corn oil diet in rats

Effects of low corn oil, high corn oil, and high fish oil diets on altered hepatic foci development in female Sprague-Dawley rats were investigated. Rats assigned to Groups 1-4 were initiated with saline as the control and those assigned to Groups 5-7 were initiated with diethylnitrosamine (DEN 15 mg/kg) at 24 hours of age. After weaning, all rats, except those in Group 1, received 500 ppm phenobarbital (PB) in their diet as tumor promoter for three months. Altered hepatic foci development was significantly lower in DEN-initiated rats fed the high fish oil + PB diet than in DEN-initiated rats fed the high corn oil + PB diets. Liver weight and relative liver weight were significantly greater in rats fed the high fish oil + PB diet than in rats fed the other diets, and hepatic biotransformation/detoxification enzyme activities were greater in rats fed the fish oil + PB diets than in rats fed the other diets. These results suggest that the effect of a high fish oil diet on altered hepatic foci may occur through regulation of hepatic biotransformation/detoxification enzyme activities, leading to alteration in the tumor-promoting action of PB. Dietary lipid significantly affected the hepatic phospholipid fatty acid composition of rats. n-3 polyunsaturated fatty acids were incorporated into membrane phospholipid at the expense of n-6 polyunsaturated fatty acids. A high fish oil diet caused greater oxidative stress in rats, as measured by plasma vitamin E level, red blood cell glutathione status, liver lipid peroxidation, and hepatic glutathione reductase activity. Pearson's correlation analysis indicated that the foci number was negatively correlated to the liver thiobarbituric acid-reactive substance and 7-pentoxyresorufin O-dealkylase activity, and the foci area was negatively correlated to the liver thiobarbituric acid-reactive substance activity (p < 0.05) in rats of groups that developed foci. These results suggest that the type of dietary lipid is the more important determinant for gamma-glutamyl transpeptidase-positive foci development than the amount of dietary lipid when rats consumed approximately the same amount of calories in all the dietary groups, and the underlying mechanisms may be partially ascribed to the antioxidant/oxidation status and biotransformation/detoxification system of rats.     

Dietary fat saturation affects glucose metabolism without affecting insulin receptor number and affinity in adipocytes from BHE rats

The effects of dietary fat source on epididymal fat cell insulin receptor binding and affinity and on glucose transport and use by genetically diabetic rats were studied. Male BHE rats were fed 6% fat/64% sucrose diets. The fat consisted of 1% corn oil plus 5% beef tallow, menhaden oil or corn oil. Glucose tolerance was assessed at 100, 300 and 600 d of age. At 100 d of age the fat pads were excised, isolated adipocytes prepared and insulin receptor number, receptor affinity, 3-O-methyl glucose uptake and glucose use determined. Insulin receptor number and binding affinity were not affected by dietary fat type. The transport and subsequent use of glucose were greater in fat cells from rats fed beef tallow compared with those from rats fed corn oil or menhaden oil. All three groups exhibited a deterioration in glucose tolerance with age. Although we observed greater glucose transport, oxidation and conversion to fatty acids in beef tallow-fed rats, we saw no differences in these measurements between cells from corn or menhaden oil-fed rats. Thus, we conclude that the effects of these dietary lipids are attributable to effects of saturated fatty acids on intracellular events rather than on the insulin receptor per se, and that the type of unsaturated fatty acid [(n-3) vs. (n-6)] is of little importance to the regulation of glucose metabolism by isolated adipocytes.     

Ca2+-Mg2+ ATPase of mouse cardiac sarcoplasmic reticulum is affected by membrane n-6 and n-3 polyunsaturated fatty acid content

White mice, 18-20 g, were fed purified diets containing two weight percent safflower oil plus ten weight percent menhaden, corn, or olive oil for 2 wk. Menhaden oil ingestion resulted in significantly higher levels of 22:6(n-3) and 20:5(n-3), particularly 22:6(n-3), and lower levels of 20:4(n-6) and 18:2(n-6) in cardiac sarcoplasmic reticulum (SR) phospholipids than did corn or olive oil ingestion. These changes in fatty acid composition resulted in a significant decrease in the value of the n-6/n-3 fatty acid ratio of cardiac SR phospholipids. The ratio was 2.8 versus 0.2 in choline phospholipids and 1.9 versus 0.2 in ethanolamine phospholipids in SR of mice fed corn or menhaden oil, respectively. This reduction in the n-6/n-3 fatty acid ratio was associated with a lower relative activity of Ca2+-Mg2+ ATPase, and a lower initial rate of calcium transport and maximum calcium uptake in SR vesicles from mice fed menhaden oil rather than olive or corn oils. The specific activity of NADPH cytochrome C reductase (EC 1.6.2.3) of cardiac SR was not affected by dietary lipids. These data indicate that modification of SR by 22:6(n-3) may change the SR bilayer structure resulting in alteration of the calcium transport properties of SR vesicles. In addition, our results suggest that reduction of calcium flux across cardiac SR following fish oil consumption may also reduce the susceptibility of myocytes to rapid changes in calcium concentrations which may occur during ischemia and reperfusion.     

Enrichment of (n-3) fatty acids of suckling rats by maternal dietary menhaden oil

The study was undertaken to determine whether the content of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in neonatal rats can be increased through milk provided by lactating mothers fed a diet containing 20% menhaden oil (experimental group), in comparison with a group fed a 20% corn oil diet (control group). The test diets were isocaloric and provided 41% of total energy as fat. Coinciding with 3-9% higher maternal body weight gain throughout the lactation period with the menhaden oil diet, the suckling rats in the experimental group at the ages of 3-9 d gained 5-10% more weight than did their control counterparts. When compared with corn oil, maternal dietary menhaden oil induced not only a higher weight percentage but also higher concentrations (microgram/mL) of EPA, DHA and total (n-3) fatty acids in milk, plasma, platelets and erythrocytes of neonates. These changes were accompanied by lower arachidonic and linoleic acid levels. EPA and DHA were detected in all three blood components of the control group, whose corn oil diet contained linolenic acid but not longer chain (n-3) fatty acids. This finding, together with the higher DHA to EPA ratios found in the three blood components than in the milk of the experimental group, suggests that neonatal rats possess the enzymes necessary for producing DHA from EPA and linolenate by desaturation and elongation mechanisms.     

A semipurified diet that suppresses phenobarbital promotion of hepatocarcinogenesis in the rat

Six groups of F344/N female rats were fed either a modified AIN‐76 diet (20% casein, 5 % corn oil, 65% cornstarch, 5% cellulose) (AIN) or a diet formulated by Dr. M. Pariza (PD) (30% casein, 10% partially hydrogenated corn oil, 40% sucrose, 15% cornstarch) beginning four days before 70% partial hepatectomy. One day after the surgery, one group fed each diet was intubated with 10 mg/kg diethylnitrosamine (DEN). One week later, these groups plus one control group fed each diet were given 0.05% phenobarbital in the diet for 6 or 14 months. After the rats were killed, blocks of liver tissue were frozen on dry ice and stored at — 70°C. Three frozen serial sections were stained for γ‐glutamyltransferase, ATPase, and glucose‐6‐phosphatase.

Numbers and volume of altered hepatic foci (AHF) were analyzed by stereological techniques. After 14 months of feeding these regimens, rats initiated with DEN and fed the AIN + PB had significantly greater numbers and a higher percent volume of the liver of most phenotypes of AHF than all other groups, including those fed PD + PB following initiation with DEN. The numbers of AHF exhibiting more complex phenotypes (i.e., scored by more than one marker) remained unaltered between 6 and 14 months. These findings indicate that the effectiveness of PB as a promoting agent in multistage hepatocarcinogenesis is significantly altered when fed with two different diets of known composition. Therefore, dietary composition can be a significant factor in studies of the stage of promotion in hepatocarcinogenesis.     

Lack of dose response by dietary n-3 fatty acids at a constant ratio of n-3 to n-6 fatty acids in suppressing eicosanoid biosynthesis from arachidonic acid

This study evaluated whether it is the ratio of n-3 to n-6 fatty acids or the absolute amount of n-3 fatty acids in diets that determines the degree of inhibition of eicosanoid biosynthesis from arachidonic acid (AA). Rats were fed diets containing different doses of linolenic acid or menhaden oil for 3 mo. Constant ratios of n-3 to n-6 fatty acids were maintained by concomitant increases in safflower oil as the n-6 fatty acid source. Results showed that AA concentrations in liver, platelet, and lung phospholipids and concentrations of eicosanoids synthesized in tissues were significantly (P less than 0.05) suppressed both by linolenic acid and menhaden oil; however, there was a lack of a dose response within groups fed different amounts of the same dietary fat. These results indicate that the ratio of n-3 to n-6 fatty acids in the diets, rather than the absolute amount of n-3 fatty acids, is the determining factor in inhibiting eicosanoid biosynthesis from AA.     

Peritoneal macrophages from mice fed dietary (n-3) polyunsaturated fatty acids secrete low levels of prostaglandins

Peritoneal macrophages from mice fed diets containing 10% menhaden oil incorporated significant amounts of n-3 polyunsaturated fatty acids (n-3 PUFA) into cellular lipids, and this lowered arachidonic acid in these lipid classes compared to those from mice fed diets containing 10% coconut oil. The n-3 PUFA-enriched macrophages secreted significantly smaller amounts of prostaglandin E, thromboxane B and 6-keto-prostaglandin F1 alpha when stimulated with opsonized zymosan or phorbol myristate acetate. These studies demonstrated that menhaden oil-enriched diets influence fatty acid composition and prostaglandin synthesis in macrophages.     

A semipurified diet that suppresses phenobarbital promotion of hepatocarcinogenesis in the rat

Six groups of F344/N female rats were fed either a modified AIN-76 diet (20% casein, 5% corn oil, 65% cornstarch, 5% cellulose) (AIN) or a diet formulated by Dr. M. Pariza (PD) (30% casein, 10% partially hydrogenated corn oil, 40% sucrose, 15% cornstarch) beginning four days before 70% partial hepatectomy. One day after the surgery, one group fed each diet was intubated with 10 mg/kg diethylnitrosamine (DEN). One week later, these groups plus one control group fed each diet were given 0.05% phenobarbital in the diet for 6 or 14 months. After the rats were killed, blocks of liver tissue were frozen on dry ice and stored at -70 degrees C. Three frozen serial sections were stained for gamma-glutamyltransferase, ATPase, and glucose-6-phosphatase. Numbers and volume of altered hepatic foci (AHF) were analyzed by stereological techniques. After 14 months of feeding these regimens, rats initiated with DEN and fed the AIN + PB had significantly greater numbers and a higher percent volume of the liver of most phenotypes of AHF than all other groups, including those fed PD + PB following initiation with DEN. The numbers of AHF exhibiting more complex phenotypes (i.e., scored by more than one marker) remained unaltered between 6 and 14 months. These findings indicate that the effectiveness of PB as a promoting agent in multistage hepatocarcinogenesis is significantly altered when fed with two different diets of known composition. Therefore, dietary composition can be a significant factor in studies of the stage of promotion in hepatocarcinogenesis.     

Influence of Dietary Fats Upon Systolic Blood Pressure in the Rat

Studies were performed to determine whether feeding diets with differing fatty acid content and composition had an influence on systolic blood pressure in the rat. Weanling male rats were fed standard laboratory chow (2.9% fat in total), or synthetic diets (10% fat in total) containing fish oil, butter, coconut oil or corn oil, for 5 weeks. Coconut oil and butter diets were rich in saturated fatty acids, whilst fish oil and corn oil were rich in the n-3 and n-6 unsaturated fatty acids respectively. Systolic blood pressure was measured using an indirect tail-cuff method at the end of the feeding period, and compared to a group of weanling rats.

Feeding the different diets did not alter the growth of the rats, so all animals were of similar weights at the time of blood pressure determination. Control (chow fed) animals, at nine weeks of age, had higher systolic blood pressures than the weanling, baseline control group. Fish oil fed rats had similar pressures to the chow fed rats. Corn oil fed rats had significantly lower systolic pressures than the controls. The rats fed the diets rich in saturated fatty acids (butter and coconut oil) had significantly higher blood pressures than all other groups. Systolic blood pressure was found to be significantly related to the dietary intakes of saturated and unsaturated fatty acids. The dietary intake of linoleic acid was significantly higher in corn oil fed rats than in other groups. Systolic blood pressure was inversely related to linoleic acid intake. Feeding a diet rich in saturated fatty acids significantly increases blood pressure in the rat. A high intake of n-6 fatty acids, and in particular linoleic acid, appears to have a hypotensive effect. Prenatal exposure of the rats to a maternal low protein diet, abolished the hypertensive effects of the coconut oil diet and the hypotensive effect of the corn oil diet upon young adult females. The intrauterine environment may, therefore, be an important determinant of the effects of these fatty acids on blood pressure in later life.     

Lymphatic transport in rats of several dietary fats differing in fatty acid profile and triacylglycerol structure

We examined in rats the intestinal absorption of nine very different dietary fats (two rapeseed oils, corn, olive, palm and menhaden oil, butter, cocoa butter and lard) to investigate the influence of fatty acid profile and triacylglycerol structure on absorption. Absorption was followed for 24 h after administration of similar amounts of fats, and the accumulated lymphatic transport and amount of triacylglycerols found in lymph in response to the administered fats were calculated, revealing major differences. The transport of olive and low alpha-linolenic rapeseed oil was significantly higher than that of the other fats (P < 0.05), except corn oil. The lymphatic transport of the other fats followed a slower course, with cocoa butter and menhaden oil having the lowest amounts transported. The amount of triacylglycerols found in lymph in response to the administered fats at 8 h ranged from 27.5% of the administered dose for cocoa butter to 72.1% for olive oil. The value for cocoa butter was significantly lower than that for most other fats. At 24 h, the values ranged from 66.5% for cocoa butter to 121.2% for olive oil. The high value for olive oil suggested transport of endogenous as well as exogenous fatty acids. The low value observed after cocoa butter resulted from decreased lipolysis and possibly also low absorption of triacylglycerols with high levels of long-chain saturated fatty acids in the sn-1/3 position. Furthermore, a low value was observed after menhaden oil administration, suggesting decreased absorption of fats containing (n-3) long-chain polyunsaturated fatty acids. Overall, these results demonstrate the influence of the fatty acid composition and triacylglycerol structure on the lymphatic absorption of dietary fat.     

Influence of dietary fats and vitamin e on plasma and hepatic vitamin a and β‐carotene levels in rats fed excess β‐carotene

Effects of different dietary lipids and excess vitamin E on plasma and hepatic concentrations of β‐carotene were evaluated in rats fed diets containing a large excess (0.2%) of β‐carotene. Male weanling Wistar Kyoto rats were fed β‐carotene‐supplemented diets containing various dietary lipids as follows: Group I, a saturated fat (coconut oil); Group II, a monounsaturated fat (olive oil); Group III, a polyunsaturated fat rich in ω‐6 fatty acids (safflower oil); Group IV, same as Group III plus vitamin E; and Group V, a polyunsaturated fat rich in ω‐3 fatty acids (menhaden oil). All diets contained 2% saf flower oil to provide sufficient amounts of linoleic acid (an essential fatty acid). Rats were killed after six weeks of feeding the various diets, and the concentrations of Q‐carotene and vitamin A were determined in plasma and liver. Plasma vitamin A levels were not altered by any of the dietary lipids or by an excess of vitamin E. The concentrations of β‐carotene in plasma were the lowest in rats fed the diet containing menhaden oil. The feeding of the diet containing an excess of vitamin E also resulted in a significant decrease in plasma β‐carotene concentration. Similarly, the hepatic β‐carotene concentration was also reduced to about one‐half in rats fed the diet containing an excess of vitamin E. Liver β‐carotene concentration was higher in Groups II and III than in the other three dietary groups. Hepatic vitamin A concentrations were also affected by the type of dietary fat. The highest levels were observed in rats fed the coconut oil diet; the lowest level of vitamin A was in rats fed menhaden oil (Group V). The results of this study suggest that the type of dietary fat and an excess of vitamin E can have a significant effect on 0‐carotene and vitamin A stores in liver and on β‐carotene content of plasma.     

Cod protein lowers the hepatic triglyceride secretion rate in rats

The objective of the present study was to determine the combined effects of cod protein and fish oil on the modulation of triglyceride metabolism in rats, and to evaluate their potential mechanisms of action. Plasma and hepatic lipid concentrations, triglyceride (TG) secretion rates and postheparin plasma lipoprotein lipase (LPL) activity were determined in rats fed for 28 d diets varying in both protein (200 g/kg) and lipid (140 g/kg) sources: 1) casein-menhaden oil, 2) casein-beef tallow, 3) cod protein-menhaden oil or 4) cod protein-beef tallow. Menhaden oil feeding diminished hepatic TG concentrations (P = 0.02), hepatic TG secretion rates (P = 0.003) and triglyceridemia (P = 0.02) compared with beef tallow. Hepatic TG concentrations (P = 0.05) and TG secretion rates (P = 0.04) were reduced in rats fed cod protein compared with those fed casein. The protein source did not exert an independent effect on triglyceridemia, whereas the combination of cod protein and menhaden oil resulted in 50% lower plasma TG compared with the casein-beef tallow mixture, whereas the combination of menhaden oil and casein did not significantly decrease triglyceridemia compared with casein-beef tallow. Menhaden oil (P = 0.005) and cod protein (P = 0.03) also lowered plasma cholesterol concentrations in comparison with beef tallow and casein, respectively. This was associated with a reduction in hepatic cholesterol concentrations when rats fed cod protein were compared with those fed casein (P = 0.006). No diet effect was observed on postheparin plasma LPL activity, but the activity of hepatic triglyceride lipase was reduced in rats fed menhaden oil compared with those fed beef tallow. These findings show that both cod protein and menhaden oil exert independent and beneficial effects on lipid metabolism in rats.     

Influence of dietary fats and vitamin E on plasma and hepatic vitamin A and beta-carotene levels in rats fed excess beta-carotene

Effects of different dietary lipids and excess vitamin E on plasma and hepatic concentrations of beta-carotene were evaluated in rats fed diets containing a large excess (0.2%) of beta-carotene. Male weanling Wistar Kyoto rats were fed beta-carotene-supplemented diets containing various dietary lipids as follows: Group I, a saturated fat (coconut oil); Group II, a monounsaturated fat (olive oil); Group III, a polyunsaturated fat rich in omega-6 fatty acids (safflower oil); Group IV, same as Group III plus vitamin E; and Group V, a polyunsaturated fat rich in omega-3 fatty acids (menhaden oil). All diets contained 2% safflower oil to provide sufficient amounts of linoleic acid (an essential fatty acid). Rats were killed after six weeks of feeding the various diets, and the concentrations of beta-carotene and vitamin A were determined in plasma and liver. Plasma vitamin A levels were not altered by any of the dietary lipids or by an excess of vitamin E. The concentrations of beta-carotene in plasma were the lowest in rats fed the diet containing menhaden oil. The feeding of the diet containing an excess of vitamin E also resulted in a significant decrease in plasma beta-carotene concentration. Similarly, the hepatic beta-carotene concentration was also reduced to about one-half in rats fed the diet containing an excess of vitamin E. Liver beta-carotene concentration was higher in Groups II and III than in the other three dietary groups. Hepatic vitamin A concentrations were also affected by the type of dietary fat.(ABSTRACT TRUNCATED AT 250 WORDS)     

Long-term feeding of corn oil, beef tallow, or menhaden oil and eicosanoid levels in BHE/cdb rats.

The effects of long-term feeding of 2 or 10% fat diets containing corn oil, beef tallow, or menhaden oil on the levels of eicosanoids in brain, plasma, and kidney medulla were studied. Male BHE/cdb rats, which carry a genetic trait for non-insulin-dependent diabetes mellitus, were fed these diets for 9 mo, at which time their glucose tolerance levels were determined, as were brain, kidney medulla, and plasma levels of PGE2, 6-keto-PGF1 alpha, and LTB4. Glucose tolerance was abnormal in the 2 and 10% corn oil groups and normal in the 10% menhaden oil groups. The glucose tolerance levels of the other groups were only slightly disturbed. The levels of LTB4 in kidney and plasma were not affected by dietary fat type or amount. LTB4 levels were significantly higher in the brains of rats fed a low level of beef tallow than in the brains of rats fed a higher level of beef tallow or a low level of menhaden or corn oil. LTB4 values for the brains of rats fed the other diets were intermediate and not different from the aforementioned values. The levels of 6-keto-PGF1 alpha were highest in rats fed the 10% corn oil diet regardless of the tissue assayed. Rats fed the 2 or 10% beef tallow or menhaden oil were not different but had lower levels of this eicosanoid metabolite than rats fed the corn oil diet. PGE2 levels followed the same pattern, suggesting that the impaired glucose tolerance of the corn oil-fed rats had a strong influence on the tissue levels of these eicosanoids.