Search

Small amounts of dietary n-3 fatty acids can have dramatic physiological effects, including the reduction of plasma triglycerides and an elevation of cellular eicosapentanoic (EPA) and docosahexanoic acids (DHA) at the expense of arachidonic acid (AA). We investigated the effects of alterations in the fatty acid compositions of cardiac sarcoplasmic reticulum (CSR) produced by dietary manipulation on the calcium pump protein that is required for energy dependent calcium transport. CSR was isolated from rats fed menhaden oil, which is rich in n-3 fatty acids, and from control animals that were given corn oil. Relative to control membranes, those isolated from rats fed menhaden oil, had a lower content of saturated phospholipids, an increased DHA/AA ratio, and an increased ratio of n-3 to n-6 fatty acids. These changes were associated with a 30% decrease in oxalate-facilitated, ATP-dependent calcium uptake and concomitant decreased Ca-ATPase activity in the membranes from the animals fed menhaden oil. In contrast, there was no alteration in active pump sites as measured by phosphoenzyme formation. Thus, the CSR Ca-ATPase function can be altered by dietary interventions that change the composition, and possibly structure, of the phospholipid membranes thereby affecting enzyme turnover.

Omega-3 fatty (n-3) acids are believed to inhibit the rate of occurrence and the growth of mammary tumors in rats treated with 7,12-dimethylbenz[a]anthracene (DMBA). Linoleic acid, on the other hand, has been shown to promote mammary tumorigenesis. This study was undertaken to see whether replacing 18% of the corn oil (high in linoleic acid) in a 20% fat diet with menhaden oil (high in n-3 fatty acids, low in linoleic acid) or coconut oil (low in n-3 fatty acids, low in linoleic acid), while keeping constant the cholesterol, antioxidant, and total fat content, would affect tumor incidence in virgin female BALB/c mice dosed with DMBA. Dietary treatment had no effect on body weight, feed intake, or survival to 44 weeks of age (36 wks after the first of 6 DMBA doses). Mammary tumor incidence was the same in the menhaden oil and coconut oil diet groups but was significantly higher in the 20% corn oil diet group. The protective effect of menhaden oil and coconut oil may be due, at least in part, to the decreased linoleic acid content of these diets relative to the corn oil diet. We conclude that n-3 fatty acids per se do not seem to inhibit tumor formation.

The effects of dietary lipid sources rich in n-6 (soybean oil) or n-3 (menhaden oil) polyunsaturated fatty acids (PUFA) on blood triacylglycerol levels and tissue fatty acid compositions in female chickens from two genetic lines were examined. Triacylglycerol concentrations in the plasma very low density and low density lipoprotein fractions were elevated in the low-weight (LW) chickens compared with the high-weight (HW) group. Chicken heterophil to lymphocyte ratios and total antibody titers to sheep red blood cells at 84 days were not influenced by genetic line or by the dietary lipid fed. Concentrations of C18:1 fatty acid isomers and total monounsaturates were highest in liver and heart tissues of HW chickens. Feeding menhaden oil enriched the plasma, liver, and heart with n-3 PUFA in both genetic lines. The data indicate a difference in hepatic fatty acid metabolism between the HW and LW lines that is unaffected by dietary n-6 or n-3 PUFA.

To determine the segment along the carcinogenic continuum at which dietary lipid exerts its principal effect, six groups of 35 Skh-HR-1 hairless mice were placed on defined isocaloric diets containing either 0.75%, 12% corn oil or 12% menhaden oil as sources of omega-6 or omega-3 fatty acids, respectively. All animals received an 11 week course of UV-radiation from fluorescent sunlamps. Upon termination of UV, diets of some groups were crossed-over to either low fat, high fat, omega-6 or omega-3 fatty acid sources. The first tumor appeared at week 14. Life-table analysis of the tumor incidence curves and Wilcoxon tests of tumor multiplicity provided evidence that high corn oil diets significantly (P less than 0.01) enhance carcinogenic expression; that tumor enhancement by the omega-6 fatty acid source occurs during the post-initiation, or promotion, stage; that replacement with a low corn oil diet after UV-initiation will negate the exacerbating effect of high corn oil; and that an omega-3 fatty acid source inhibits UV-carcinogenesis even at high dietary levels, although not during the post-initiation stage.

We tested two hypotheses, i) whether the type and the amount of fat in the diet will affect the formation of cholesterol gallstones in the hamsters, and ii) whether palmitic acid, a major fatty acid component of butterfat, can act as a potentiator of cholesterol cholelithiasis in the hamster. Young, male golden Syrian hamsters (Sasco) were fed a semipurified diet containing casein, corn starch, cellulose and cholesterol (0.3%) to which various types and amounts of fat (butterfat, olive oil, menhaden oil, corn oil) were added. All diets contained 2% corn oil to supply essential fatty acids to the growing hamsters. No deaths or illness occurred during the experiment. Animals fed the semipurified diet plus 4% butterfat (group 1) had a gallstone incidence of 63%. Replacement of butterfat with either olive oil, corn oil or menhaden oil prevented the formation of cholesterol gallstones entirely (groups 2–4). When total butterfat was increased from 4% to 8% (group 8), the incidence of cholesterol gallstones increased to 80%. Substitution of 4% olive oil (group 5), corn oil (group 6), or menhaden oil (group 7) for the additional 4% butterfat significantly reduced gallstones to 35%, 45% and 30%, respectively. The replacement of 4% butterfat with 1.2% palmitic acid gave the highest incidence of cholesterol gallstones (95%). These results suggest that butterfat (and one of its components, palmitic acid) intensifies gallstone formation in this model whereas mono- and polyunsaturated fats act as inhibitors of cholesterol cholelithiasis. A fatty acid, possibly palmitic acid, appears to act as lithogen in our model.

The influence of feeding 6% hydrogenated coconut oil, corn oil or menhaden oil on hepatocyte insulin binding, receptor number and glucose use was studied. Hepatocytes isolated from rats fed menhaden oil had a significantly greater affinity for insulin than hepatocytes from rats fed hydrogenated coconut oil. Glucose use was not influenced by diet; uniformly labeled glucose was metabolized to CO2 or to lipid similarly in cells isolated from rats fed the three oils. Thus, dietary fat type in a low fat diet influenced events at the plasma membrane without influencing intracellular events.

Addition of fish oils to infant formula provides (n-3) long-chain polyenoic fatty acids (LCP), specifically 22:6(n-3), to infants fed formula rather than human milk. Most fish oils, however, contain high levels of 20:5(n-3) and low (n-6) LCP. These studies determined the brain total, synaptic plasma membrane phosphatidylethanolamine and phosphatidylcholine, and plasma and liver phospholipid fatty acids of piglets fed from birth to 15 d with formula containing (percent fatty acids) 34% 18:2(n-6), 0.8% 18:3(n-3) and 0, 2 or 6 g/L menhaden oil, or sow milk. The brain 22:6(n-3) was higher and 22:4(n-6) lower in piglets fed 6 g/L menhaden oil compared with sow milk. Brain levels of 20:5(n-3) did not increase, or levels of 20:4(n-6) decrease, with increasing dietary (n-3) LCP. A diet concentration-dependent increase in 20:5(n-3) and decrease in 20:4(n-6) (P less than 0.0001) in liver phospholipid showed no evidence of maximum saturation or depletion, respectively, over the range of (n-3) LCP intake studied. The fish oil supplementation was effective in supplying 22:6(n-3) to the developing brain. The accompanying increase in 20:5(n-3) and decrease in 20:4(n-6), important eicosanoid precursors, in plasma and liver phospholipid show the need for caution in the use of fish oils low in (n-6) LCP as a source of (n-3) LCP for infant formula.

The aim of the present investigation was to study the effects of fish oil feeding in obese Zucker rats to establish its suitability as an animal model of hyperlipidaemia, and to understand the possible mechanism of fish oil-induced perturbations in cell metabolism. Lean and obese Zucker rats were fed on diets containing 180 g coconut, safflower, or menhaden oil/kg for 10 weeks. Body-weights and food intakes of lean coconut (LC), safflower (LS), and menhaden (LM) groups were similar. Obese menhaden (OM) rats had lower food intakes and body-weights compared with obese coconut (OC) and obese safflower (OS) groups, but values for all obese rats were higher than those for lean rats. Liver weights were higher in obese compared with lean rats, but on a percentage body-weight basis menhaden oil rats had higher values within genotype. Serum cholesterol and triacylglycerol levels were lower in the OM group compared with the OC and OS groups, and in the LM group compared with the LC group. Glucose and insulin levels were highest in OS rats followed by OC and OM rats and then the lean rats. Serum triiodothyronine and thyroxine were lower in OM rats compared with OC and OS rats. Liver mitochondrial state 3 rates with glutamate-malate and succinate were lower; mitochondrial β-oxidation was unaffected and peroxisomal β-oxidation was higher in menhaden oil rats compared with both coconut and safflower oil rats. In general, consumption of menhaden oil lowered hepatic malic enzyme (EC1.1.1.38, 1.1.1.40), glucose-6-phosphate dehydrogenase (EC1.1.1.49) and glutathione peroxidase (EC1.11.1.9) activities and elevated long-chain fatty acyl-CoA hydrolase (EC3.1.2.2) activity when compared with the two other diets. It is concluded that obese Zucker rats do respond like human subjects to fish oil feeding but not to vegetable oils. The hypolipidaemic effect of fish oil appears to be mediated through a lowering of lipogenic enzymes, glucose-6-phosphate dehydrogenase and malic enzyme.

We evaluated the effects of menhaden oil on growth and development of the small intestinal mucosa in growing rats and on the progression and resolution of methotrexate-induced mucosal injury in the rats. One study compared effects of diets containing 10% safflower oil(SO), 9% SO and 1% menhaden oil (MO), 10% MO, or 9% MO and 1% SO on mucosal growth and development for 125 d. In another study, animals fed the 10% MO or the 10% SO diet for 5 wk were subjected to subcutaneous methotrexate injections for 3 consecutive days. Feeding rats a diet containing large amounts of menhaden oil resulted in lower prostaglandin E2 and leukotriene B4 synthesis and lower sucrase activities. Indicators of mucosal mass after methotrexate-induced injury were significantly improved in both the jejunum and ileum at 3 and 10 d after methotrexate administration. Our data suggest that dietary menhaden oil stimulates mucosal regeneration after methotrexate-induced injury.

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.

Due to the numerous proposed cardiovascular benefits associated with consumption of omega-3 fatty acids, marketing of an egg enriched by omega-3 fatty acid may benefit the egg producer. Effects on yolk composition of a standard laying hen diet enriched with 3% menhaden oil (test diet), versus an isocaloric (control) diet containing no added fat, were evaluated for 18 wk. Dietary menhaden oil did not alter egg production, egg weight, total yolk fat, or yolk cholesterol. However, yolk contents of omega-6 and omega-3 fatty acids were influenced by diet. Arachidonic acid decreased and eicosapentaenoic acid increased in eggs from hens fed the test diet following 1 wk of dietary treatment. Docosahexaenoic acid and linolenate increased in eggs from hens fed the test diet at 2 and 3 wk of the trial, respectively. These alterations in yolk composition resulted in a decrease in the ratio of omega-6 to omega-3 fatty acids from 18 for eggs from hens fed the control diet to 3 for eggs from hens fed the test diet. At Weeks 14 and 18, hens (n = 10 per diet) were killed and necropsied. No change in gross scoring of hepatic lipidosis was observed. Histologically, significantly greater scores for hepatocellular lipid infiltration were recorded for liver sections from hens fed menhaden oil than for control hens. Increased microscopic hepatic lipid infiltration observed with dietary omega-3 administration may have significance for flocks predisposed to fatty liver syndrome and may also provide a unique system in which to study the effects of dietary omega-3 fatty acids on liver lipid metabolism.

Fish oil has been shown to have a protective effect in some cancer models. To determine whether fish oil alters skin tumorigenesis, a study was designed using the initiation-promotion mouse skin carcinogenesis model, feeding mice during the promotion stage a constant overall amount of dietary fat (10%) in which the levels of menhaden oil (MO) varied from 0 to 8.5% or corn oil (CO) at 10%. SENCAR mice were initiated with 10 nmol dimethylbenz[a]anthracene. Two weeks later mice were divided into five groups and maintained on one of the following AIN-76 based diets consisting of: 8.5% coconut oil (CT)/1.5% CO (diet A); 1% MO/7.5% CT/1.5% CO (diet B); 4% MO/4.5% CT/1.5% CO (diet C); 8.5% MO/1.5% CO (diet D); or 10% CO (diet E). Two weeks later, promotion with twice weekly applications of 1 micrograms 12-O-tetradecanoylphorbol-13-acetate (TPA) was begun and continued for 24 weeks. No statistically significant differences in kcal food consumed or body wts were observed between diet groups during the study. The final papilloma and carcinoma incidence was not different among the diet groups. However, differences were seen in the rate of papilloma appearance with the group fed diet E (10% CO) being the slowest and diet B being the most rapid. In a parallel study, ornithine decarboxylase activity, a suggested marker of promotion, was greatly elevated in the epidermis of all TPA-treated mice and the effect of diet tended to reflect the different rates of tumor formation observed among the groups. These data indicate that the diets containing fish oil were not protective in the final incidence of tumor formation and suggest that a better understanding of the complex interactions is warranted before recommendations are made to alter the human diet for cancer prevention.

Feeding vitamin E-deficient diets containing either fish oils such as menhaden, salmon, or anchovy oil or fish oil concentrates based on n-3 ethyl esters or free fatty acids protected mice against Plasmodium yoelii as indicated by decreased parasitemia and improved survival. The fish oil concentrates depressed plasma tocopherol levels more strongly in vitamin E-supplemented mice than the menhaden oil. The free fatty acid concentrate appeared to suppress parasitemia in vitamin E-deficient mice better than the menhaden oil, although ultimate survival was similar in both groups. Dietary manipulation of host antioxidant status offers promise as a possible means of malaria control.

The relative cellular uptake and incorporation into prechylomicrons and chylomicrons was investigated for the menhaden and rapeseed oil fatty acids, when given by stomach tube as the original oils or the corresponding methyl and ethyl esters. The intermediates and final products of cellular acylation were determined by chromatographic methods at various times over a period of 1–24 h. There was little selectivity in the uptake among the oligo- and poly-unsaturated fatty acids of menhaden oil, when either oil or esters were fed. In contrast, the long-chain saturated and monounsaturated fatty acids of rapeseed oil were discriminated against during both cellular uptake and reacylation (60% overall reduction in utilization). Also, there was detectable discrimination against the long-chain polyunsaturated monoacylglycerols of menhaden oil and against the long-chain saturated and monounsatured monoacylglycerols of rapeseed oil during both cellular uptake and reacylation (30% overall reduction in utilization). Evidence was obtained for an indiscriminate cellular uptake of variable amounts (4–22%) of intact dietary methyl and ethyl esters of fatty acids, which, however, appeared in the chylomicrons only to a very limited extent (0.1–1.0% of total lipid). During peak absorption the cellular and lymphatic appearance of fatty acids from the digestion and absorption of the alkyl esters was nearly 50% lower than that from the corresponding triacylglycerols. The slower absorption of the fatty acids from the alkyl ester feeding is hypothetically attributed to a lower efficiency of the phosphatidic acid pathway, which is required in the absence of dietary 2-monoacylglycerols, but other mechanisms cannot be excluded.Key words: villus cells, prechylomicrons, chylomicrons, triacylglycerol biosynthesis, monoacylglycerol pathway, phosphatidic acid pathway.

In order to distinguish between possible fatty acid differences during lumenal lipolysis and cellular absorption, we have reinvestigated the in vitro hydrolysis of menhaden oil and its alkyl esters by pancreatic lipase. For this purpose we incubated menhaden oil or its fatty acid methyl and ethyl esters with porcine pancreatic lipase in the presence of bile salts and determined the composition of the released free fatty acids, monoacylglycerols, diacylglycerols, and residual triacylglycerols, or the free fatty acids and residual alkyl esters, respectively, by thin-layer and gas-liquid chromatography. There was significant discrimination against the delta 4- to delta 7-unsaturated fatty acids of both medium and long chain lengths during the hydrolysis of menhaden oil and its fatty acid ethyl esters. In general, the ethyl esters were hydrolyzed 10-50 times more slowly than the corresponding glyceryl esters, depending on the exact ratio of the two substrate types. None of the triacylglycerols or ethyl esters, however, was completely resistant to hydrolysis resulting in an eventual cleavage of all the alkyl esters and presumably all the primary ester bonds in the triacylglycerol molecules. Since the rate of release of the least resistant fatty acid exceeded that of the most resistant acid by only a factor of 6, it is concluded that in the presence of a large excess of lipase the liberated fatty acids would approach the composition of the dietary alkyl or glyceryl esters, as observed during lumenal lipolysis (Yang, L.-Y., A. Kuksis, and J. J. Myher. 1989. Biochem. Cell Biol. 67: 192-204).

Cholesterol gallstone formation in the prairie dog is accompanied by an increase in the percentage of biliary phospholipids containing arachidonic acid, and an increase in gallbladder prostaglandin (PG) synthesis, but the pathogenetic significance of these changes is unclear. Dietary supplementation with eicosapentaenoic acid (EPA), an omega-3 fatty acid which is commonly found in fish oil, decreases prostaglandin synthesis in some tissues by replacing arachidonic acid, and by competitively inhibiting prostaglandin synthesis. We studied the effect of dietary fish oil on gallbladder PG synthesis, and the relative abundance of various molecular species of phosphatidylcholines and phosphatidylethanolamines in bile and gallbladder epithelium in the cholesterol-fed prairie dog. Prairie dogs were maintained for 4 weeks on one of four diets: i) control, ii) cholesterol-supplemented (0.34%), iii) menhaden oil (50 g/kg chow), or iv) cholesterol plus menhaden oil. Supplementation with menhaden oil resulted in a replacement of arachidonic and linoleic acids with EPA and docosahexaenoic acids in the phospholipids of bile and gallbladder mucosa. In cholesterol-fed animals, supplementation with menhaden oil prevented increased gallbladder PG synthesis. Menhaden oil also reduced the incidence of cholesterol monohydrate crystals among cholesterol-fed animals (9/20 with cholesterol plus menhaden oil vs 21/22 with cholesterol alone), but the improvement could not clearly be attributed to decreased PG synthesis since supplementation with menhaden oil also increased the total phospholipid concentration in bile, and decreased the degree of cholesterol saturation. These results demonstrate that dietary supplementation with omega-3 fatty acids significantly influences biliary phospholipids, and decreases the incidence of cholesterol monohydrate crystal formation in this animal model.

The absorption of equivalent doses of eicosapentaenoic and docosahexaenoic acids was compared in rats when administered as the ethyl ester concentrate, ethyl ester concentrate plus olive oil, free fatty acid or triacylglycerol (menhaden oil). Lymph was collected from a thoracic duct cannula for 24 hr after dosing via an indwelling duodenal catheter. After 24 hr, the absorption of eicosapentaenoic acid was greater for the free fatty acid and menhaden oil than for the ethyl ester form, but docosahexaenoic acid absorption was comparable for all forms. Other rats had greater plasma levels of eicosapentaenoic and docosahexaenoic acids 5 hr after oral gavage dosing with menhaden oil than did rats dosed with the ethyl ester form.

LEARNING OUTCOME: The learner will describe the lipid composition of poultry meat designed to serve as a functional food for increasing n-3 fatty acid consumption The U.S. Dietary Guidelines recommend fish as a low-fat source of protein and n-3 fatty acids (n-3 FA). Dietary n-3 FA are believed useful for reducing heart disease risk and promoting neonatal development. Unfortunately, a disparity exists between nutritional recommendations and dietary practice, as consuming 2–3 fish meals per week is considered healthful but the current average U.S. consumption offish is only 1.3 meals per week. Functional foods have been proposed as food-based alternatives to dietary supplements for increasing the availability of certain desirable nutrients. The current study investigated the manipulation of poultry diets to include n-3 FA for the production of n-3 FA rich poultry meat. Meat-type chickens were fed diets containing either 8.4 g of docosahexaenoic acid (DHA; 22:6n-3) from marine algae (MA) or 8.4 g DHA from menhaden oil (MO) for 28 days prior to commercial processing. Both diets yielded breast meat with similar total fat as typical breast meat, 2.0 and 1.7 g per 100 g serving, respectively. Importantly, however, both diets yielded significantly greater n-3 FA than that found in typical chicken breast meat (44±5 mg/100 g). The MA diet, however, produced breast meat containing 190±10 mg total n-3 FA per 100 g serving compared to the MO diet which yielded breast meat containing only 87±11 mg total n-3 FA per serving. An equivalent serving of lean fish typically contains between 100 and 300 mg total n-3 FA per 100 g serving, therefore, a serving of breast meat from a chicken fed MA would provide a similar n-3 FA content as lean fish. These data indicate that the manipulation of poultry rations to include MA results in a breast meat that can serve as a functional alternative to fish for increasing n-3 fatty acid consumption and thus promoting health.

Although omega-3 (n-3) fatty acids which are polyunsaturated would be predicted to reduce plasma lipids, data have not been consistent. The objective of this research was to assess whether dietary intake of other nutrients and energy was related to the manner in which n-3 fatty acids affected plasma cholesterol and triglyceride. Healthy male and female subjects (n=30) were assigned randomly to consume self-selected diets restricted in n-3 fatty acids plus either regular (C) or n-3 enriched shell eggs (4/week), the latter from hens fed flaxseed (F, high in linolenic acid) or menhaden oil [(M, high in docosahexaenoic acid (DHA)]. Subjects consumed all types of eggs for 6 weeks with a 4-week washout period between each. Plasma total cholesterol (TC) and triglycerides (TG) were measured enzymatically and dietary intake assessed from 3-day food records (2/period) by the Nutrient Data System (University of Minnesota, 1994). Pearson's product moment correlation coefficients between plasma lipids and dietary components were determined. Plasma TC was correlated (P

In numerous in vivo systems it has been shown that diets high in menhaden oil (a fish oil high in omega-3 fatty acids) can inhibit the carcinogenic process. In the present study, we have assessed the effects of a diet containing menhaden oil on 2-amino-3-methylimidazo[4,5-f]quinoline (IQ)-DNA adduct formation in target tissues of the male Fischer 344 rat. Young adult male Fischer 344 rats were maintained on either a) an AIN-76A diet containing 5% corn oil, b) an isocaloric AIN-76A diet modified to contain 2% corn oil and 19% menhaden oil (MO diet), or c) a regular laboratory rodent diet (chow diet) for 6 weeks prior to receiving a single oral dose of 10 or 50 mg IQ/kg. Groups of four animals were killed 1 or 6 days after IQ administration. Using 32P-postlabeling assays, IQ-DNA adducts were isolated and quantitated in the liver, small intestine, and large intestine. Adduct patterns were similar in all cases. Adduct levels, expressed as relative adduct labeling values (RAL x 10(7)), were related to dose in all three tissues, with liver levels up to 10-fold higher than the large intestine and up to 20-fold higher than the small intestine. On day one, liver adduct levels in animals on the AIN-76A diet were similar to those in animals on the chow diet, but those in animals on the MO diet were approximately 2-fold lower.(ABSTRACT TRUNCATED AT 250 WORDS) Images Figure 1. a Figure 1. b Figure 1. c

The significance of the lipid composition of membranes became important once it was established that membranes are dynamic lipid bilayers, consisting primarily of phospholipid, neutral lipids and cholesterol that provide a supporting matrix for proteins [ I ] . The physical properties of the membrane are determined by many factors including the phospholipid head group [2], the length and degree of unsaturation of the fatty acyl chains [3] and the molar ratio of cholesterol to phospholipid [4]. Rainbow trout, like all poikilotherms. alter the lipid composition of their membranes to maintain a coxtant membrane fluidity [5,6] thus preventing temperature induced alterations to membrane-mediated processes. When this homeostatic mechanism is compromised, either by extreme diet or by in virro supplementation of lipids, certain cellular functions are altered or rendered inoperative (7.81. In the present study, rainbow trout, Oncorhynchus mykiss, were maintained on two diets, using either sunflower or fish (menhaden) oil as the sole source of lipid. Leucocyte phospholipids isolated from fish maintained on the menhaden oil based diet for at least eight weeks displayed a greater mean number of double bonds per fatty acyl chain than those fed the sunflower oil diet (Ashton er al. unpublished data). When the membrane fluidity of macrophages was determined using the fluorescence polarization of I .6-diphenyl1.3.5-hexatriene. the membranes of cells from fish maintained on the sunflower oil diet were found to be more fluid (Table I). This was in contrast, however, to the expected result i.e. that the membranes containing the more unsaturated lipids would have been more fluid [2]. Cholesterol is known to have an ordering influence upon membrane fluidity when the lipids are in the liquid-crystalline state [9]. The possibility therefore exists that the differing concentrations of cholesterol in the diets were affecting membrane composition and fluidity. The diets were extracted and analysed for cholesterol by using the Lieberman-Burchard reaction [lo]. The serum cholesterol concentrations of fish from both diets were also determined using a cholesterol assay kit (Sigma Chemical Co. Ltd.) to ensure that any difference observed between the two diets was reflected in the tissues of the trout. As can be seen from Table I , the group of fish fed on the menhaden oil diet exhibited a significantly higher serum cholesterol concentration than those fish maintained on the sunflower oil diet. To investigate if serum factors alter membrane fluidity, macrophages isolated from fish maintained on a commercial diet (Mainstream expanded diet, B.P. Nutrition) were incubated for 21 hr at the environmental temperature in RPMI 1640 medium containing 5% serum of known cholesterol content from fish fed on either the sunflower or menhaden diets. The cells incubated with serum from the menhaden oil fed fish, displayed reduced membrane fluidity that correlated with the raised concentrations of cholesterol in the serum semples (Figure I ) . Macrophages incubated with the serum from fish maintained on the sunflower oil diet did not exhibit any significant alteration

The ability of a menhaden oil (MO) diet to influence cercarial penetration into mouse tail skin was evaluated. Male CD-1 mice 4-6 wk old (15.2 g average weight) were fed a 0, 10%, or 20% MO-supplemented diet for 2 wk. After this time mice were infected with either 65 +/- 3 or 145 +/- 3 [35S]methionine/cysteine-labeled cercariae for 1 hr by tail immersion. Twenty-four hours and 7 days later groups of mice were killed and their tail skin removed and autoradiographed. At 24 hr postinfection, mice fed a 20% MO diet had significantly higher cercarial penetration than controls and 10% MO diets (56% +/- 5.2 vs. 44% +/- 2.9, P = 0.02, 1-tailed t-test). After 7 days mice fed a 20% MO diet retained more radioactive foci than controls or 10% MO diets (21% +/- 2.0 vs. 15% +/- 1.3, P = 0.01, 1-tailed t-test).

Groups of Atlantic salmon held in marine net-pens were fed Oregon Moist Pellets in which herring oil was replaced with either menhaden oil, soybean oil, or tallow. The lipid sources constituted approximately 37% of the total lipid in the diet, the remainder being contributed by the other dietary ingredients. After 23 weeks of feeding, the fish were harvested and growth, chemical composition, and sensory attributes were measured. Dietary lipid source did not affect growth or proximate composition of the fillets. Fatty acid composition of the fillets reflected the fatty acid composition of the diets, although the differences in fatty acid composition among groups of fish were less than the differences in fatty acid composition among the experimental diets. Sensory attributes were not affected by dietary lipid source. This study shows that Atlantic salmon can utilize alternate lipid sources in the diet without compromising growth or organoleptic quality and that dietary lipid substitution offers the possibility of producing fish containing fatty acid profiles preferred in the market.

The Mrl lpr/lpr (Mrl/l) mouse is a model for systemic lupus erythematosus and rheumatoid arthritis in humans. The diet of Mrl/l mice was supplemented with EPA (see Introduction) in menhaden oil or in the commerical fish oil MaxEPA. The survival of mice was not affected by the dietary manipulations. The addition of menhaden oil decreased the severity of the renal pathology. However, MaxEPA containing the same amount of eicosapentaenoic acid was considerably less effective. A diet deficient in polyunsaturated fatty acids did not ameliorate any manifestations of the disease. Anti-DNA antibody levels in serum were not influenced by the therapy. Myocardial abscesses and/or ulcerating valvular lesions were observed in about one third of the mice, irrespective of the diet given.

A study was conducted to evaluate the effects of feeding, varying levels of menhaden oil on weight gain, feed conversion, and whole-body proximate and fatty acid composition of red drum. The experiment was conducted utilizing a brackishwater (5–6 ppt) recirculating system which supplied water to a series of 40-l aquaria. Fish (1.8g) were stocked at a rate of 12 fish per aquarium (48 fish/treatment) and fed the appropriate diet twice a day for a period of 6 weeks. All diets contained 40% protein and an estimated digestible energy value of 15.4 kJ/g of diet. Dietary lipid levels ranged from 1.7 to 18.8%. Weight gain, feed conversion, and survival were best at dietary lipid levels of 7.4 and 11.2%. Fish fed the diet containing 18.8% lipid had lower weight gains and higher feed conversion ratios than fish fed lower levels of lipid. Whole-body lipid concentrations increased as dietary lipid increased up to 7.4% then decreased when dietary levels were elevated to 15% or greater. Whole-body fatty acids generally reflected dietary lipid, particularly in respect to the n3 polyunsaturated fatty acids.

To complement studies on monoethylenic fatty acids produced from the major polyunsaturated fatty acid (20:5A5,8,11,14,17) during hydrogenation of a menhaden oil of iodine value (IV) 159, the C10 dienoic and trienoic fatty acid isomers of partially hydro-genated menhaden oils (PHMO) of IV 131.5, 96.5 and 85.5 were isolated by a combination of preparative gas liquid chromatography (GLC), mercuric adduct fractionation, and silver nitrate thin layer chromatography (AgNO3-TLC). The 20:2 fatty acid methyl esters of the three PHMO samples were transformed to the corresponding alcohols and ozonized in BF3-MeOH, followed by GLC analysis of the ozonolysis fragments. During the hydrogenation process, re-sidual ethylenic bonds in the 20:2 isomers tend to migrate both towards the carboxyl group and towards the methyl end of the molecule. The hydrazine reaction results revealed that thetrans ethylenic bonds in the 20:2 and 20:3 isomers were distributed all along the the carbon chain, but thecis ethylenic bonds were more localized in the Δ11,Δ14 and Δ17 positions of the preexisting major menhaden oil component 20:5Δ5,8,11,14,17. Iatroscan analyses on AgNO3-chromarods revealed that, as a result of the hydrogenation process, almost half of the 20:2 isomers were non-methylene-interruptedcis, trans/trans, cis structures.

Feeding rats and guinea pigs on a diet containing 5% menhaden oil altered the fatty acid composition of lung microsomes. The lung microsomal phospholipids contained increased amounts of n-3 fatty acids, eicosapentaenoic (20:5) and docosahexaenoic acid (20:6), following the ingestion of menhaden oil. There was a concomitant decrease in arachidonic acid (20:4) levels in rat lung microsomes, but no significant change of this fatty acid was observed in the microsomes from guinea pigs. The ability of lung microsomes to convert 14C-arachidonic acid. into thromboxane (TXB) was reduced by the enrichment of n-3 fatty acids in the microsomal lipids.

Studies on the effects of feeding various sources of n-3 fatty acids on the fatty acid composition of lipids in edible tissues and lipoproteins in chickens were conducted. Commercial meat-type chicks were fed one of four dietary lipids: (1) linseed oil, (2) menhaden oil, (3) soybean oil, or (4) chicken fat, at 50 g/kg of the diet from hatch through 56 days. Chickens fed the polyunsaturated lipids, linseed oil, menhaden oil, and soybean oil, all had similar plasma and VLDL + LDL (very low density lipoproteins and low density lipoproteins) triacylglycerol levels all of which were lower than those for chickens fed chicken fat. The fatty acid compositions of the VLDL + LDL fractions and tissue lipids were similar to the dietary lipids fed. However, the fatty acid compositions of the abdominal fat pads and brains reflected de novo synthesis in addition to the influence of dietary lipids. The levels of 20:50 in tissue lipids of chickens fed linseed oil approached those levels found in chickens fed menhaden oil. Chickens fed linseed oil had the highest levels of polyunsaturates in tissues while those fed chicken fat had the lowest levels. Chickens fed soybean oil maintained the highest levels of 18:2n6 and 20:4n6 in tissue lipids. Both the linseed oil and menhaden oil treatments exhibited lower levels of 20:4n6 in tissue lipids compared with the soybean oil and chicken fat treatments. These data indicate that dietary n-3 lipid sources influence the fatty acid composition of tissues and can be effectively used to enrich chicken meat with n-3 polyunsaturated fatty acids.

Channel catfish (Ictalurus punctutus) were grown in tank culture on diets containing either tallow or menhaden oil at 10% of diet. Processed fish were frozen in air at —18°C or in nitrogen spray at -77°C, sealed in polyethylene, and stored at either -18 or -35°C. Levels and fatty acid profiles were determined for total lipid, triglyceride, phospholipid, and free fatty acids in fresh fish that had been held on ice for 2 days and in frozen fish at 0, 94, 220, and 312 days. Dietary lipids strongly affected fatty acid profiles of all lipid fractions. Free fatty acid production occurred only in fish held on ice and in fish stored at -18°C. Changes in free fatty acid profiles and decreases in phospholipid levels indicated phospholipase activity. After 312 days storage at -18°C free fatty acid levels reached approx 0.93%. Measurable oxidative deterioration did not occur under either condition of frozen storage.

Fish oils, often an abundant source of C20 and C22 fatty acids, could supplement rapessed oil in the manufacture of long chain saturated fatty acids. Herring oil, traditionally the fish oil of choice, is in very short supply due to depletion of fishery stocks. Menhaden oil, when made from fish caught in the Atlantic, could furnish a steady supply with long chain acids at about the 30% level. Oil made from other species such as anchovy or pilchard need further data on fatty acid content and variability. Manufacture of polyunsaturated fatty acids from fish oils is hampered by lack of suitable procedures. Potential markets for fish oil polyunsaturates especially in the pharmaceutical field seem promising.

The interacting effects of fat type and carbohydrate source on the hepatic lipogenic response to starvation-refeeding were studied. Three experiments were conducted using male rats fed ad libitum or starved for 48 hours and refed one of four diets. The diets contained corn or menhaden oil and glucose or sucrose. The activities of NADP-linked glucose 6-phosphate dehydrogenase and malic enzyme were determined as were liver lipid (Experiments 1 and 2) and de novo fatty acid synthesis (Experiment 3). Experiment 1 used Sprague-Dawley rats while experiments 2 and 3 used BHE rats. Rats refed the menhaden oil diets had less of a lipogenic response to starvation-refeeding compared to rats refed the corn oil diets. Sucrose-refed rats had more of an enzyme response and a greater fatty acid synthesis response to refeeding than BHE rats refed either of the menhaden oil diets or the corn oil-glucose diet. The percent increment in these parameters was strain dependent. We conclude that the effectiveness of menhaden oil in decreasing fatty acid synthesis is dependent on the type of carbohydrate in the diet and the genetic character of the animal used.

Menhaden oil (MO), whose polyunsaturated fatty acids consist mainly of (n-3) fatty acids, was fed to spontaneously hypertensive rats to determine the effect of (n-3) fatty acid on the in vitro production of prostaglandins produced from arachidonic acid (20:4[n-6]). Capacity to form PGE2 and PGF2 alpha was impaired in homogenates of kidney medullae and cortices from rats fed the MO diet compared to rats fed the control diet. The lower amounts of diene prostaglandins produced corresponded to the decrease in the amount of 20:4 (n-6) in the tissue. Possibly changes produced in tissue lipids by dietary fatty acids affect prostaglandin production by reducing the availability of substrate in tissue lipids.

US menhaden oil is rich in long-chain polyethylenic fatty acids, chiefly C20 (eicosapentaenoic) and C22 (docosahexaenoic) fatty acids, unlike Canadian herring oil, which is rich in long-chain (C20 and C22) monoethylenic fatty acids. An examination of the product fatty acids from hydrogenation of menhaden oil therefore comple-ments studies previously published for herring oil. During a commer-cial hydrogenation of menhaden oil, iodine value (IV) 159.0, on nickel catalyst, samples were collected at IV 150.0, 140.0, 131.5, 120.5, 96.5, 90.0 and 84.5. The fatty acid compositions were deter-mined using a combination of mercuric adduct fractionation and gas liquid chromatographic (GLC) analyses, and the totaltrans content by infrared spectroscopy. The partial hydrogenation resulted in the disappearance of the pentaenoic and hexaenoic fatty acids, a de-crease in tetraenes, and a definite increase in trienes, 8.3% at IV 84.5 compared to 4.2% at IV 159.0. The dienoic fatty acids in-creased to 13.2% at IV 84.5 compared to 4.1% at IV 159.0, and the monoenoic fatty acids increased to 34.2% from 24.0%. No impor-tant changes in the saturated acids were observed, 43.8% at IV 84.5 compared to 41.6% at IV 159.0. The totaltrans content varied from 3.4% at IV 150.0 to 45.1% at an IV of 84.5. The isomer composi-tions of thecis andtrans C20 monoethylenic fatty acids were deter-mined using a combination of preparative GLC, AgNO3 thin layer chromatography and ozonolysis. Thecis 20:1 acids at IV 84.5 still retained 27.5% of the major isomer (All) originally present at 72%. The parent A5, A8, All, A14 and A17 bonds of the 20:5 originally present could be detected in thecis 20:1 isomers at IV 96.5 but not at IV 84.5. At IV 84.5, 58% of the 20:1was trans, the major isomer being All (9.4% of total 20.1), accompanied by important quanti-ties of Δ10 and Δ12, respectively, 6.9% and 6.6% of the total 20:1.

Prostaglandins and related compounds are active mediators of inflammation, but data concerning their role in the pathogenesis of the glomerulonephritis of New Zealand Black x New Zealand White (NZB x NZW) F1 mice are conflicting. Dietary eicosapentaenoic acid (EPA, C20:5), a fatty acid analogue of arachidonic acid (C20:4), has been shown to impair platelet aggregation in humans, apparently through inhibition of the synthesis of prostaglandins and thromboxanes from arachidonic acid. We report here the effects of a diet high in EPA on the development of renal disease and survival in female NZB x NZW F1 mice. Animals from 4--5 wk of age were fed diets containing 25% lipid, supplied either as beef tallow or menhaden oil, with fatty acid analysis of less than 0.05 and 14.4% EPA, respectively. In the first experiment, by 13.5 mo of age, mice on the beef tallow diet had all (9/9) developed proteinuria and the majority (6/9) had died, with renal histologic examination revealing severe glomerulonephritis. In contrast, none of 10 menhaden oil-fed animals had developed proteinuria, and all were alive at this time (P less than 0.005 for both proteinuria and survival). In a second experiment using 50 mice in each dietary group, 56% of the beef tallow group vs. none of the menhaden oil group had developed proteinuria at 9 mo of age (P less than 0.005). Native DNA binding at 6 mo of age was 23.9 +/- 14.7 vs. 10.1 +/- 9.7% in the beef and menhaden oil groups, respectively (P less than 0.01). Weights were similar in all groups, and there was no evidence of essential fatty acid deficiency in any group. These results demonstrate that a diet high in EPA protects NZB x NZW F1 mice from the development of glomerulonephritis.

The regulation of hepatic and intestinal 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase and acyl-CoA; cholesterol acyltransferase (ACAT) activities by dietary fish oil was examined in the rabbit. Rabbits were fed 10% menhaden oil or menhaden oil plus 1% cholesterol for 14 days. They were compared with animals fed a control diet or one enriched with long-chain saturated fats consisting of 10% cocoa butter oil or cocoa butter oil plus 1% cholesterol. Plasma cholesterol was increased in rabbits fed the fish oil and the two cholesterol-containing diets. In the liver, ACAT activity was increased and HMG-CoA reductase activity was decreased in rabbits ingesting the fish oil. The same was true for animals ingesting both cholesterol-containing diets. In the intestine, ACAT activity was not affected by the ingestion of the fish oil compared to control rabbits; however, it was significantly higher in animals fed the fish oil compared to animals ingesting the cocoa butter. HMG-CoA reductase activity was decreased in the distal two-thirds of the intestine in animals fed the menhaden oil compared to activities observed in controls. In animals ingesting the cholesterol diets, intestinal reductase was significantly decreased, whereas intestinal ACAT activity was increased in rabbits ingesting the cocoa butter and cholesterol diet when compared to their controls. Lipid analysis of hepatic and intestinal microsomes demonstrated an enrichment of n-3 polyunsaturated fatty acids in membranes from rabbits ingesting the menhaden oil.(ABSTRACT TRUNCATED AT 250 WORDS)

Three species of nonhuman primates were fed an atherogenic diet for 6 months (baseline period) and a menhaden oil (EPA)-containing diet for 8 weeks (test period) during which various hemostatic and lipid parameters were compared. The EPA-rich diet prolonged bleeding times, inhibited platelet aggregation response to ADP and collagen, and increased mean platelet lifespan. This diet elicited an increase in the polyunsaturated fatty acids C20 : 5 (EPA) and C22 : 6 (docosahexaenoic acid) at the expense of C18 : 2 (linoleic acid) and C20 : 4 (arachidonic acid) in pooled samples of platelet membranes, creating an increase in the ratio of n-3/n-6 polyunsuturated fatty acids. The serum lipid response to a menhaden oil diet comprised a nonsignificant decrease in total serum cholesterol and a significant decrease in HDL cholesterol.

Adult channel catfish (Ictalurus punctatus) were fed diets containing menhaden oil (MHO), soybean oil (SBO), or beef tallow (BFT) as lipid sources for 116 d. The effects of these diets on two important hepatic xenobiotic-metabolizing enzyme systems, cytochrome P-450-dependent monooxygenases (MOs) and glutathione S-transferases (GSTs), were evaluated. Microsomal MO and cytosolic GST activities were consistently greater in fish fed MHO than in those receiving SBO or BFT. Generally, enzyme activities in fish fed SBO and BFT were similar. The different diets also markedly influenced the fatty acid composition of the liver, particularly with respect to the relative abundance of specific fatty acid families. These data demonstrate that dietary lipid does affect the activities of xenobiotic-metabolizing enzymes in fishes, and thereby could influence the sensitivity of fishes to certain organic toxicants.

Florida pompano (Trachinotus carolinus) juveniles were fed to satiation twice daily on one of four experimental diets containing 12, 8, 4, or 0% menhaden fish oil for 48 days in flowing-water tanks at 28 C (82 F). Basalingredients of the diets were lipid-extracted menhaden fish meal (50%), lipid-extracted, dehulled soybean meal (20%), dextrin (8.9%), cellulose (variable with fish oil) and vitamin and mineral supplements. Fish fed the 8% oil diet gained more weight than those fed the 0 to 12% fish oil diet. Fish fed the diet containing no fish oil gained less weight than those fed any of the diets containing fish oil and had deformed gill opercula and filaments. The gill anomalies are presumed to have been caused by essential lipid deficiencies in the diet. Energy deficiency could also have been responsible for poor growth by the fish fed the diet without fish oil. Energy excess could have caused the fish fed the highest level of fish oil to consume less diet and, therefore, been responsible for t...

Four groups of New Zealand White rabbits (n=8) were fed semi-synthetic diets containing 7.6% fat (w/w) for 20 weeks. The fats were: 1. hydrogenated soybean oil (HSBO), 80% stearic acid, with 2% safflower oil (SO), 2. safflower oil, 78% linoleic acid, 3. linseed oil (LO), 54% linolenic acid, and 4. menhaden oil (MO), 21% palmitic acid, 13% eicosapentaenoic acid (EPA), and 8% docosahexaenoic acid (DHA). The diets contained 20% of calories from protein, 56% from carbohydrate, and 24% from fat. The MO diet also contained 0.06% cholesterol while the other diets were cholesterol free. Before assignment to experimental diets, the animals had serum cholesterol values of 62.1±20.3 mg/dl and triglyceride concentration of 40.3±14.3 mg/dl (mean±S.D.). After 4 weeks on the diets, the cholesterol values in the four groups were: HSBO, 70.9±21.2 mg/dl; SO, 59.1±15.9 mg/dl; LO, 65.1±50.7 mg/dl; and MO, 141.7±67.2 mg/dl. Only the MO value differed significantly from the pre-diet value (P

The characteristics of the cardiac adenylate cyclase system were studied in rats fed diets containing fish oil (menhaden oil) and other oils. Adenylate cyclase activity generally was higher in cardiac homogenates and membranes of rats fed diet containing 10% menhaden oil than in the other oils. The increase in enzyme activity, especially in forskolin-stimulated activity, was associated with an increase in the concentration of the [3H] forskolin-binding sites in cardiac membranes of rats fed menhaden oil. The beta-adrenergic receptor concentration was not significantly altered although the affinity for [3H]dihydroalprenolol-binding was lower in membranes of rats fed menhaden oil than those fed the other oils. omega-3 fatty acids from menhaden oil were incorporated into the cardiac membrane phospholipids. The results suggest that the observed increase in myocardial adenylate cyclase activity of rats fed menhaden oil may be due to an increase in the number of the catalytic subunits of the enzyme or due to a greater availability of the forskolin-binding sites.

The effects of corn or menhaden oil and thyroxine treatment on hepatic mitochondrial respiration was studied. BHE rats were fed a 64% sucrose, 6% corn, or menhaden oil diet until they were 60-70 days of age. Succinate-supported mitochondrial respiration was studied at 3 degrees C intervals from 4 to 40 degrees C. Upper and lower activation energies and transition temperatures were determined through the calculation of Arrhenius plot. Menhaden oil plus daily thyroxine injection resulted in higher and lower activation energies than the other treatments. This combined treatment also resulted in lower state 3 and higher state 4 respiration rates and tighter coupling of respiration to ATP synthesis. These effects were thought to be due to the effect this treatment combination had on membrane fluidity.

Methyl-branched fatty acids, which are usually minor components (equal or less than 0.1%) in fish oils, were concentrated in the non-urea-complexing fraction along with polyunsaturated fatty acids during the enrichment of omega-3 fatty acids from certain fish oils via the urea complexation process. The methyl-branched fatty acids in the omega-3 polyunsaturated fatty acid concentrates, which were prepared from three fish body oils, were characterized by gas chromatography and gas chromatography/mass spectrometry. Among the major branched-chain fatty acids expected and identified were the known isoprenoid acids--mainly 4,8,12-trimethyltridecanoic, pristanic, and phytanic--and the well-known iso and anteiso structures. Two novel phytol-derived multimethyl-branched fatty acids, 2,2,6,10,14-pentamethylpentadecanoic and 2,3,7,11,15-pentamethylhexadecanoic, were identified in redfish (Sebastes sp.) oil. These two fatty acids were absent in oils from menhaden (Brevoortia tyrannus) and Pacific salmon (mixed, but mostly from sockeye, Oncorhynchus nerka). The major branched-chain fatty acid in the salmon oil, 7-methyl-7-hexadecenoic acid, was also present to a moderate extent in menhaden oil. A novel vicinal dimethyl-branched fatty acid, 7,8-dimethyl-7-hexadecenoic was detected in all of the fish oils examined, but was most important in the salmon oil. Three monomethyl-branched fatty acids, 11-methyltetradecanoic acid, and 11- and 13-methylhexadecanoic, hitherto undescribed in fish lipids, were also detected in salmon, redfish and menhaden oils.

The influence of phenobarbital on the activity of hepatic mixed function oxidases responsible for benzo[a]pyrene hydroxylation was studied in rats fed diets containing menhaden fish oil (rich in n-3 fatty acids). Male rats were starved for 2 days and refed diet devoid of fat or containing 0.5, 10, or 20% menhaden oil for 4 days. Phenobarbital increased the apparent Km value as well as Vmax for benzo[a]pyrene hydroxylase in microsomes from rats fed the 20% menhaden oil diet. The increased Km was due to a progressive decrease in benzo[a]pyrene metabolism at the lower substrate concentrations, even in the presence of increased cytochrome P-450 content. The phenobarbital-induced increase in Km and the decreases in benzo[a]pyrene hydroxylation were not observed in rats fed 0.5% menhaden oil or a diet devoid of fat.