MO Diet Research Articles

Plasma molybdenum reflects dietary molybdenum intake

The relationship between plasma molybdenum (Mo) and dietary intake has not been investigated in humans. We developed an isotope dilution method to determine molybdenum in 0.5 mL blood plasma by ICP-MS and conducted a study to determine the effect of dietary intake on plasma molybdenum. Twelve young men consumed a very low Mo diet (22 μg/day) for 24 days while confined to the WHNRC metabolic research unit and plasma molybdenum was monitored. 97Mo was infused in four of the subjects (Group 1) to follow its clearance from the blood. The other eight remained in unit for 120 days (an additional 96 days). Four consumed the 22 μg/day molybdenum diet for 102 days followed by 467 μg/day for 18 days (Group 2). and four consumed five levels of dietary molybdenum for 24 days each (Group 3). 100Mo was added to the diet one or more times at each dietary level. Total plasma molybdenum and 100Mo were monitored throughout the study. Plasma molybdenum in the 12 subjects decreased from 8.2 ± 0.5 to 6.1 ± 0.5 nmol/L after 13 days of low molybdenum intake and was 5.1 ± 0.5 nmol/L after 24 days. In Group 2, average plasma molybdenum was 7.8 ± 0.9 nmol/L at the beginning of the study, 5.4 ± 0.4 nmol/L during the 102 days low molybdenum period, and 16.5 ± 0.6 nmol/L during the high molybdenum period. Plasma molybdenum in Group 3 was 4.2 ± 2.1 nmol/L at 22 μg/day; 5.8 ± 2.5 nmol/L at 72 μg/day; 6.6 ± 2.3 nmol/L at 121 μg/day; 19.7 nmol/L ±2.1 at 467 μg/day; and 43.9 ± 2.1 nmol/L at 1490 μg/day. The results demonstrate that, in contrast to most other essential minerals, plasma molybdenum reflects low and high dietary molybdenum intakes within 14 days and may a useful indicator of low and high dietary intakes.

Feeding value of wild Napier grass ( Pennisetum macrourum) for cattle supplemented with protein and/or energy rich supplements

Two experiments were conducted to evaluate the feeding value of Pennisetum macrourum, commonly known as wild Napier grass, as a feed for cattle. Experiment 1 was a nutritive value determination using four crossbred steers and four diets in a 4×4 Latin square design experiment. The four diets were: wild Napier grass + mineral/vitamin mixture (WN), wild Napier grass + 0.5 kg fishmeal + 0.5 kg maize bran + mineral/vitamin mixture (MB+FM), wild Napier grass + 0.5 kg molasses + mineral/vitamin mixture (MO) and wild Napier grass + 0.5 kg fishmeal + 0.5 kg molasses + mineral/vitamin mixture (MO+FM). Wild Napier grass contained 668, 256 and 78 g/kg DM of NDF, ADF and CP, respectively. The DM intake (67.9, 118.9, 96, 132.9 g/kg for animals on WN, MB+FM, MO and MO+FM, respectively) differed ( P<0.05) among diets. Metabolizable energy (ME) intake increased ( P<0.05) from 17.6 to 32.7 (MJ per day) for steers on diets WN and MO+FM, respectively and N retention was increased ( P<0.05) from 7.6 to 51.5 g per day in diets WN and MO+FM, respectively. N absorbed was more efficiently retained ( P<0.05) with MO+FM supplements. Experiment 2, used 16 milking cows fed on similar diets to Experiment 1 in a completely randomized experiment. DM intake differed ( P<0.05) among diets, except between BM+FM and MO and ranged from 6.3 to 8.7 kg in diets WN and MO+FM, respectively. All cows lost weight, with those on MO diet losing ( P<0.05) the most weight. Milk yield differed ( P<0.05) among diets ranging from 7.8 to 15.5 kg per cow per day for cows on WN and MO+FM, respectively. Although steers and cows performed better when supplemented with FM, its high cost suggests that feeding of molasses as an inexpensive source of fermentable carbohydrates in the rumen may be recommended as it results in adequate performance.

Dietary (n-3) Fat and Cholesterol Alter Tissue Antioxidant Enzymes and Susceptibility to Oxidation in SHR and WKY Rats

Previously, 8% fish oil blend diets, compared to butter and soybean oil blend diets, reduced specific antioxidant enzyme activities and tissue susceptibility to in vitro oxidative stress in spontaneously hypertensive (SHR) and Wistar Kyoto (WKY) rats. Moreover, high cholesterol (5.0 g/kg diet) diets protected against in vitro tissue lipid oxidation. In this study, we hypothesized that 160 g fat/kg diet as blends of (n-6) or (n-3) oils and cholesterol would alter antioxidant enzyme activities and thus increase tissue susceptibility to oxidation. The effects of diet blends of saturated (butter, B), (n-6) (soybean oil, SBO) or (n-3) (menhaden oil, MO) oils with cholesterol (0.5 or 5.0 g/kg) on systolic blood pressure (SBP), plasma lipids, antioxidant enzymes and susceptibility to oxidation were examined in SHR and WKY rats. SBP at 13 wk of age was greater (P < 0.001) in SHR than in WKY rats, but was not affected by diets. Plasma cholesterol and triacylglycerols were decreased (P < 0.001) by MO diets. Hepatic glutathione reductase activities were reduced (P < 0.001) in SBO-fed SHR and enhanced in SBO- and MO-fed WKY rats. Glutathione levels were reduced (P < 0.001) in RBC and enhanced (P < 0.001) in livers of MO-fed rats. Lipid oxidation was enhanced (P < 0.001) in red blood cells (RBC) from SBO groups, and hearts and livers of MO groups. High cholesterol diets reduced (P < or = 0.001) susceptibility to lipid peroxidation in RBC and liver of SHR and WKY rats. Greater amounts of dietary (n-3) fat enhance tissue susceptibility to oxidation, which can be modulated by increased dietary cholesterol in SHR and WKY rats.

Effects of Monounsaturated Enriched Sunflower Oil on CHD Risk Factors Including LDL Size and Copper-Induced LDL Oxidation

Objective: To compare the effects of a diet high in monounsaturated enriched sunflower oil and a low fat diet on CHD risk factors including in vitro Cu-induced LDL oxidation and LDL size, lipids, lipoproteins, glucose and insulin.Design: A randomized crossover dietary intervention.Setting: Free living individuals.Subjects: Fourteen healthy males 35 to 55 years of age and 14 healthy postmenopausal women 50 to 60 years of age completed the dietary intervention. Two subjects did not complete the study, and their data were not included.Interventions: A low fat, high carbohydrate diet (22% to 25% of energy from total fat, 7% to 8% of energy from monounsaturated fat and 55% to 60% of energy from carbohydrate) was compared to a monounsaturated enriched sunflower oil (MO) diet (40% to 42% of energy from fat, with 26% to 28% from monounsaturated fat and 40% to 45% of energy from carbohydrate) in an isocaloric substitution. Each dietary period was one month.Results: Total cholesterol, LDL cholesterol, triglycerides and glucose were not significantly different between the two diets. HDL cholesterol, HDL3 cholesterol and insulin were significantly higher on the MO diet, mean 7%, 7% and 17% higher respectively. Copper-induced LDL oxidation lag phase was significantly longer (mean 18%) after the MO diet compared to the low fat, high carbohydrate diet. LDL particle size was not significantly different.Conclusions: The significant increase in LDL oxidation lag phase and the significantly higher HDL cholesterol on the MO diet would be expected to be associated with a decrease in CHD risk.

Copper balance in mature geldings fed supplemental molybdenum

Four mature sedentary geldings were used in a 4×4 Latin square designed experiment to evaluate the effects of supplemental molybdenum (Mo) on copper (Cu) balance. Four diets were formulated to contain 0 (control), 5, 10 and 20 ppm of supplemental Mo and were fed for a 21-day adjustment period followed by a 72-hour fecal and urine collection. Diets consisted of a pelleted concentrate based on corn, soybean meal and cotton seed hulls fed in a 50:50 ratio of concentrate to native prairie grass hay. All diets were formulated to be isonitrogenous and isocaloric with similar concentrations of Cu. Urine was collected every four hours for 72 hours and multiple fecal grab samples were taken every two hours post feeding. On the third collection day, blood samples were drawn at the time of feeding, each hour for five hours post feeding, and eight hours post feeding for serum Cu analysis. Balance data were analyzed using a general linear model procedure with horse, period and treatment as main effects. Serum Cu data were analyzed using the general linear model procedure with horse, treatment and period as main effects and time as the repeated variable. The intake of Cu was similar among all diets fed. There was no difference (p>.05) in serum Cu concentrations over time or between treatments due to supplemental Mo. Urinary and fecal excretion of Cu did not differ (p>.05) between diets. Consequently, the balance of Cu was similar among diets consumed. Excretion of Mo in the urine was higher (p<.05) in horses fed the 20 ppm Mo diet versus the 0, 5 and 10 ppm Mo diet. As Mo intake increased, fecal excretion increased (p<.05) across all diets. Additionally, Mo balance was higher (p<.05) on the 20 ppm Mo diet than all other diets. In conclusion, supplemental Mo appeared to have no adverse effect on the absorption and retention of Cu when fed to mature geldings.

Effects of Dietary Copper and Molybdenum on Copper Status, Cytokine Production, and Humoral Immune Response of Calves

Twenty-four male Holstein calves were used to determine the effects of dietary Cu and Mo on performance, Cu status, and immune function of calves. Calves were fed a milk replacer that was deficient in Cu for 8 wk and then were randomly assigned after weaning to one of four treatments: 1) control (no supplemental Cu or Mo), 2) 10mg of Cu (from CuSO4)/kg of dry matter (DM) (Cu diet), 3) 5mg of Mo (from Na2MoO4)/kg of DM (Mo diet), or 4) 5mg of Cu (from CuSO4) and 5mg of Mo (from Na2MoO4)/kg of DM (Cu + Mo diet). The basal diet was a semipurified diet that contained approximately 1.1mg of Cu and 1.1mg of Mo/kg of DM. Calves fed the Cu and Mo diets gained weight more efficiently than those fed the control and Cu + Mo diets during the 112-d study. By d 84 of the study, calves fed the Cu diet had higher plasma Cu concentrations and plasma ceruloplasmin activities than did calves fed the other three diets and had higher liver Cu concentrations on d 136. Plasma and liver Cu concentrations did not differ among calves fed the control, Mo, and Cu + Mo diets. At d 112, activity of Cu-Zn superoxide dismutase was lower in calves fed the Mo diet than in calves fed the Cu diet. Serum total antibodies to porcine erythrocytes (primary response) were lower in calves fed the Mo diet than in calves fed the Cu diet at 7, 14, and 21 d postinoculation. Production of tumor necrosis factor and interleukin-1 by isolated peripheral blood monocytes was not significantly affected by treatment. Although no differences were apparent in plasma or liver Cu concentrations among calves fed the control, Mo, and Cu + Mo diets, calves fed the Mo diet had a more severe Cu deficiency based on depressed humoral immune response and superoxide dismutase activity.

The influence of dietary fatty acids on the activity and metabolic control of peroxisomal carnitine palmitoyltransferase in the liver

Peroxisomes play an important role in the β-oxidation of fatty acids and they possess a membrane-bound carnitine palmitoyltransferase (CPT). Whether this enzyme is regulated by the amount and type of fat consumed in the diet has not been investigated. Therefore weanling male Lewis rats were fed for various times (2 days to 4 weeks) on a low-fat (2.5% w/w) diet (LF) or on high-fat diets containing 20% (w/w) of either hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO), evening primrose oil (EPO) or menhaden (fish) oil (MO). Hepatic peroxisomal CPT activity and sensitivity to inhibition by malonyl CoA were examined. In general, feeding the high-fat diets resulted in higher CPT activity per mg peroxisomal protein (specific activity) and per g liver (capacity) than feeding the LF diet throughout the 4 week feeding period. The most rapid induction of CPT specific was seen in the livers of animals fed the SO, EPO and MO diets. Induction of CPT specific activity was maximal after one week of feeding each of the diets. Feeding the MO diet resulted in the highest CPT specific activity at most time points examined and the highest CPT capacity at all time points. In relation to feeding the LF diet, the HCO and EPO diets increased CPT specific activity and capacity by approximately 2-fold while the OO, SO and MO diets increased the CPT specific activity by 3- to 4-fold; these diets increased CPT capacity by 3.5-fold (OO), 4.5-fold (SO) and 7.4-fold (MO). These observations are consistent with previous observations that dietary fish oils increase peroxisomal β-oxidation. Peroxisomal CPT from animals fed the LF diet was the most sensitive to inhibition by malonyl CoA at each time point ([I 50] = approx. 0.5 μM). Each of the high-fat diets decreased the sensitivity of peroxisomal CPT to inhibition by malonyl CoA. The decrease in sensitivity was apparent after feeding the OO, SO or MO diets for 2 days. At all time points peroxisomal CPT from MO-fed rats was the least sensitive to malonyl CoA inhibition. At its least sensitive (after 7 days of feeding) peroxisomal CPT from MO-fed rats required a 5.7-fold higher malonyl CoA concentration to induce 50% inhibition than did the enzyme from LF-fed rats. These data indicate that both the level of fat in the diet and the fatty acid composition of high-fat diets influence CPT activity and its sensitivity to the inhibitor malonyl CoA.

Characterization of lipoprotein composition in rats fed different dietary lipids and of the effects of lipoproteins upon lymphocyte proliferation

Weanling Lewis rats were fed for 10 weeks on a low fat (2.5% by weight; LF) diet or on diets containing 20% by weight of hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO), evening primrose oil (EPO), or menhaden (fish) oil (MO); all other components of the diets were identical. The chylomicron (CM), very low density lipoprotein (VLDL), low density lipoprotein (LDL), and high density lipoprotein (HDL) fractions were isolated from the serum. The serum from MO-fed animals had lower LDL and HDL cholesterol concentrations than the serum from animals fed each of the other diets. The apolipoprotein A-1 concentration in the HDL fraction from animals fed the MO diet was also low. The serum from HCO-fed animals had a higher CM triacylglycerol concentration than serum from animals fed each of the other diets. The serum from OO-fed animals had a higher VLDL triacylglycerol concentration than serum from animals fed each of the other diets. The concentration of apolipoprotein B was also high in the VLDL fraction from OO-fed animals. The fatty acid composition of each lipoprotein fraction was affected by the nature of the lipid in the diet; the greatest effects were observed in the CM and VLDL fractions. Each lipoprotein fraction isolated from LF-fed rats inhibited mitogen-stimulated rat spleen lymphocyte proliferation in a concentration-dependent manner; LDL and HDL caused greater inhibition than CM and VLDL. Dietary lipid manipulation did not alter the inhibitory effects of any of the lipoprotein fractions upon lymphocyte proliferation, except that CM and HDL from MO-fed animals and HDL from OO-fed animals resulted in enhanced proliferation compared with either CM or HDL from animals fed the other diets. We conclude that the inhibition of lymphocyte proliferation caused by feeding rats certain dietary lipids (OO, EPO, MO) may be mediated by non-lipoprotein serum components.

Dietary Oils with Added Tocopherols: Effects on Egg or Tissue Tocopherols, Fatty Acids, and Oxidative Stability

The effect of dietary oils [menhaden (MO), flax (FL), palm (PO), and sunflower oils (SF)] with added tocopherols on the tocopherol deposition, fatty acid composition, and thiobarbituric acid (TBA) values of egg or tissues (liver, adipose tissue, white meat, and dark meat) were examined. Addition of tocopherols increased (P < 0.05) the total egg or tissue tocopherol content. The enhancement of total tocopherols in the different tissues in the order of magnitude were egg yolk > liver > adipose tissue > dark meat > white meat. Dark meat contained higher (P < 0.05) total tocopherols than white meat. Dietary MO or FL resulted in a significant (P < 0.05) incorporation of C20:5 n-3 and C22:6 n-3 with a concomitant reduction in C20:4 n-6 in liver, egg, white meat, and dark meat. Dietary SF resulted in a significant (P < 0.05) incorporation of C18:2 n-6 and C20:4 n-6 in all the tissues. Addition of PO did not result in any change in the yolk saturated fatty acid content. The content of monounsaturated fatty acids were greater (P < 0.05) in all the tissues from PO diets than in diets with other oils. Dietary tocopherols resulted in a significant increase (P < 0.05) in the content of C20:5 n-3 and C22:6 n-3 in the yolk, adipose tissue, and white meat from birds fed MO + T diets. Inclusion of tocopherols resulted in a significant (P < 0.05) reduction in TBA values in eggs, in liver for MO and FL diets, and in dark and white meat for the MO diet. Tocopherol supplementation did not result in any change in TBA values in the PO diet.

Effects of Dietary Lipid Manipulation upon Graft vs Host and Host vs Graff Responses in the Rat

The popliteal lymph node (PLN) assay was used to establish whether dietary lipids with differing fatty acid compositions could affect cell-mediated immunity in the rat. Weanling rats were fed for 4 weeks on a low-fat (2.5% by weight; LF) diet or on diets containing 20% (by weight) hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO), evening primrose oil (EPO), or menhaden (fish) oil (MO). Feeding the MO diet suppressed the graft vs host response compared with feeding the LF, HCO, SO, or EPO diets, while feeding the OO diet suppressed this response compared with feeding the LF or EPO diets. Feeding the MO diet suppressed the host vs graft response compared with feeding each of the other diets. Following the graft vs host reaction, PLN lymphocytes from animals fed the MO diet had significantly lower levels of expression of LFA-1 and CD2 compared with PLN lymphocytes from animals fed the LF diet; furthermore, they had lower levels of expression of T-cell receptor (TcR), CD4, CD8, LFA-1, and CD2 compared with lymphocytes from animals fed some, and in the case of CD2 each, of the other high-fat diets, Feeding the MO diet resulted in a lower proportion of cells expressing the interleukin-2 receptor, indicating an inhibition of lymphocyte activation, and a lower proportion of CD16 +/CD3 - cells, indicating a decrease in the proportion of NK cells within the PLN. Following the host vs graft reaction, PLN lymphocytes from animals fed the MO diet had significantly lower levels of expression of TcR and CD8 compared with lymphocytes from animals fed each of the other diets; furthermore, they had lower levels of expression of CD4, CD2, and LFA-1 compared with lymphocytes from animals fed the LF, HCO, OO, or SO diets. These observations indicate that the smaller PLN size of animals fed the MO diet results from an inhibition of activation and subsequent proliferation of cells within the node and perhaps also a suppression of movement of cells from the bloodstream to the PLN, due to decreased level of expression of adhesion molecules. These lowered levels of expression might be due to an inhibitory effect of the n-3 polyunsaturated fatty acids found in MO upon components of the signal transduction pathways involved in lymphocyte activation or upon expression of the genes for the surface molecules or both.

Effects of dietary fish oil on calcium homeostasis in rat platelets

Mechanisms to explain the differential effects of dietary n-6 and n-3 polyunsaturated fatty acids (PUFA) on cellular functions are not completely understood. In this study, we investigated the effects of these two types of PUFA on ionized calcium (Co 2+ ) fluxes in platelets. Adult male rats were fed either an n-6 PUFA-rich diet (corn oil, CO) or an n-3 PUFA-rich diet (menhaden oil, MO) for 8 to 12 days. Receptor-stimulated release and basal membrane fluxes of Ca 2+ were studied in platelets using two different reporter molecules. The fluorescent indicator chlorotetracycline (CTC) was employed to investigate Ca 2+ mobilization from internal storage compartments upon stimulation. Aequorin, a photoprotein, was used to monitor calcium movements through platelet membranes. Platelets with n-3 PUFA in membrane lipids as a consequence of the MO diet demonstrated a delay in the mobilization of Co 2+ from intracellular stores in response to stimulation to several doses of thrombin compared with control platelets (CO). This delayed response was significantly different compared with that found for controls at the lowest dose of agonist (MO, 40.2 ±3.2 sec; CO, 28.5 .9 sec, mean EM, P = 0.02). Decay rates for aequorin in rat platelets were found to be linear for 30 min and were similar after exposure to either 0.75 or 1.5 mM external calcium. The rates in platelets from animals fed MO were significantly lower compared with those observed in platelets from the animals fed CO (```P`` = 0.003). The combined results with the reporter molecules suggest that incorporation of n-3 PUFA into membranes delays calcium release and flux under stimulated and basal conditions, respectively. Such alterations would contribute to changes in cellular responses and suggest additional actions of n-3 PUFA beyond those attributed to their inhibitory actions on eicosanoid production from n-6 PUFA.

Effects of Dietary Lipid Manipulation upon Inflammatory Mediator Production by Murine Macrophages

This study investigated the effects of feeding mice lipids with different fatty acid compositions upon the ability of stimulated macrophages to produce inflammatory mediators. Weanling mice were fed for 8 weeks on a low-fat (LF; 2.5% by weight) diet or on diets containing 20% by weight of hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO), or menhaden (fish) oil (MO). Thioglycollate-elicited peritoneal macrophages were isolated. Macrophages isolated from MO-fed mice produced less PGE2, 6-keto-PGF1a, TXB2, and interleukin-6 in response to lipopolysaccharide (LPS) stimulation than those from mice fed each of the other diets. Macrophages from mice fed the OO, SO, or MO diets produced less tumor necrosis factor a in response to LPS stimulation than those from mice fed the LF or HCO diets. There was no effect of dietary lipid manipulation upon the production of interleukin-1 by LPS-stimulated macrophages. Macrophages from mice fed the MO diet produced more superoxide and hydrogen peroxide in response to phorbol ester stimulation than those from mice fed each of the other diets. In response to unopsonized zymosan, macrophages from mice fed the SO or MO diets produced more hydrogen peroxide than macrophages from mice fed the other diets. LPS-stimulated nitric oxide production was greater from macrophages from OO-, SO-, or MO- fed mice than from those fed the LF or HCO diets. Thus, the nature of the lipid consumed in the diet has significant effects upon the production of a variety of inflammatory mediators by macrophages. The most potent effect is caused by fish oil consumption. Possible mechanisms by which dietary fatty acids, particularly the n-3 polyunsaturated fatty acids found in fish oils, could affect mediator production by macrophages are described. The clinical relevance of such effects is discussed.

Comparison of the effects of a range of dietary lipids upon serum and tissue lipid composition in the rat

Since the type of fat consumed in the diet may play a role in the development of several disorders, it is important to ascertain the effects of different dietary fats upon parameters such as serum lipid levels and adipose deposition. The aim of this study was to determine the effects of feeding rats a range of fats with differing fatty acid compositions. Weanling male rats were fed for 10 weeks on a low fat (LF) diet or on one of five high fat diets, which contained 20% by weight of either hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO), evening primrose oil (EPO) or menhaden (fish) oil (MO). Food intake, animal growth, tissue weights at sacrifice, serum and liver lipid concentrations and serum, heart, brain and adipose tissue fatty acid compositions were studied. The food intake of the LF-fed animals was greater than that of animals fed on the high fat diets; there were no differences in food intake between animals fed the high fat diets. The total energy intake was lower for animals fed on the HCO diet than for those fed on the LF, OO, EPO or MO diets; there were no other differences in energy intake between the groups. Animals fed the different diets had almost identical rates of weight gain up to 5 weeks; after this period of rapid growth, the increase in weight was slower in all groups but especially in the LF-fed animals. The LF-fed rats had a lower total weight gain and smaller final weights than rats fed on the high fat diets. Animals fed on the MO diet had a greater weight gain than those fed on the OO or EPO diets and their final weights were greater. The MO diet resulted in greatly increased liver weight compared with each of the other diets. The HCO, OO and EPO diets also increased liver weight compared with the LF diet. The total lipid content of the livers from rats fed the high fat diets was greater than that of those from rats fed the LF diet; the livers from animals fed the MO diet contained more lipid than those from animals fed each of the other diets. MO feeding increased the free cholesterol, cholesterol ester and triacylglycerol contents of the liver. Each of the high fat diets resulted in an increase in epididymal fat pad weight compared with the LF diet, but the high fat diets resulted in different degrees of adipose deposition; the EPO and MO diets resulted in smaller epididymal fat pads than the HCO, OO and SO diets. Serum total cholesterol concentrations were higher after feeding the OO, SO or EPO diets than after feeding the LF or MO diets. The MO diet resulted in a total serum cholesterol concentration which was lower than that of animals fed each of the other diets. The serum cholesterol ester concentration of the MO-fed animals was lower than that of the LF-, SO- or EPO-fed animals. Serum triacylglycerol concentrations of the HCO- and OO-fed rats were higher than those of the LF-, SO-, EPO- or MO-fed animals. The fatty acid compositions of the serum, adipose tissue and the neutral lipid and phospholipid fractions of the heart reflected those of the diets themselves, apart from those from the HCO-fed animals, which contained much lower proportions of medium chain fatty acids than did the diet. The fatty acid composition of the phospholipid fraction of the brain was not affected by dietary lipid manipulation. The fatty acid composition of the diet affects animal growth, tissue weights, serum cholesterol, cholesterol ester and triacylglycerol concentrations and the fatty acid compositions of the serum, adipose tissue and heart. The fatty acid composition of the brain is relatively resistant to dietary modification.

The effect of fatty acids on leucocyte subsets and proliferation in rat whole blood

Polyunsaturated fatty acids (PUFA) have been shown to suppress immune cell functions in vitro. Dietary studies investigating the effects of PUFA-containing oils on lymphocyte functions have yielded contradictory findings; such studies are difficult to compare since there are many variations in protocols. The present study investigated the effects of exogenously added fatty acids on proliferation of leucocytes to whole blood in vitro and the effects of feeding diets containing oils rich in saturated fatty acids, monounsaturated fatty acids, n-6 PUFA or n-3 PUFA on rat leucocyte proliferation in whole blood and on receptor and surface marker expression by peripheral blood leucocytes. When added exogenously to whole blood all fatty acids tested, except myristic acid, inhibited leucocyte proliferation; the greatest inhibition of proliferation was seen with arachidonic and eicosapentaenoic acids. To investigate the effects of dietary lipids on proliferation and surface marker expression by leucocytes, rats were fed for ten weeks on a low fat (LF) diet (approximately 2% fat by weight) or on one of five high fat diets, which contained 20% (by weight) hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO), evening primrose oil (EPO) or menhaden (fish) oil (MO). Compared with feeding the LF, SO or EPO diets, the HCO, OO and MO diets suppressed the proliferation of leucocytes in whole blood at low concentrations of Con A. High fat feeding decreased the sensitivity of B-cells to LPS, but had no effect on the magnitude of the response to this mitogen. Dietary lipid manipulation had no effect on leucocyte subpopulations (T-cells, B-cells, CD4 + cells, CD8 + cells, monocytes/macrophages, natural killer cells) or on the expression of adhesion molecules (LFA-1, ICAM, CD2). The effects of dietary lipid manipulation on leucocyte proliferation are clearly very different from the effects of addition of single fatty acids to whole blood in vitro. This is likely to be due to alterations in blood triacylglycerol and cholesterol concentrations brought about by different dietary lipids, suggesting that dietary lipids have marked effects on leucocyte proliferation and that the use of the whole blood system may be a more physiological way of determining the effects of dietary lipids on immune function than the use of single exogenously added fatty acids with purified cells.

Effects of Dietary Lipid Manipulation upon Rat Spleen Lymphocyte Functions and the Expression of Lymphocyte Surface Molecules

Rats were fed for 12 weeks on a low fat (LF; 2.5% by weight) diet or on one of five high fat (20% by weight) diets; the latter contained hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO), evening primrose oil (EPO) or menhaden (fish) oil (MO). Feeding the EPO or MO diets resulted in inhibition of mitogen-stimulated spleen lymphocyte proliferation compared with feeding any of the other diets; in addition, feeding the OO diet resulted in inhibition of proliferation compared with feeding the LF diet. Feeding the OO, EPO or MO diets resulted in inhibition of spleen lymphocyte natural killer (NK) cell activity compared with feeding the LF or HCO diets; feeding the SO diet resulted in inhibition of NK cell activity compared with feeding the HCO diet. There was no effect of dietary lipid manipulation upon the proportion of T-cells or of CD4+ or CD8+ cells in the spleen. The level of expression of CD2 on CD4+ and CD8+ spleen lymphocytes was decreased by MO feeding compared with feeding the LF, HCO, SO or EPO diets; OO feeding decreased the level of expression of CD2 on CD4+ spleen lymphocytes compared with feeding the LF diet. The level of expression of LFA-1 was decreased on both CD4+ and CD8+ spleen lymphocytes from animals fed the OO or MO diets compared with that on lymphocytes from animals fed some of the other diets. Following mitogenic stimulation the level of expression of CD8, CD2, ICAM-1, LFA-1 and the interleukin-2 receptor was lower on spleen lymphocytes from animals fed the MO diet and, for some of the markers, on those from animals fed the OO or EPO diets. These observations indicate that diets containing MO, OO and EPO exert immunomodulatory effects by influencing the expression of important molecules upon the lymphocyte surface. This may occur through effects on signal transduction pathways and/or gene expression.

Dietary polyunsaturated fatty acid effects on immune cells of the porcine lung

The effects of various dietary polyunsaturated fatty acids (PUFAs) on the function of immune cells of the porcine lung was studied. Groups of six pigs were fed diets containing 10.5% corn oil [CO; enriched in linoleic acid (18:2, n-6)], linseed oil (LO; enriched in alpha-linolenic acid (18:3, n-3)], menhaden oil (MO; enriched in eicosapentaenoic (20:5; n-3) and docosahexaenoic (22:6; n-3) acids], linseed + corn oil (1:1; LC), and menhaden + corn oil (1:1; MC) for 28-30 days. Basal levels of alveolar macrophage (m phi) tumor necrosis factor-alpha (TNF-alpha) production were higher (P < .05) for LC- and MC-fed pigs than for CO- and LO-fed pigs. Lipopolysaccharide (LPS)-stimulated LC and MC m phi s produced more TNF than m phi s from pigs fed CO, LO, and MO diets. Macrophages from pigs receiving the CO and LC diets had higher (P < .05) levels of leucine aminopeptidase than m phi s from the other dietary groups. Lipopolysaccharide did not increase m phi nitrite production over basal levels except in the MO diet group. However, LPS-stimulated m phi s from the CO, MO, and LC dietary groups produced more nitrite than m phi s from MC-fed pigs. Alveolar lymphocytes from pigs receiving the MC diet produced more T cell growth factors than LO and MO m phi s. Alveolar m phi s from the different dietary groups did not differ in their capacity for non-immune-mediated phagocytosis of fluorescent latex beads. These results indicate that dietary PUFAs can modulate some functions of porcine alveolar immune cells and that this may prove significant for host response to respiratory disease agents.

Dietary modulation of DNA adduct formation of the food mutagen 2-amino-3-methylimidazo[4,5-f]quinoline in the male Fischer 344 rat.

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)

A High α-Linolenate Diet Suppresses Antigen-Induced Immunoglobulin E Response and Anaphylactic Shock in Mice

Mice were fed for 2 mo diets having ratios of alpha-linolenate [18:3 (n-3)] to linoleate [18:2(n-6)] of < 0.01, 0.36, 1.0 and 3.9. Proportions of safflower seed oil and perilla seed oil were adjusted to obtain these ratios. The dietary alpha-linolenate to linoleate balance was reflected in the proportion of (n-3) and (n-6) highly unsaturated fatty acids with 20- and 22-carbon chains in spleen phospholipids, but the ratio did not affect the proportion of T lymphocyte subsets expressing CD4 and CD8 antigens in splenic leukocytes. The immunoglobulin (Ig) G and IgM responses against sheep red blood cells when estimated as plaque-forming cells present in spleen, were not affected significantly by the diets. However, the serum hemagglutinin titer was slightly but significantly higher in the high alpha-linolenate diet group [18:3(n-3)/18:2(n-6) = 3.9] than in the dietary group with 18:3(n-3) to 18:2(n-6) ratios of 0.36 and < 0.01. In contrast, the IgE antibody response against egg albumin, as well as the mortality from anaphylactic shock induced by a second challenge with antigen, was significantly lower in the high alpha-linolenate diet group [18:3(n-3)/18:2(n-6) = 3.9] than in the high linoleate diet [18:3(n-3)/18:2(n-6) < 0.01] group. These results, together with the reported suppressive effects of a high alpha-linolenate diet on the formation of lipid-derived allergic mediators, support the hypothesis that raising the (n-3) to (n-6) ratios of diets would be effective in reducing the severity of immediate-type allergic hypersensitivity.

Inhibition of natural killer cell activity by dietary lipids

Natural killer (NK) cells are a subset of cytotoxic lymphocytes found mainly in blood and the spleen. NK cells play a role in natural immunity to microbes, viruses and tumor cells and are involved in the rejection of grafts. The present study investigated the effects of diets containing oils rich in saturated fatty acids, mono-unsaturated fatty acids, n-6-poly-unsaturated fatty acids (PUFA) or n-3-PUFA on the NK cell activity and on the lymphokine-activated killer (LAK) cell activity of rat spleen lymphocytes. Weanling rats were fed for 10 weeks on a low-fat (LF) diet (∼ 2% fat by weight) or on 1 of 5 high-fat (HF) diets, which contained 20% (by weight) hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO), evening primrose oil (EPO) or menhaden (fish) oil (MO). Each of the HF diets suppressed the NK activity of freshly prepared spleen lymphocytes compared with the LF diet; cells from the MO-fed rats exhibited the lowest NK activity. Culture with IFNα for 3 h increased the NK activity of spleen lymphocytes from all animals, except those fed the OO diet; the increase in NK activity varied from 20% (LF) to 50% (MO). Although feeding the OO, EPO or MO diets resulted in lower IFN α-stimulated NK activity than that obtained by feeding the LF diet, the only consistent significant difference was the lower activity of the cells from the OO-fed rats compared with those from the LF-fed rats. LAK cells were generated by culture of spleen lymphocytes with ConA for 24 h followed by IL-2 for 72 h. All of the HF diets decreased LAK cell activity; statistically significant effects were observed for lymphocytes from rats fed the MO diet compared with those from rats fed the LF-fat diet. These observations show that dietary PUFA, particularly those of the n-3 family inhibit NK cell activity. This may be useful in prolonging graft survival, but may also decrease the ability of the host to destroy invasive microbes, viruses and tumor cells.

Effects of dietary linseed oil and marine oil on lipid peroxidation in monkey liverin vivo andin vitro

Diets rich in linoleic acid (CO) from corn oil, or in linoleic acid and either alpha-linolenic acid (LO) based on linseed oil or n-3 fatty acids (MO) from menhaden oil were fed to male and female Cynomolgus monkeys for 15 wk. In the liver a 40% reduction of alpha-tocopherol occurred in the MO group relative to the CO and LO groups followed by increased formation of lipofuscin in vivo. A four-fold increase of alpha-tocopherol in the MO diet (MO + E) brought the level in the liver to that found with CO and LO. The increased peroxidation in the MO group in the liver phospholipids was associated with the replacement of 60% of the n-6 fatty acids by n-3 fatty acids from menhaden oil. Similar fatty acid profiles were found in groups fed MO and MO + E, respectively. Compared to the CO fed group, feeding alpha-linolenic acid only resulted in a slight incorporation of n-3 fatty acids in the liver membranes mainly due to a direct incorporation of alpha-linolenic acid. However, in monkeys fed menhaden oil more than 30% of the total fatty acids in the liver phospholipids were n-3 fatty acids. The various diets did not influence the activity of liver catalase (EC 1.11.1.6) nor superoxide dismutase (EC 1.15.1.1), but glutathione-peroxidase activity (EC 1.11.1.9) was higher in monkeys fed the MO diet. The catalase activity in females was 20% higher than in males.(ABSTRACT TRUNCATED AT 250 WORDS)