Effects of peroxidation products in thermoxidised dietary oil in female rats during rearing, pregnancy and lactation on their reproductive performance and the antioxidative status of their offspring

The present study was performed to investigate whether lipid peroxidation products in thermoxidised dietary oil fed during rearing, pregnancy and lactation influences the reproductive performance of female rats and the antioxidant status of their offspring. Twenty-four female rats were divided into two groups at 4 weeks of age. They were fed diets containing fresh or oxidised oil (the latter prepared by heating at a temperature of 50 degrees C for 16 d) for 14 weeks. At the age of 12 weeks female rats were mated. The number of total pups and pups born alive was not different between both groups. However, individual pups and litters of dams fed oxidised oil were lighter at birth and gained less weight during the suckling period than those of dams fed fresh oil (P < 0.05). Pups of dams fed oxidised oil contained less protein and more fat in their carcasses than those of dams fed fresh oil (P < 0.05). The milk of dams fed oxidised oil had a lower concentration of triacylglycerols and a lower energy content than that of dams fed the fresh oil (P < 0.05). The pups of dams fed oxidised oil had higher concentrations of lipid peroxidation products in the liver at birth and day 19 of lactation than those of dams fed fresh oil (P < 0.05). In conclusion, the present study shows that feeding oxidised oil with a high concentration of lipid peroxidation products to female rats during rearing, pregnancy and lactation influences the development and antioxidant status of fetus and suckling pups.     

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

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

Effects of marginal zinc deficiency on subclinical lead toxicity in the rat neonate

Influence of maternal dietary zinc intake on tissue distribution of lead and zinc in neonatal rats administered lead acetate by gavage during lactation was examined. Milk from dams fed a marginally deficient diet (6 micrograms Zn/g diet) contained a lower zinc concentration at the beginning of lactation than did that from control dams (30 micrograms Zn/g diet); no differences were seen by d 11 of lactation. Dams fed the deficient diet had lower plasma zinc values in comparison with pair-fed or ad libitum-fed dams and lower femur zinc concentration in comparison with pair-fed dams. Pups suckling marginally deficient dams had lower concentrations of zinc in plasma, femurs and kidneys although hippocampal and cerebellar zinc were unaltered. Body weights of pups from marginally zinc-deficient dams were lower than those from ad libitum-fed dams, but similar to those from pair-fed dams. Lead ingestion had no effect on body weight. Marginally zinc-deficient pups had greater lead accumulation in blood, femurs, hippocampi and cerebella, but not kidney, than did zinc-adequate pups. Marginal zinc deficiency during lactation increases the body lead burden of suckling rats, an effect not attributable to increased transfer of lead into milk in response to suboptimal maternal zinc status.     

Effect of fish oil and safflower oil in common Japanese diet on human plasma fatty acid composition

The influence of fish oil and safflower oil contained in the common Japanese diet as the main dietary polyunsaturated fatty acid source on plasma fatty acids in ten female student volunteers (21-22 years old) was investigated. The subjects were divided into two groups and fed the experimental diets for five days. The total daily fat intake in the fish diet and safflower oil diet was 54.4 g and 56.2 g, respectively, and the fat derived from fish and safflower oil was 16 g and 23 g, respectively. The proportion of linoleic acid was reduced in the plasma of subjects fed the fish diet and increased in the plasma of subjects fed the safflower oil diet. The plasma levels of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) were significantly elevated in the fish diet group. The ratio of EPA/arachidonic acid (AA) was higher, and those of n-6/n-3 and n-9/n-3 were lower in the plasma of subjects fed the fish diet when compared to the results obtained from plasma of subjects fed the safflower oil diet. From these results, it seems likely that fish oil in the common Japanese diet is a favorable source of plasma EPA and DHA even in such short term supplementation and with such a small amount of daily consumption.     

Long-Term Effect of Docosahexaenoic Acid Feeding on Lipid Composition and Brain Fatty Acid-Binding Protein Expression in Rats

Arachidonic (AA) and docosahexaenoic acid (DHA) brain accretion is essential for brain development. The impact of DHA-rich maternal diets on offspring brain fatty acid composition has previously been studied up to the weanling stage; however, there has been no follow-up at later stages. Here, we examine the impact of DHA-rich maternal and weaning diets on brain fatty acid composition at weaning and three weeks post-weaning. We report that DHA supplementation during lactation maintains high DHA levels in the brains of pups even when they are fed a DHA-deficient diet for three weeks after weaning. We show that boosting dietary DHA levels for three weeks after weaning compensates for a maternal DHA-deficient diet during lactation. Finally, our data indicate that brain fatty acid binding protein (FABP7), a marker of neural stem cells, is down-regulated in the brains of six-week pups with a high DHA:AA ratio. We propose that elevated levels of DHA in developing brain accelerate brain maturation relative to DHA-deficient brains.     

Auditory Brainstem Evoked Response in Juvenile Rats Fed Rat Milk Formulas with High Docosahexaenoic Acid

Abstract

Previous studies found that juvenile offspring of rats fed high docosahexaenoic acid (DHA; 22:6n-3) diets through gestation and lactation had longer auditory brainstem-evoked response (ABR) accompanied by higher 22:6n-3 and lower arachidonic acid (ARA; 20:4n-6) in brain. In the present study, ABR was assessed in juvenile rats fed high-DHA diets only postnatally.

Methods: Rat pups were fed rat milk formulas with varying amounts of DHA and ARA to 19 days of age followed by diets with the corresponding fatty acids. The high-DHA group was fed 2.3% of fatty acids as DHA, the DHA+ARA group was fed DHA and ARA at 0.6 and 0.4% of fatty acids, levels similar to those in some infant formulas, and the unsupplemented group was fed no DHA or ARA. ABR and fatty acid and monoamine levels in brain were measured on postnatal days 26-28. Statistical analyses were measured by ANOVA.

Results: ARA and DHA levels in brain increased with supplementation. ABR was shorter in the high-DHA group than the DHA+ARA group and not different from the unsupplemented or dam-reared suckling group. Norepinephrine levels in the inferior colliculus were lower in the high-DHA group than the DHA+ARA group and higher in all formula groups compared to the dam-reared group.

Conclusion: In contrast to the longer ABR in juvenile offspring of rats fed high-DHA through gestation and lactation, ABR was shorter in juvenile rats fed high-DHA diets only after birth than rats fed ARA+DHA. Further studies are needed to understand the relationship between dietary DHA, norepinephrine, and auditory system development over a range of DHA intakes and discrete periods of development.     

Vitamin A during lactation: relationship of maternal diet to milk vitamin A content and to the vitamin A status of lactating rats and their pups

We have investigated the effects of maternal vitamin A intake during pregnancy and lactation or during lactation alone on the concentration of vitamin A in rat's milk and on vitamin A levels in plasma and liver of dams and their pups. Groups of Sprague-Dawley rats were fed diets having either a high vitamin A content [15 retinol equivalents (R.E.)/g diet] or a low vitamin A content (0.6 R.E./g) for 42 d, including 7-8 d prior to pregnancy, pregnancy, and for 14 d of lactation. The concentration of vitamin A in milk on d 14 of lactation was significantly greater on the high vitamin A diets [114 +/- 16 micrograms/dl (mean +/- SEM; n = 8) versus 52 +/- 7.3 micrograms/dl (n = 11), P less than 0.005]. However, milk vitamin A concentration on d 1 of lactation did not vary with maternal vitamin A intake during pregnancy. In a second study in which supplementation with vitamin A (30 R.E./g diet) was begun on d 1 postpartum, the milk vitamin A content increased progressively with duration of lactation. Maternal plasma vitamin A concentrations did not differ between rats fed the higher or lower vitamin A diets. However, liver vitamin A concentrations both of dams and of their 14-d-old pups were significantly higher when dams were fed the higher vitamin A diets during pregnancy and/or lactation. The results of these studies indicate that the transfer of vitamin A from mother to offspring by milk and the vitamin A status of dams and their suckling neonates is influenced by maternal vitamin A intake during lactation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Administration of low doses of fish oil derived N-3 fatty acids to elderly subjects

OBJECTIVES: To assess the incorporation of n-3 polyunsaturated fatty acids (PUFA) in plasma and erythrocyte lipids of elderly subjects after ingestion of very low doses of fish oil. The effects on alpha-tocopherol and retinol concentrations were also studied. SETTING: Municipal nursing home in Barcelona, Spain. SUBJECTS: Forty-five elderly subjects aged 60-92 y. DESIGN AND INTERVENTION: Subjects received a non-commercialized milk formula containing 1% fish oil for 15 months, which provided 0.40 g/d of n-3 PUFA. Fatty acid profiles and antioxidant concentrations were measured before and after the intervention period. RESULTS: Fish oil ingestion was associated with significant increases in total n-3 PUFA in plasma and erythrocytes by 32% and 18%, respectively. Eicosapentaenoic (EPA) and docosahexaenoic (DHA) acid concentrations were higher after the ingestion period both in plasma and erythrocytes (P < 0.05), whereas linoleic and arachidonic acids remained unchanged. The n-6/n-3 ratio decreased by 21% in plasma and by 16% in erythrocytes (P < 0.05). Moreover, younger subjects showed a greater incorporation of EPA and DHA than older subjects. Plasma alpha-tocopherol and retinol concentrations did not vary significantly, whereas erythrocyte alpha-tocopherol was significantly higher after the intervention period. CONCLUSION: This study shows that low doses of n-3 PUFA supplemented with adequate amounts of alpha-tocopherol can be incorporated into blood lipids in elderly subjects without lowering their antioxidant concentrations.     

Copper metabolism in iron-deficient maternal and neonatal rats

Groups of rats were fed diets providing 8 ppm iron (-Fe) and 250 ppm iron (+Fe) throughout pregnancy and lactation. In spite of the increase in apparent absorption of iron in pregnant -Fe dams, iron deficiency anemia developed, resulting in decreased iron levels in placenta, amniotic fluid and fetal liver. Copper concentration of amniotic fluid was elevated in -Fe dams. On day 17 of lactation, -Fe dams and their suckling pups had hematologic evidence of iron deficiency. While liver and spleen iron decreased in 17-day-old pups, levels of copper increased. Subcellularly, the greatest increase in hepatic copper in -Fe pups was found in the cytosol, thus the increased copper deposition is not similar to copper loading. Serum ceruloplasmin activity was significantly elevated in -Fe lactating dams and was slightly, but not significantly, increased in -Fe pregnant dams and suckling pups.     

Neonatal dietary zinc deficiency in artificially reared rat pups retards behavioral development and interacts with essential fatty acid deficiency to alter liver and brain fatty acid composition.

The objective of this study was to investigate whether short-term zinc deficiency in the early neonatal period would exacerbate the effects of essential fatty acid (EFA) deficiency on liver and brain long-chain polyunsaturated fatty acid (LCPUFA) composition, as well as on behavioral development in artificially reared rat pups. Using a 2 x 2 factorial design, male Long-Evans rat pups were reared artificially from postnatal d 5 to 16; pups were fed through gastrostomy tubes with rat formula deficient in zinc and/or EFA. As expected, EFA deficiency significantly reduced levels of arachidonic acid [AA, 20:4(n-6)] and docosahexanoic acid [DHA, 22:6(n-3)] in liver phosphatidylcholine (PC) and brain phosphaditylethanolamine (PE), and increased 22:5(n-6) levels in liver and brain PC and PE. There were significant interactions between zinc and EFA in liver such that zinc deficiency reduced AA and DHA in the EFA-adequate groups, but significantly increased AA in the EFA-deficient groups. Contrary to the hypothesis, short-term zinc deficiency did not exacerbate the effects of EFA deficiency in liver phospholipids. In brain PE, a significant interaction between EFA and zinc was observed such that zinc deficiency increased 22:5(n-6) concentrations in EFA-adequate but not in EFA-deficient groups. Regardless of their EFA status, zinc-deficient rats were growth retarded and demonstrated deficits in locomotor skills. Possible effects of long-term zinc and EFA deficiency on brain function should be investigated in future studies.     

Oxidation of plasma proteins is not increased after supplementation with eicosapentaenoic and docosahexaenoic acids

BACKGROUND: It is generally thought that as the intake of dietary polyunsaturated fatty acids increases, so should that of alpha-tocopherol, to protect the polyunsaturated fatty acids from increased in vivo peroxidation. However, there are little quantitative data about the concentration of alpha-tocopherol that is necessary when eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) are consumed. OBJECTIVE: The purpose of this study was to measure changes produced in 2 indexes of lipid oxidation after supplementation with EPA and DHA from fish oil and 3 doses of RRR-alpha-tocopheryl acetate in postmenopausal women. DESIGN: Daily supplements of fish oil providing 2.5 g EPA and 1.8 g DHA and 0, 100, 200, or 400 mg alpha-tocopheryl acetate were given to 46 postmenopausal women in a 4-treatment, 4-period crossover design. RESULTS: The supplements increased plasma concentrations of EPA, DHA, and alpha-tocopherol. The fish-oil supplement increased the plasma concentration of thiobarbituric acid-reactive substances (TBARS) (P: = 0.0001) but not that of oxidatively modified protein, as indicated by the carbonyl content. The alpha-tocopheryl acetate and fish-oil supplements had no significant effect on plasma concentrations of TBARS or oxidized protein. CONCLUSIONS: Although these data show a small but statistically significant increase in oxidative stress on the basis of plasma TBARS concentrations after the consumption of EPA and DHA, the clinical relevance of this change is questionable. In addition, as supplements of alpha-tocopheryl acetate were added to the diet, neither the plasma TBARS concentration nor the protein oxidation changed. Consequently, the results of this study indicate that there is no basis for vitamin E supplementation after consumption of EPA and DHA.     

Dietary sesame lignans decrease lipid peroxidation in rats fed docosahexaenoic acid

We have previously reported that dietary sesamin and sesaminol, major lignans of sesame seed, elevate the alpha-tocopherol concentration and decrease the thiobarbituric acid reactive substance (TBARS) concentration in the plasma and liver of rats. In this study, the effects of dietary sesamin and sesaminol on the lipid peroxidation in the plasma and tissues of rats fed docosahexaenoic acid (DHA, 22:6 n-3) were examined. Male Wistar rats (4-wk-old) were divided into the following six experimental groups: control group, fed a basal diet: sesamin group, fed a diet with sesamin (2 g/kg); sesaminol group, fed a diet with sesaminol (2 g/kg); DHA group, fed a diet containing DHA (5 g/kg); DHA + sesamin group, fed a diet containing DHA with sesamin; and DHA + sesaminol group, fed a diet containing DHA with sesaminol. Each diet contained either 0.01 or 0.05 g D-alpha-tocopherol/kg, and the rats were fed the respective experimental diet for 5 wk. The dietary DHA elevated the TBARS concentration and also increased the red blood-cell hemolysis induced by the dialuric acid. The dietary sesamin and sesaminol lowered the TBARS concentrations and decreased the red blood hemolysis. The dietary sesamin and sesaminol elevated the alpha-tocopherol concentrations in the plasma, liver, and brain of the rats fed a diet with or without DHA. These results suggest that dietary sesame lignans decrease lipid peroxidation as a result of elevating the alpha-tocopherol concentration in rats fed DHA.     

Water maze performance is unaffected in artificially reared rats fed diets supplemented with arachidonic acid and docosahexaenoic acid

Four groups of male Long-Evans rats were reared artificially from postnatal d 5 to 18 by being fed through a gastrostomy tube with rat milk substitutes containing oils providing 10% linoleic acid and 1% alpha-linolenic acid (g/100 g fat); with the use of a 2 x 2 design, they were fed one of two levels of arachidonic acid (AA) and docosahexaenoic acid (DHA) (0.0 and 2.5 g/100 g of fatty acids). A fifth artificially reared group was fed a diet high in saturated fat, and a sixth group was reared by dams fed a standard AIN-93M diet. The pups were weaned onto modified AIN-93G diets, with a fat composition similar to that fed during the artificial rearing period. Behavioral testing was conducted between 6 and 9 wk of age; brain lipid composition was then assessed. Relative to the unsupplemented group (0.0 g/100 g AA and DHA), dietary supplementation resulted in a wide range of AA (84-103%) and particularly DHA (86-119%) levels in forebrain membrane phospholipids. AA supplementation increased AA levels and decreased DHA levels, and DHA supplementation increased DHA levels and decreased AA levels, with the magnitude of these effects dependent on the level of the other fatty acid. DHA levels were very low in the saturated fat group. The groups did not differ on the place or cued version of the Morris water-maze, but on a test of working memory, the saturated fat group was impaired relative to the suckled control group. Further correlational analyses in the artificially reared animals did not support a relationship between the wide range of DHA and AA levels in the forebrain and working-memory performance.     

Lead exposure and (n-3) fatty acid deficiency during rat neonatal development alter liver, plasma, and brain polyunsaturated fatty acid composition

Lead (Pb) exposure has been reported to increase arachidonic (AA) and docosahexaenoic (DHA) acids. To determine whether Pb effects on fatty acid composition are influenced by dietary (n-3) fatty acid restriction, weanling female rats were fed either an (n-3)-adequate or -deficient diet to maturity and mated. At parturition, dams in each group were subdivided to receive either 0.2% Pb or Na-acetate in their drinking water during lactation only. Pups were analyzed for fatty acid content in liver, plasma, and brain at either 3 or 11 wk. The (n-3)-deficient diets markedly decreased total (n-3) fatty acids, and increased total (n-6) fatty acids including both AA and docosapentaenoic (n-6) in each compartment (P < 0.05). The main effects of Pb were in the livers of weanling rats where there was a 56% loss in total fatty acid concentration concurrent with increased relative percentages of AA and DHA. Thus, because there was a greater percentage of liver nonessential fatty acid lost relative to the essential fatty acids (EFA), there was no net change in AA concentration. There was a diet x Pb interaction for a decrease in liver DHA concentration evident only in the (n-3)-adequate group. There were also diet x Pb interactions in plasma at 11 wk and in brain at 3 wk. These data are consistent with the hypothesis of a Pb-induced increase in fatty acid catabolism, perhaps as a source of energy.     

Maternal fish oil supplementation ameliorates maternal high-fructose diet-induced dyslipidemia in neonatal mice with suppression of lipogenic gene expression in livers of postpartum mice

Maternal fructose consumption during pregnancy and lactation is associated with metabolic dysregulation in offspring. We tested the hypothesis that fish oil (FO) supplementation during pregnancy and lactation improves fructose-induced metabolic dysregulation in postpartum dams and offspring mice. We therefore aimed to determine the effects of FO supplementation on metabolic disruption in neonatal mice and dams induced by a maternal high-fructose diet (HFrD). The weight of the offspring of dams fed with HFrD on postnatal day 5 was significantly low, but this was reversed by adding FO to the maternal diet. Feeding dams with HFrD significantly increased plasma concentrations of triglycerides, uric acid, and total cholesterol, and decreased free fatty acid concentrations in offspring. Maternal supplementation with FO significantly suppressed HFrD-induced hypertriglyceridemia and hyperuricemia in the offspring. Maternal HFrD induced remarkable mRNA expression of the lipogenic genes Srebf1, Fasn, Acc1, Scd1, and Acly in the postpartum mouse liver without affecting hepatic and plasma lipid levels. Although expression levels of lipogenic genes were higher in the livers of postpartum dams than in those of nonmated mice, HFrD feeding increased the hepatic lipid accumulation in nonmated mice but not in postpartum dams. These findings suggest that although hepatic lipogenic activity is higher in postpartum dams than nonmated mice, the lipid consumption is enhanced in postpartum dams during pregnancy and lactation. Maternal FO supplementation obviously suppressed the expression of these lipogenic genes. These findings coincide with reduced plasma triglyceride concentrations in the offspring. Therefore, dietary FO apparently ameliorated maternal HFrD-induced dyslipidemia in offspring by suppressing maternal lipogenic gene expression and/or neonatal plasma levels of uric acid.     

Ratio of high-fat diet intake of pups nursed by dams fed combination diet was lower than that of pups nursed by dams fed high-fat or low-fat diet

To investigate the influence of fat-feeding dams on the food choice of their pups after weaning, each of three groups of dams was fed a low-fat diet (LHD), a high-fat diet (HFD) or a two-choice diet of LFD and HFD during pregnancy and lactation. Immediately after weaning, all pups were placed on a two-choice diet program for 5 wk. The fat energy ratio (F ratio) for dams fed the two-choice diet was 31%. Although no significant differences in body weight or calorie intake were observed between these three groups of dams, liver and perirenal fat tissue weights and plasma and liver trigluceride and total-cholesterol concentrations were lower in dams fed the two-choice diet than in dams fed LHD or HFD. Both groups of pups nursed by dams fed LFD or HFD continued to eat a large amount of HFD after weaning (F ratio was over 40%). Although within first week after weaning, no significant difference in the ratio of HFD intake was observed among the three groups of pups, the ratio for pups nursed by dams fed the two-choice diet decreased after the second week. The F ratio for pups nursed by dams fed the two-choice diet was 32%. These data lead us to conclude that if dams ate more than one diet in an adequate PFC ratio, their pups would have the ability to eat adequately after weaning.     

Dietary conjugated linoleic acids lower the triacylglycerol concentration in the milk of lactating rats and impair the growth and increase the mortality of their suckling pups

Recent studies showed that conjugated linoleic acids (CLA) lower triacylglycerol concentrations in the milk of lactating animals. This study was performed to determine the reasons for this phenomenon; we also investigated whether there is a relation between altered lipid metabolism in the liver and the reduction in milk triacylglycerols in rats fed CLA. Two groups of female rats were fed diets containing 0 [sunflower oil (SFO) group] or 14.7 g/kg diet of a CLA mixture (CLA group) at the expense of sunflower oil during growth, pregnancy, and lactation. CLA-fed rats had 49 and 80% lower mRNA concentration and activity of fatty acid synthase, respectively, a 51% lower mRNA concentration of lipoprotein lipase (LPL) in their mammary glands at d 17 of lactation, and a 46% lower milk fat content than SFO rats (P < 0.05). Although CLA rats had lower concentrations of triacylglycerols in the liver than SFO rats (20.8 +/- 2.6 vs. 62.6 +/- 27.7 micromol/g, P < 0.05), concentrations of triglycerides in plasma, which are the substrates of LPL, did not differ between the groups. Moreover, the number of pups per litter, litter weights, and pup weights at d 17 of lactation were 41, 35, and 22% lower, respectively, in the CLA group than in the SFO group. In conclusion, the present study suggests that dietary CLA reduces triacylglycerol concentrations in the milk via reduced de novo fatty acid synthesis in the mammary gland and an impaired uptake of fatty acids from lipoproteins into the mammary gland. This might be the reason for reduced growth rates and an increased mortality of suckling pups.     

Fatty acid composition of serum lipid classes in mice following allergic sensitisation with or without dietary docosahexaenoic acid-enriched fish oil substitution

Dietary fatty acids have been shown to influence allergic sensitisation. Both n-3 and n-6 PUFA are involved in targeted mediation of inflammatory responses during allergic sensitisation and manifestation of atopic diseases. In the present experiments we investigated whether supplementation of DHA-enriched fish oil partly substituting dietary sunflower-seed oil, in comparison with sunflower-seed oil, supplemented to mice influences fatty acid composition of serum lipid classes. The effects of the two different diets were also investigated depending on allergic sensitisation. Supplementation of DHA and EPA in doses of 2 and 0.12 % (w/w) to non-sensitised and sensitised mice resulted in significantly increased percentile contributions of DHA to all lipid classes. In contrast, serum values of the n-6 PUFA arachidonic acid (AA) were significantly lower, both in non-sensitised and sensitised mice fed the DHA-enriched diet. The fatty acid composition of serum lipids also reflected allergic sensitisation: the EPA:AA ratio in TAG, cholesteryl esters and phospholipids in non-supplemented animals fell to 23, 29 and 29 % respectively of the original value after allergic sensitisation, whereas it decreased to 70, 80 and 76 % respectively only in the animals supplemented with DHA. In summary, allergic sensitisation alone decreased significantly the EPA:AA ratios in serum TAG, while concomitant supplementation of DHA-enriched fish oil ameliorated this decrease. We postulate from the present results that the amelioration of the severity of allergic sensitisation after DHA supplementation may be linked to altered ratios of the eicosanoid precursors EPA and AA as well as DHA needed for further metabolic activation to pro- or anti-inflammatory bioactive lipids.     

Marginal maternal Zn intake in rats alters mammary gland Cu transporter levels and milk Cu concentration and affects neonatal Cu metabolism

Marginal zinc intake is common and leaves women particularly vulnerable to Zn deficiency due to increased demand for Zn as a consequence of reproduction. Zn deficiency during pregnancy and lactation has been associated with secondary affects on copper metabolism in the offspring; however, the underlying mechanisms are unknown. The effects of marginal maternal Zn intake on maternal and neonatal Cu metabolism were determined in rats. Plasma, milk and tissue Cu and Zn concentrations and plasma and milk ceruloplasmin (Cp) activity were measured in dams fed a control (CON, 25 mg Zn/kg diet) or a marginal Zn diet (ZD, 10 mg Zn/kg diet) and their suckling pups. There was no effect on maternal tissue Cu or Zn or milk Zn concentration; however, plasma Cp activity was higher in dams fed ZD, suggesting that Cp activity may be a useful marker for identifying marginal Zn status. Rats fed ZD had high mammary gland Ctr1, Atp7A and Atp7B levels, milk Cp activity and Cu concentration. Immunostaining and differential centrifugation indicated that ZD also altered Ctr1 and Atp7A localization in the mammary gland. Pups from dams fed ZD had higher small intestine Cu and lower plasma Cu than CON pups. These results suggest that marginal maternal Zn intake during pregnancy and lactation increase mammary gland Cu transporter levels and alter their localization, resulting in high milk Cu levels, possibly in response to transiently elevated plasma Cu levels. The combination of high milk Cu concentration and immature neonatal Cu transport exposes the suckling neonate to excess Cu; however, whether this occurs in humans is not yet known.     

Effect of diet during pregnancy and lactation on the activity of HMG-CoA reductase in the developing rat

Wistar rats were fed a control diet or a diet containing either cholestyramine or high fat and cholesterol throughout gestation and the first 14 d of lactation. New-born litters were cross-fostered from rats fed the control diet to rats fed either cholestyramine or high fat and cholesterol, or from rats fed cholestyramine to rats fed the control diet. Hepatic hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase activity, plasma cholesterol and triglycerides were assayed on gestation d 20 and postnatal d 8, 14, 22 and 30. Cholestyramine had no effect on maternal or fetal plasma lipid levels but increased fetal hepatic HMG-CoA reductase activity by approximately 50%. The increased reductase activity persisted on postnatal d 8 and 14. Control pups suckled by dams fed cholestyramine also had significantly increased HMG-CoA reductase activities on postnatal d 8 and 14. The high fat and cholesterol diet significantly increased maternal plasma cholesterol but had no effect on HMG-CoA reductase activity in the fetus or suckling pups. Neither cholestyramine nor high fat and cholesterol altered the rat milk cholesterol levels. The studies demonstrate that HMG-CoA reductase activity in the developing rat can be altered by factors dependent on maternal diet. They do not support a hypothesis for regulation by maternal dietary or milk cholesterol supply.