Low arachidonic acid rather than alpha-tocopherol is responsible for the delayed postnatal development in offspring of rats fed fish oil instead of olive oil during pregnancy and lactation

This study was designed to compare in rats the effects of dietary fish oil and olive oil during pregnancy and lactation on offspring development, fatty acid profile and vitamin E concentration. From d 0 of pregnancy, female Sprague-Dawley rats were divided into two groups that were fed purified diets that differed only in their nonvitamin lipid components. One diet contained 10 g fish oil/100 g diet (FOD), whereas the other contained 10 g olive oil/100 g diet (OOD). At d 20 of gestation, maternal adipose tissue fatty acid profile did not differ between rats fed the two diets, whereas both maternal and fetal plasma and liver arachidonic acid (AA) contents were proportionally lower and eicosapentaenoic (EPA) and docosahexaenoic (DHA) acid contents were higher in the FOD group than in the OOD group. alpha-Tocopherol concentration was lower in maternal and fetal plasma, liver and brain in the FOD group than in the OOD group. The postnatal increase in body weight and length was less and body and psychomotor maturation indices were delayed in pups from FOD-fed dams compared with those from OOD-fed dams. This difference was maintained when pups were cross-fostered at birth, with the delay in postnatal development present in the pups suckling dams fed FOD during lactation. At age 21 d, pups suckling dams fed FOD had lower AA and higher EPA and DHA concentrations in brain phospholipids. Although alpha-tocopherol in plasma and liver was lower in pups suckling dams fed FOD rather than OOD, brain alpha-tocopherol concentrations did not differ. Milk yield and milk alpha-tocopherol and AA concentrations were lower and EPA and DHA were higher in the milk of dams fed FOD compared with those fed OOD. Postnatal development indices and the proportion of plasma, liver and brain AA concentrations, although not plasma, liver and brain alpha-tocopherol concentrations, recovered to the values found in dams fed OOD when the FOD was supplemented with gamma-linolenic acid. However, postnatal development indices were not recovered when the FOD was supplemented with sufficient exogenous vitamin E to increase plasma and liver alpha-tocopherol concentrations above those in dams fed OOD. Thus, although feeding FOD during pregnancy and lactation decreases both alpha-tocopherol and AA concentrations, the latter deficiency rather than the former seems to be responsible for delayed postnatal development of rat pups.     

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.     

Dietary canola and soybean oil fed to SHRSP rat dams differently affect the growth and survival of their male pups

Canola oil (Can), as well as some other oils, shortens the survival of SHRSP rats compared with soybean oil (Soy). Although detrimental factors other than phytosterols have not been identified, they are likely to be hydrophobic and transmissible to pups. To test this possibility, female SHRSP rats (F0) were fed a diet supplemented with Can or Soy and mated at 11 wk of age. The growth of suckling pups (F1) from the Can-fed dams was significantly retarded compared with that of pups from the Soy-fed dams. Half of the male pups (F1) were weaned to the same diet as their dams (Can-->Can and Soy-->Soy groups) and the rest were weaned to the other diet (Can-->Soy and Soy-->Can groups). The survival rate of the male pups (F1) was significantly lower in the Can-->Can group than in the Soy-->Can group, and in the Can-->Soy group than in the Soy-->Soy group, indicating that the oils fed to dams differently affected the growth and survival of pups. There were fewer pups per dam in the Can-fed dams (F0) than in the Soy-fed dams, and in the dams (F1) of the Can-->Can and Soy-->Can groups than in those of the Can-->Soy and Soy-->Soy groups. Although Can is nutritionally detrimental to SHRSP rats compared with Soy, no direct evidence has been obtained thus far relating these observations to human nutrition.     

A high dietary lipid intake during pregnancy and lactation enhances mammary gland lipid uptake and lipoprotein lipase activity in rats.

Rats fed a diet with high fat concentration produce larger amounts of milk with a higher lipid concentration than rats fed a lower fat diet. This investigation was designed to study the relationship between dietary fat intake, mammary gland lipid uptake and lipogenesis in rat dams fed, during pregnancy and lactation, one of two purified diets, with equal energy density, containing 2.5 (LL) or 20 g fat/100 g diet (HL). Milk lipid concentration and fatty acid composition were determined at d 14 of lactation. Mammary gland lipogenesis, lipoprotein lipase (LPL) activity and the uptake of [1-(14)C]triolein by the mammary gland and its transfer to the pups was measured. The intestinal absorption of oral (14)C-lipid, (14)CO(2) production and the amount of (14)C-lipid transferred to the pups (milk clot + pups carcass) were significantly higher in the HL group than in the LL group (P < 0.05). Mammary gland lipogenesis was 75% lower and LPL activity was 30% higher in the HL group (P < 0.05). Medium-chain fatty acids (C6-C14) excretion was 46% lower and that of long-chain fatty acids was 142% (P < 0.001) higher in the HL group than in the LL group. The higher milk lipid excretion in the rats fed a high-fat diet resulted from a larger uptake of dietary lipid by the mammary gland, indicated by a larger transfer of (14)C-lipid to the pups and by a higher LPL activity in the mammary gland.     

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.     

A thermally oxidized dietary oil does not lower the activities of lipogenic enzymes in mammary glands of lactating rats but reduces the milk triglyceride concentration

It was shown that dietary thermoxidized oils suppress gene expression of lipogenic enzymes in the liver. This study was performed to investigate whether oxidized oils also influence the activities of lipogenic enzymes in the mammary gland of lactating rats. Female rats (n = 24) were divided into two groups at 4 wk of age. They were fed for 14 wk diets with either fresh oil (a mixture of sunflower oil, linseed oil, and palm oil, 73:15:12) or oxidized oil (a mixture of sunflower oil and linseed oil, 80:20) prepared by heating at a temperature of 50 degrees C for 16 d. At the age of 12 wk, the rats were mated. At birth, litters were adjusted to 7 pups/dam. Milk was sampled at d 14 of lactation; mammary glands were taken at d 19 of lactation. Rats fed the oxidized oil had a lower activity of glucose-6-phosphate dehydrogenase (G6PDH) in their mammary glands than those fed the fresh oil (P < 0.05); the activities of fatty acid synthase (FAS) and acetyl-CoA-carboxylase in mammary glands did not differ. Relative mRNA concentrations of G6PDH, FAS, and sterol-regulatory element binding protein-1, a regulator of lipogenesis, in the mammary gland did not differ between groups. The concentrations in the milk of medium-chain fatty acids (C8-C14), the major products of fatty acid synthesis in mammary glands, also did not differ. The concentrations of triglycerides and long-chain fatty acids (C18-C22), however, were lower in the milk of rats fed the oxidized oil than in the milk of rats fed the fresh oil (P < 0.05). In conclusion, this study shows that feeding oxidized oils to lactating rats does not affect lipogenic enzymes in mammary glands but reduces the triglyceride concentrations in their milk.     

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.     

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)     

Influence of heated linseed oil on reproduction in the female rat and on the composition of hepatic lipids in young rats]

During gestation and lactation, six month old female Wistar rats were fed diets containing 10 p. 100 by weight of various vegetable oils; thermopolymerized linseed oil at 275 degrees C for 12 hours under nitrogen atmosphere (group T), oxidized linseed oil at 200 degrees C for 100 hours under air atmosphere (group O). The two oils contain respectively 11,5 and 1,1 p. 100 of cyclic monomers (18 C). Control groups were fed either fresh linseed oil or fresh peanut oil under the same conditions. In group T, most of the newborn rats die at birth or during the first three days of life; none of them survive 13 days after birth. In group O, mortality of youngs is not so high but is still significantly higher than in control groups. Moreover, dead young rats of group T have heavier livers and higher lipid content in the organ. Cyclic monomers were detected in liver fatty acids. In surviving young rats of group O,the body growth during lactation is significantly slower than in control animals. Young rats of group O were sacrificed at the age of 14 days. Liver weight and lipid content of the organ are increased and cyclic monomers were detected. The effects are however less pronounced than in group T. One can assume that among abnormal compounds formed during heating of linseed oil, cyclic monomers are responsible for the toxic effects observed in the present experiment since they have been transmitted to the litters either during gestation or lactation.     

Ethanol intake during lactation impairs milk production in rats and affects growth and metabolism of suckling pups.

From parturition, lactating Wistar rats were given 20% alcohol in drinking water and fed a solid diet ad lib (group AL). Pair-fed (PF) and control (C) rats were fed solid diet and given water ad lib (C). All animals were sacrificed on the 12th day of lactation. Ethanol treatment decreased food intake and milk production in lactating rats to a greater level than in PF rats, and a greater reduction in body weight of the AL pups was noted. Brain weight, protein concentration, and DNA content were also lower in pups of AL dams than of PF dams, whereas liver glycogen concentration was higher in the former. Pups from AL dams had higher circulating levels of beta-OH-butyrate, triglyceride, and free fatty acids than those from either C or PF dams. Plasma glucose concentration was lower in both PF and AL than in C pups, whereas the AL group had lower plasma protein concentration than any of the other groups. We conclude that maternal alcohol intake during lactation greatly impairs milk production, and although the known increase of lipid content in milk in rats studied under similar conditions allows an enhanced lipidic components in the pups, this adaptation does not allow normal growth and brain development.     

Maternal dietary restriction during pregnancy and lactation: effect on digestive organ development in suckling rats

To examine the relative effects of maternal malnutrition during pregnancy and lactation on development of the pancreas and small intestine in suckling pups, rats were restricted to 50% of control (C) intake beginning at day 5 of pregnancy. Immediately after birth, some litters were exchanged such that some C dams were suckling pups born to 50%-restricted dams (C/50) and vice versa (50/C). Other litters were allowed to stay with their own mothers, which received a control or restricted diet as during pregnancy (C/C and 50/50). Pups nurtured by restricted dams had reduced body weights, intestinal lengths, hepatic and pancreatic weights, and specific activities of pancreatic lipase and small intestinal brush border sucrase and maltase. Small intestinal lactase levels were higher in the groups of pups from mothers restricted during lactation. In nearly all cases, the 50/C group was the most severely affected while the C/50 group was intermediate between the C/C and 50/50 groups.     

Conjugated linoleic acid is a growth factor for rats as shown by enhanced weight gain and improved feed efficiency

We studied the effect of conjugated linoleic acid (CLA) on rat development and growth. Primigravid female Fischer rats were fed control or CLA-supplemented (0.25% or 0.5% CLA) diets during gestation and/or lactation. Conjugated linoleic acid was incorporated into milk fat and tissue lipids proportional to the level of CLA fed and the duration of CLA feeding. Conjugated linoleic acid was incorporated into fetal and neonatal tissues; it did not affect litter size nor induce apparent abnormalities. To the contrary, feeding CLA to the dams during gestation and lactation improved the postnatal body weight gain of pups (P < 0.05), measured on d 10 of lactation. Pups that continued to receive the CLA-supplemented diet after weaning had significantly greater body weight gain and improved feed efficiency relative to control animals (P < 0.05).     

Depressed folate incorporation into milk secondary to iron deficiency in the rat

The present study was designed to determine whether reduced folate incorporation into milk can account for folate depletion of iron-deficient suckling rats. Dams were fed diets containing 2 mg/kg folate and either 8, 12 or 250 mg/kg iron throughout gestation and lactation to produce severely iron-deficient, moderately iron-depleted and iron-sufficient states in 17-d-old pups (n = 15 litters/group). On d 17 of lactation, dams were separated from litters and given intraperitoneal injections of [3',5',7,9-3H]pteroylmonoglutamic acid ([3H]PteGlu) or physiological saline. Mean [3H]PteGlu incorporation into milk of severely iron-deficient dams was 67% of that in iron-sufficient controls, while "total" and "free" milk folate activities were 54 and 61%, respectively. Values for milk [3H]PteGlu incorporation and folate activities were intermediate in moderately iron-depleted dams. Pup red blood cell folate activity was positively correlated with both free (r = 0.43, P = 0.004) and total (r = 0.37, P = 0.015) milk folate activities. Mean plasma folate activities of severely and moderately iron-deficient pups were 68 and 86% of control values, respectively. Results show that in both mild and severe iron deficiency, reduced folate secretion into milk is at least partially responsible for impaired folate status of suckling pups.     

Increased rat mammary tissue vitamin A associated with increased vitamin A intake during lactation is maintained after lactation

Although increases in dietary vitamin A increase milk vitamin A, little is known about effects of vitamin A intake on mammary tissue vitamin A levels during and after the reproductive cycle. First, we measured vitamin A concentrations in milk, mammary tissue and liver of lactating rats fed 0, 4, or 50 micromol of vitamin A/kg diet during pregnancy and through d 12 of lactation. Liver vitamin A concentration was significantly affected by diet in lactating females and pups 12 d after parturition. Milk vitamin A concentrations were significantly higher (7.1 +/- 2.2 micromol/L, n = 8) in dams fed 50 micromol/kg than in those fed 0 or 4 micromol/kg (1.9 +/- 0.3, n = 5 and 2.9 +/- 0.7 micromol/L, n = 7; P < 0.001), as were mammary tissue vitamin A concentrations (5.1 +/- 1.1 versus 2.2 +/- 0.4 and 2.4 +/- 0.6 nmol/g; P < 0.001). Next, we maintained female rats on 50 or 10 micromol vitamin A/kg diet during pregnancy and lactation and then on 4 micromol/kg diet after pups were weaned on d 21. On d 21, mammary tissue vitamin A concentrations were 3.14 +/- 0.75 versus 1.52 +/- 0.21 nmol/g in dams fed 50 versus 10 micromol/kg (n = 4/group; P < 0.001). Mammary tissue vitamin A concentrations were not significantly affected by time from 7 to 49 d after lactation and averaged 8.5 +/- 0.4 and 4.9 +/- 0.8 nmol/g on d 49 in dams fed 50 versus 10 micromol/kg (n = 4; P < 0.001). We conclude that diet-induced differences in rat mammary tissue vitamin A developed during pregnancy and lactation are maintained for > or =7 wk after lactation.     

Effects of maternal chronic alcohol administration in the rat: lactation performance and pup's growth

Summary A fostering/crossfostering analysis of the effects of maternal ethanol exposure on lactation performance and offspring growth was performed. Wistar rats were kept under one of the three experimental nutritional treatments: alcohol-treated (EG), pair-fed-treated (PFG) (as a nutritional control of alcohol-associated malnutrition), and control or normal diet (CG). Rats from the EG group were accustomed to increased amounts of ethanol (5 % during the first week to 20 % in the fourth week). The 20 % ethanol level was maintained throughout three additional weeks and during gestational and lactational period. Daily food intake, fluid consumption, body weight and gestational parameters were studied in control (CG), pair-fed (PFG) and ethanol dams (EG). At birth, half the litters were fostered to other dams of the same treatment (GLG) and half were cross-fostered to dams of the opposite treatment (GG, LG). No cross-fostering analyses were performed on the pair-fed group. Offspring body weight was controlled throughout lactation. Liver, kidney and spleen weights as well as milk consumption were also studied at the end of lactation period. In dams, a significant reduction of body weight was described throughout the suckling period. No ethanol detrimental effects were observed on body weight at birth, but in spite of a normal birth weight, alcohol during lactation was responsible for a growth deficit. Milk consumption was significantly reduced in offspring exposed to ethanol during gestation and/or lactation. Curiously, prenatal alcohol exposure affects adversely the suckling behaviour in pups at the time of weaning. In our study, alcohol treatment and malnutrition affects liver and spleen weights. However, malnutrition decreases spleen weights more than alcohol treatment. In the case of the kidney weights the alcohol decreases kidney weight more than malnutrition. Collectively, the data from the present study show similar effects following pre/postnatal and postnatal alcohol exposure. The findings suggest that chronic alcohol administration during gestation and/or lactation adversely affects pup growth at weaning as indicated by its effect on milk consumption, pup and organ weight. Received: 3 January 2001, Accepted: 8 June 2001     

Maternal-iron-deficiency effects on peritoneal macrophage and peritoneal natural-killer-cell cytotoxicity in rat pups.

Cytotoxicity of peritoneal macrophages (pMs) and peritoneal natural killer (pNK) cells toward xenogenic tumor cells was studied in anemic, suckling rats. Dams were fed 6, 12, or 250 mg Fe/kg diet ad libitum throughout gestation and lactation. Pups were injected intraperitoneally with 10(5) plaque-forming units of virus. Four days later cytotoxicity of pMs and pNK cells against YAC-1 mouse lymphoma cells was measured. Body weight, hemoglobin, hematocrit, and viable cell yield of pups were significantly decreased with decreasing dietary iron. pM cytotoxicity was significantly impaired in anemic pups at pM-target-cell ratios of 10:1 and 30:1 at 4 and 16 h (P less than or equal to 0.03). pNK-cell cytotoxicity was significantly impaired in anemic pups at pNK-target-cell ratios of 10:1 and 50:1 at 16 h. Iron-deficient diet consumed by dams throughout gestation and lactation resulted in anemic offspring whose immunologic defense by pMs and pNK cells against xenogenic tumor cells was significantly reduced.     

Polyunsaturated (n-3) fatty acids susceptible to peroxidation are increased in plasma and tissue lipids of rats fed docosahexaenoic acid-containing oils

Docosahexaenoic acid [DHA, 22:6(n-3)], a major component of membrane phospholipids in brain and retina, is profoundly susceptible to oxidative stress in vitro. The extent of this peroxidation in organs when DHA is ingested in mammals, however, is not well elucidated. We investigated the effect of dietary DHA-containing oils (DHA 7.0-7.1 mol/100 mol total fatty acids), in the form of triacylglycerols (TG), ethyl esters (EE) and phospholipids (PL), on tissue lipid metabolism and lipid peroxidation in rats. Groups of Sprague-Dawley rats were fed semipurified diets containing 15 g/100 g test oils and were compared with those fed 80% palm oil and 20% soybean oil as the control (unsupplemented group) for 3 wk. The DHA oil diets markedly increased (P: < 0.05) the levels of DHA in the plasma, liver and kidney, 1.5-1.9, 2.5-3.8 and 2.2-2.5 times the control values, respectively, whereas there was a concomitant reduction (P: < 0.05) in arachidonic acid. All forms of DHA oil caused lower TG concentrations in plasma (P: < 0.05) and liver (P: < 0.05), but had no effect in kidney. The DHA oil-fed rats had greater phospholipid hydroperoxide accumulations in plasma (191-192% of control rats), liver (170-230%) and kidney (250-340%), whereas the alpha-tocopherol level was reduced concomitantly (21-73% of control rats). Consistent with these results, rats fed DHA-containing oils had more thiobarbituric reactive substances in these organs than the controls. Thus, high incorporation of (n-3) fatty acids (mainly DHA) into plasma and tissue lipids due to DHA-containing oil ingestion may undesirably affect tissues by enhancing susceptibility of membranes to lipid peroxidation and by disrupting the antioxidant system.     

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.     

Interactions between protein and vegetable oils in the maternal diet determine the programming of the insulin axis in the rat

The available evidence suggests that metabolic control mechanisms are programmed early in life. Previous studies of pregnant rats fed low-protein diets have suggested that the vegetable oils used in the experimental diets influence the outcome. The present study investigated the offspring of female rats fed semi-synthetic diets containing either 180 or 90g casein/kg with 70 g/kg (w/w) of either corn oil or soya oil during gestation. During lactation, the dams received stock diet, and the offspring were subsequently weaned onto the stock diet. The offspring of dams fed the low-protein diets were smaller at birth. At 25 weeks of age, the offspring were subjected to an oral glucose tolerance test. In the offspring of dams fed the diet containing soya oil, the area under the insulin curve was affected by the protein content of the maternal diet. There was no effect of protein on the area under the insulin curve in the offspring of dams fed the diet prepared with corn oil. There were no differences in plasma glucose concentrations. The levels of mRNA for acetyl-CoA carboxylase- in the livers of female offspring were affected by the protein and oil content of the maternal diet. The level of carnitine palmitoyl transferase mRNA was affected by the protein content of the maternal diet. The present study suggests that PUFA in the maternal diet can interact with protein metabolism to influence the development of the offspring. This may involve the higher content of alpha-linolenic acid in soya oil compared with corn oil.     

Oxidized fat reduces milk triacylglycerol concentrations by inhibiting gene expression of lipoprotein lipase and fatty acid transporters in the mammary gland of rats

Feeding oxidized fats to lactating rats causes a strong reduction of triacylglycerol concentration in the milk. The reason for this, however, has not yet been elucidated. Pregnant Sprague-Dawley rats were assigned to 2 groups of 11 rats each and fed diets containing either fresh fat (FF group) or an oxidized fat (OF group) from d 1 to d 20 of lactation. Concentrations of triacylglycerols and long-chain fatty acids in the milk and weight gain of suckling pups were lower in the OF group than in the FF group (P < 0.05). Concentrations of medium-chain fatty acids in the milk and messenger RNA (mRNA) abundance of lipogenic enzymes in the mammary gland did not differ between the 2 groups of rats. However, the OF group had a lower concentration of triacylglycerols and nonesterified fatty acids (NEFA) in plasma and lower mRNA concentrations of lipoprotein lipase and fatty acid transporters in the mammary gland than the FF group (P < 0.05). Moreover, the OF group had higher mRNA concentrations of hepatic lipase, fatty acid transporters, and several genes involved in fatty acid oxidation in the liver than the FF group (P < 0.05). The present findings suggest that a dietary oxidized fat lowers the concentration of triacylglycerols in the milk by a reduced uptake of fatty acids from triacylglycerol rich-lipoproteins and NEFA into the mammary gland. The study, moreover, indicates that an oxidized fat impairs normal metabolic adaptations during lactation, which promote the utilization of metabolic substrates by the mammary gland for the synthesis of milk.