Supplementing sow diets with palm oil during late gestation and lactation: effects on milk production, sow hormonal profiles and growth and development of her offspring.

The supplementing of sow diets with lipids during pregnancy and lactation has been shown to reduce sow condition loss and improve piglet performance. The aim of this study was to determine the effects of supplemental palm oil (PO) on sow performance, plasma metabolites and hormones, milk profiles and pre-weaning piglet development. A commercial sow ration (C) or an experimental diet supplemented with 10% extra energy in the form of PO, were provided from day 90 of gestation until weaning (24 to 28 days postpartum) in two groups of eight multiparous sows. Gestation length of PO sows increased by 1 day (P<0.05). Maternal BW changes were similar throughout the trial, but loss of backfat during lactation was reduced in PO animals (C: -3.6±0.8 mm; PO: -0.1±0.8 mm; P<0.01). Milk fat was increased by PO supplementation (C day 3: 8.0±0.3% fat; PO day 3: 9.1±0.3% fat; C day 7: 7.8±0.5% fat; PO day 7: 9.9±0.5% fat; P<0.05) and hence milk energy yield of PO sows was also elevated (P<0.05). The proportion of saturated fatty acids was greater in colostrum from PO sows (C: 29.19±0.31 g/100 g of fat; PO: 30.77±0.36 g/100 g of fat; P<0.01). Blood samples taken on 105 days of gestation, within 24 h of farrowing, day 7 of lactation and at weaning (28±3 days post-farrowing) showed there were no differences in plasma concentrations of triacylglycerol, non-esterified fatty acids, insulin or IGF-1 throughout the trial. However, circulating plasma concentrations of both glucose and leptin were elevated during lactation in PO sows (P<0.05 and P<0.005, respectively) and thyroxine was greater at weaning in PO sows (P<0.05). Piglet weight and body composition were similar at birth, as were piglet growth rates throughout the pre-weaning period. A period of 7 days after birth, C piglets contained more body fat, as indicated by their lower fat-free mass per kg (C: 66.4±0.8 arbitrary units/kg; PO: 69.7±0.8 arbitrary unit/kg; P<0.01), but by day 14 of life this situation was reversed (C: 65.8±0.6 arbitrary units/kg; PO: 63.6±0.6 arbitrary units/kg; P<0.05). Following weaning, PO sows exhibited an increased ratio of male to female offspring at their subsequent farrowing (C: 1.0±0.3; PO: 2.2±0.2; P<0.05). We conclude that supplementation of sow diets with PO during late gestation and lactation appears to increase sow milk fat content and hence energy supply to piglets. Furthermore, elevated glucose concentrations in the sow during lactation may be suggestive of impaired glucose homoeostasis.

Influence of fatty acid profile of total parenteral nutrition emulsions on the fatty acid composition of different tissues of piglets.

Total parenteral nutrition (TPN) studies in human babies of very-low-birth-weight suggest that the lipid emulsions currently available are not optimum for neonatal nutrition. Since fatty acid metabolism in human and pigs is very similar, the present study examines how lipid emulsions used in clinical TPN (i.e. ClinOleic, Intralipid, Lipofundin or Omegaven), with different fatty acid compositions, administered to neonatal piglets for 7 days, influenced their tissue fatty acid composition as compared to those enterally fed with a sow milk replacer. A positive linear relationship was found between the proportion of all individual fatty acids in the lipid emulsions or in the milk replacer versus those in plasma, skeletal muscle, subcutaneous fat, liver, heart, pancreas, stomach or intestine total lipids or in brain phospholipids, the latter showing the lowest correlation coefficient. With the exception of brain, the proportion of either oleic acid or alpha-linolenic acid in the individual tissues was correlated with those present in the corresponding lipid emulsion or milk replacer, whereas the proportion of linoleic acid correlated significantly with all the tissues studied. With the exception of brain phospholipids, both eicosapentaenoic and docosahexaenoic acids were higher in the tissues of piglets receiving Omegaven than in all other groups. In conclusion, with the exception of the brain, fatty acid composition of plasma and different tissues in piglets are strongly influenced by the fatty acid profile of TPN emulsions. Fatty acid composition of brain phospholipids are, however, much less influenced by dietary composition, indicating an active and efficient metabolism that ensures its appropriate composition at this key stage of development.

Maternal lipid metabolism and placental lipid transfer.

During early pregnancy, long-chain polyunsaturated fatty acids (LC-PUFA) may accumulate in maternal fat depots and become available for placental transfer during late pregnancy, when the fetal growth rate is maximal and fetal requirements for LC-PUFAs are greatly enhanced. During this late part of gestation, enhanced lipolytic activity in adipose tissue contributes to the development of maternal hyperlipidaemia; there is an increase in plasma triacylglycerol concentrations, with smaller rises in phospholipid and cholesterol concentrations. Besides the increase in plasma very-low-density lipoprotein, there is a proportional enrichment of triacylglycerols in both low-density lipoproteins and high-density lipoproteins. These lipoproteins transport LC-PUFA in the maternal circulation. The presence of lipoprotein receptors in the placenta allows their placental uptake, where they are hydrolysed by lipoprotein lipase, phospholipase A(2) and intracellular lipase. The fatty acids that are released can be metabolized and diffuse into the fetal plasma. Although present in smaller proportions, maternal plasma non-esterified fatty acids are also a source of LC-PUFA for the fetus, their placental transfer being facilitated by the presence of a membrane fatty acid-binding protein. There is very little placental transfer of glycerol, whereas the transfer of ketone bodies may become quantitatively important under conditions of maternal hyperketonaemia, such as during fasting, a high-fat diet or diabetes. The demands for cholesterol in the fetus are high, but whereas maternal cholesterol substantially contributes to fetal cholesterol during early pregnancy, fetal cholesterol biosynthesis rather than cholesterol transfer from maternal lipoproteins seems to be the main mechanism for satisfying fetal requirements during late pregnancy.

Lipid metabolism during the perinatal phase, and its implications on postnatal development.

During pregnancy, lipid metabolism plays a major role to warrant the availability of substrates to the foetus. By using different experimental designs in the rat we have been able to answer several questions that were open about the short- and long-term effects of alterations of lipid metabolism during the perinatal stage. The first one was to demonstrate the importance of maternal body fat depot accumulation during the first half of pregnancy. We found that conditions like undernutrition circumscribed to this specific period when foetal growth is still small, that impede such fat accumulation not only restrain intrauterine development but also have long-term consequences, as shown by an impaired glucose tolerance when adults. Secondly, undernutrition during suckling has major long-term effect decreasing body weight, even though food intake was kept normal from the weaning period. Present findings also show that a diet rich in omega-3 fatty acids during pregnancy and lactation has negative effects on offspring development, but cross fostered experiments showed that the effect was a consequence of the intake of these fatty acids during the lactation period rather than during pregnancy. Pups from dams that were fed a fish oil-rich diet during pregnancy and lactation were found to have altered glucose/insulin relationship at the age of 10 weeks. Since a omega-3 fatty acid-rich diet decreases milk yield during lactation, additional experiments were carried out to determine whether decreased food intake, altered dietary fatty acid composition, or both were responsible for the long-term effects on the glucose/insulin axis. Results show that the decreased food intake caused by a omega-3 fatty acid-rich diet rather than the change in milk composition during suckling was responsible for the reduced pancreatic glucose responsiveness to insulin release at 16 weeks of age. In conclusion, present findings indicate that impaired maternal fat accumulation during early pregnancy and food intake during lactation, rather than a difference in dietary fatty acid composition have a greater influence on postnatal development and affect glucose/insulin relationships in adult rats.

Experimental models for studying perinatal lipid metabolism. Long-term effects of perinatal undernutrition.

By using different experimental designs in the rat we have been able to answer several unanswered questions on the short- and long-term effects of alterations of lipid metabolism during the perinatal stage. The first was to demonstrate the importance of maternal body fat accumulation during the first half of pregnancy, since undernutrition in this critical period when fetal growth is slow, impedes fat depot accumulation and not only restrains intrauterine development but has long-term consequences, as shown by an impaired glucose tolerance when adults. Secondly, undernutrition during suckling has major long-term effect of decreasing body weight, even though food intake is kept normal from the weaning period. Our findings also show that a diet rich in n-3 fatty acids during pregnancy and lactation has adverse effects on offspring development, but cross fostered experiments showed that this effect was a consequence of the intake of these fatty acids during the lactation period rather than during pregnancy. Pups from dams that were fed a fish oil-rich diet during pregnancy and lactation were found to have altered glucose/insulin relationship at the age of 10 weeks. Since a n-3 fatty acid-rich diet decreases milk yield during lactation, additional experiments were carried out to determine whether decreased food intake or altered dietary fatty acid composition, or both, were responsible for the long-term effects on the glucose/insulin axis. Results show that the decreased food intake caused by a n-3 fatty acid-rich diet rather than the change in milk composition during suckling was responsible for the reduced pancreatic glucose responsiveness to insulin release at 16 weeks of age. In conclusion, present findings indicate that impaired maternal fat accumulation during early pregnancy and food intake during lactation, rather than a difference in dietary fatty acid composition, have major effects on postnatal development and affect glucose/insulin relationships in adult rats.

Relationship between plasma fatty acid profile and antioxidant vitamins during normal pregnancy.

OBJECTIVE: To study the changes of plasma fatty acids and lipophilic vitamins during normal pregnancy. DESIGN: Plasma fatty acid profile and the concentration of carotenoids, tocopherols and retinol were measured in healthy women at the first and third trimesters of pregnancy, at delivery, and in cord blood plasma. RESULTS: Maternal plasma cholesterol and triglycerides increased from the first to the third trimester of gestation, while free fatty acids progressively increased from the first trimester through the third trimester to delivery, suggesting an enhanced lipolytic activity. Plasma levels of alpha- and gamma-tocopherols, lycopene and beta-carotene also progressively increased with gestation, but values in cord blood plasma were lower than in mothers at delivery. Retinol levels declined with gestational time and values in cord blood plasma were even lower. The proportion of total saturated fatty acids increased with gestation, and it further increased in cord blood plasma. Total n-9 fatty acids remained stable throughout pregnancy, and slightly declined in cord blood plasma, the change mainly corresponding to oleic acid. Total n-6 fatty acids declined with gestation and further decreased in cord blood plasma, and a similar trend was found for linoleic acid. However, arachidonic acid declined in women at the third trimester and at delivery as compared to the first trimester, but was enhanced in cord blood plasma. The proportion of total n-3 fatty acids remained stable throughout pregnancy at the expense of decreased alpha-linolenic acid at delivery but enhanced eicosapentaenoic acid, with small changes in docosahexaenoic acid. The proportion of these n-3 fatty acids was similar in cord blood plasma and maternal plasma at delivery. CONCLUSIONS: Owing to the different placental transfer mechanisms and fetal capability to metabolize some of the transferred fatty acids and lipophilic vitamins, the fetus preserves the essential compounds to assure their appropriate availability to sustain its normal development and to protect itself from the oxidative stress of extrauterine life. SPONSORSHIP: The studies reported herein have been carried out with financial support from the Commission of the European Communities, specific RTD programme 'Quality of Life and Management of Living Resources', QLK1-2001-00138 'Influence of Dietary Fatty Acids on the Pathophysiology of Intrauterine Foetal Growth and Neonatal Development' (PeriLip). It does not necessarily reflect its views and in no way anticipates the Commission's future policy in this area.

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.

Changes in dietary fatty acids modify the decreased lipolytic beta3-adrenergic response to hyperinsulinemia in adipocytes from pregnant and nonpregnant rats.

The effect of dietary olive oil and fish oil on the lipolytic dose-response of the beta3-adrenergic agonists, epinephrine, isoproterenol, BRL-37344, and CGP-12177, in adipocytes was studied in pregnant and virgin rats either untreated or under hyperinsulinemic-euglycemic conditions. Rats were fed a semisynthetic diet containing 5% of either olive oil or fish oil and studied at day 20 of treatment and/or gestation. Plasma glucose was lower and plasma insulin, triglycerides, and free fatty acids (FFAs) were higher in pregnant versus virgin rats, and the insulin sensitivity index was lower in the former. Lumbar adipose tissue phospholipid fatty acids showed a significantly higher monounsaturated fatty acid and a lower (n - 3) fatty acid content in rats fed the olive oil diet versus the fish oil diet. The lipolytic dose-response curve of either adrenergic agent was always lower in adipocytes from untreated pregnant rats versus virgin rats, and whereas the hyperinsulinemic-euglycemic clamp decreased these responses in adipocytes from virgin rats fed the olive oil diet only, adipocytes from pregnant rats always showed a decreased dose-response lipolytic curve. Thus, the lipolytic responsiveness of beta3-adrenoceptor (beta3-AR) agonists by adipocytes is impaired in cells from rats made hyperinsulinemic chronically by pregnancy or acutely by the hyperinsulinemic-euglycemic clamp, but such response to the acute condition disappears when the adipocyte phospholipid composition is modified by changes in dietary fatty acids.

Lipid metabolism in the fetus and the newborn.

During late gestation, although maternal adipose tissue lipolytic activity becomes enhanced, lipolytic products cross the placenta with difficulty. Under fasting conditions, free fatty acids (FFA) are used for ketogenesis by the mother, and ketone bodies are used as fuels and lipogenic substrates by the fetus. Maternal glycerol is preferentially used for glucose synthesis, saving other gluconeogenic substrates, like amino acids, for fetal growth. Placental transfer of triglycerides is null, but essential fatty acids derived from maternal diet, which are transported as triglycerides in lipoproteins, become available to the fetus owing to the presence of both lipoprotein receptors and lipase activities in the placenta. Diabetes in pregnancy promotes lipid transfer to the fetus by increasing the maternal-fetal gradient, which may contribute to an increase in body fat mass in newborns of diabetic women. Deposition of fat stores in the fetus is very low in the rat but high in humans, where body fat accretion occurs essentially during the last trimester of intra-uterine life. This is sustained by the intense placental transfer of glucose and by its use as a lipogenic substrate, as well as by the placental transfer of fatty acids and to their low oxidation activity. During the perinatal period an active ketonemia develops, which is maintained in the suckling newborn by several factors: (i) the high-fat and low-carbohydrate content in milk, (ii) the enhanced lipolytic activity occurring during the first few hours of life, and (iii) both the uptake of circulating triglycerides by the liver due to the induction of lipoprotein lipase (LPL) activity in this organ, and the presence of ketogenic activity in the intestinal mucose. Changes in LPL activity, lipogenesis and lipolysis contribute to the sequential steps of adipocyte hyperplasia and hypertrophia occurring during the extra-uterine white adipose tissue development in rat, and this may be used as a model to extrapolate the intra-uterine adipose tissue development in other species, including humans.

[Effect of variation of the dietary fat content in rats during gestation on the fatty acid profile in maternal and fetal plasma]. / Efecto de variaciones en el contenido graso de la dieta de la rata durante la gestación sobre el perfil de ácidos grasos en plasma materno y fetal.

With the aim of knowing how changes in the fatty acid composition of the diet affect the fatty acid profile in the plasma during gestation, and the repercussions on the fetuses, in the present study we have administered semi-synthetic diets containing palm oil, olive oil, sunflower seed oil, or fish oils as the sole non-vitamin fat component to pregnant rats. The animals were studied on day 20 of the gestation and after being fed the corresponding diet. As was expected, in the palm oil diet the most abundant fatty acids were saturated, in the olive oil diet is was oleic acid, in the sunflower seed and fish oil diets while the linoleic acid was considerably higher in the sunflower seed oil diet is was linoleic acid, and the fish oil diet it was the only one to show appreciable amounts of eicosepentaenoic and docosehexacnoic acids. In turn, none of the diets contained arachidonic acid. In the plasma of the mothers the proportion of saturated fatty acids was similar in all the groups, the oleic acid was higher in the palm and olive oil diets than in the sunflower seed oil diet. In turn, although a certain proportion of arachidonic acid was found in all the groups, its proportion was lowest in the group of rats with the fish oil diet and these same fish oil rats showed a higher proportion of eicosepentaenoic and docosehexaenoic acids than the other groups did. The profile of the saturated and monounsaturated fatty acids in the plasma of the fetuses differed from that of the mothers, and the changes in the rest of the fatty acids studied were similar to those of the mother with there being a linear and significant correlation of the polyunsaturated acids values between the maternal and the fetal plasma. The fetuses of rats fed with the first dietshowed and intense deficiency of arachidonic acid, and this could have negative consequences for the post-natal development.