Linseed oil in the maternal diet increases long chain- PUFA status of the foetus and the newborn

January 1, 2010 Human Health and Nutrition Data 0 Comments

Linseed oil in the maternal diet increases long chain- PUFA status of the foetus and the newborn

Year: 2010
Authors: de Quelen, F. Boudry, G. Mourot, J.
Publication Name: British Journal of Nutrition
Publication Details: doi:10.1017/S0007114510000772

Abstract:

Linseed oil, being rich in 18:3n-3, represents an alternative source of n-3 PUFA in the maternal diet. However, little is known about the effect of this oil on the long chain n-3 PUFA composition of offspring, which are required for normal growth and maturation of numerous organs. The main objective of the experiment was therefore to investigate fatty acid composition of tissues from sows at the end of gestation and from piglets during the first week of postnatal life in response to maternal dietary linseed oil intake. Sows received either a lard (LAR)-based diet or a linseed oil (LSO)-based diet during gestation and lactation. Fatty acid composition was evaluated in sow plasma, placenta and milk, and in different tissues of piglets on days 0, 3, 7, 21 and 32. The LSO diet increased the proportions of n-3 PUFA and especially 22:6n-3 in the placenta. The carcass of LSO piglets at birth contained greater proportions of 20:5n-3, 22:5n-3 and 22:6n-3. The LSO sow milk exhibited greater proportions of 18:3n-3 compared with the LAR sow milk. The piglets suckling LSO sows had greater proportions of 18:3n-3, 20:5n-3 and 22:5n-3 in plasma and carcass. The proportions of 22:5n-3 and 22:6n-3 were greater in the brain of LSO piglets than in that of LAR piglets during the suckling period. In conclusion, LSO in the maternal diet during gestation and lactation increases 22:6n-3 concentrations in the placenta and in the foetus carcass, and it maintains 22:6n-3 concentrations in the brain during the first week of postnatal life. (Author's abstract)
The PUFA composition of the maternal diet during gestation and lactation can affect the composition of the foetus and the neonate (through the maternal milk). An inadequate n-6 to n-3 PUFA ratio may lead to an imbalance in the concentrations of n-6 LC-PUFA and n-3 LC-PUFA, and it may have  consequences for the development of physiological functions. Many human and animal studies show that 18:3n-3 supplementation can increase LC-PUFA status in the newborn. The main objective of this experiment was to investigate, in sows and piglets, the effect of maternal LSO intake on the fatty acid composition of the sow plasma and placenta and on the fatty acid composition of different tissues of the newborn before any suckling. The effect of maternal LSO intake on the evolution of the fatty acid composition of sow milk and piglet tissues at different time points during the suckling period was also established. The results show high contents of n-3 LC-PUFA in the placenta suggesting that sows are capable of synthesising n-3 LC-PUFA from dietary 18:3n-3 during gestation, although the site of synthesis is not known.
LSO in the maternal diet increased LC-PUFA accumulation in the placenta. The fatty acid composition of piglet tissues before suckling was influenced by the maternal diet. At birth, the carcasses of piglets from the LSO sows had greater proportions of n-3 LC-PUFA than the carcasses of piglets from the LAR sows, whereas in the plasma, the proportions of 20:5n-3 and 22:6n-3, but not of 22:5n-3, were greater with the LSO diet. In the present study, sows were fed 42g/d of LSO, which increased the proportion of 20:5n-3 by 2�4 times and of 22:6n-3 by 1�7 times in the plasma of the LSO piglets compared with the LAR piglets at birth. In the present study, the milk of the LSO sows had greater proportions of 18:3n-3 compared with the other n-3 LC-PUFA. The maternal LSO diet influenced the fatty acid composition of piglet tissues during the postnatal life. Piglets suckling the LSO sows consumed high levels of 18:3n-3 through the milk. This resulted in the increased plasma and carcass proportions of 18:3n-3, 20:5n-3 and 22:5n-3, with the proportion of 18:3n-3 in the plasma and carcasses of LSO piglets increasing with time.  The evolution of fatty acid composition in piglet brain was different from that of fatty acid composition in piglet plasma and carcasses. Although not different during the first week after birth, the proportion of 22:5n-3 and 22:6n-3 were greater from day 7 in the brain of the LSO piglets than in that of the LAR piglets, with no difference for 18:3n-3 and 20:5n-3. The 22:6n-3 could, in part, be transported via the circulation from the carcass to the brain. In conclusion, LSO in the maternal diet during gestation and lactation increases LC-PUFA content in the placenta and 22:6n-3 deposition in the carcasses and brain of piglets at birth. Furthermore, this diet maintains the proportion of 22:6n-3 in the brain of the LSO piglets compared with the LAR piglets during the postnatal period. Further work is needed to understand the dietary regulation of fatty acid transporters in the placenta, and to explore the capacity of neonatal piglets to transform maternal 18:3n-3 in n-3 LC-PUFA, especially in the brain. (Editor's comments)



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