Dietary (n-3) Fatty Acids and Brain Development1

Effects of a marine oil-based n-3 LCPUFA supplement (mLCPUFA) fed from weaning until the end of the next lactation to sows with a predicted low litter birth weight (LBW) phenotype on growth performance and carcass quality of litters born to these sows were studied, based on the hypothesis that LBW litters would benefit most from mLCPUFA supplementation. Sows were allocated to be fed either standard corn/soybean meal-based gestation and lactation diets (CON), or the same diets enriched with 0.5% of the mLCPUFA supplement at the expense of corn. The growth performance from birth until slaughter of the litters with the lowest average birth weight in each treatment (n = 24 per treatment) is reported in this paper. At weaning, each litter was split between two nursery pens with three to six pigs per pen. At the end of the 5-week nursery period, two barrows and two gilts from each litter that had individual birth weights closest to their litter average birth weight, were moved to experimental grow-finish pens (barn A), where they were housed as two pigs per pen, sorted by sex within litter. Remaining pigs in each litter were moved to another grow-finish barn (barn B) and kept in mixed-sex pens of up to 10 littermates. After 8 weeks, one of the two pigs in each pen in barn A was relocated to the pens holding their respective littermates in barn B. The remaining barrows and gilts were individually housed in the pens in barn A until slaughter. Maternal mLCPUFA supplementation increased docosahexaenoic acid (DHA) concentration in the brain, liver and Semitendinosus muscle of stillborn pigs ( P < 0.01), did not affect eicosapentaenoic acid and DHA concentrations in sow serum at the end of lactation, and did not affect average daily gain, average daily feed intake or feed utilization efficiency of the offspring. BW was higher ( P < 0.01) in the second half of the grow-finish phase in pigs from mLCPUFA sows compared with controls in barn A, where space and competition for feed was minimal, but not barn B. Carcass quality was not affected by treatment for pigs from barn A, but maternal mLCPUFA supplementation negatively affected carcass quality in pigs from barn B. Collectively, these results suggest that nutritional supplementation of sows can have lasting effects on litter development, but that feeding mLCPUFA to sows during gestation and lactation was not effective in improving growth rates or carcass quality of LBW litters.

Section: Discussionsupporting

confidence: 90%

Effects of dietary enrichment with a marine oil-based n-3 LCPUFA supplement in sows with predicted birth weight phenotypes on growth performance and carcass quality of offspring

Smit

Spencer

Patterson

et al. 2015

“…Finally, n-3 LCPUFA can influence postnatal growth rate and survival through a change in piglet behaviour. DHA is important for brain development (Innis, 2007) and in central dopamine metabolism (Ng and Innis, 2003), which in turn affects feeding behaviour (McEntee and Crook, 1991). Rooke et al (2001a) showed that inclusion of salmon oil (rich in n-3 LCPUFA) in the sow's diet decreased pre-weaning mortality from 11.7% to 10.2%, mainly because of a reduction in piglets crushed by the sow.…”

Section: Discussionmentioning

confidence: 99%

Responses to n-3 fatty acid (LCPUFA) supplementation of gestating gilts, and lactating and weaned sows

Smit

Patterson

Webel

et al. 2013

Feeding n-3 long-chain polyunsaturated fatty acids (LCPUFA) to gilts or sows has shown different responses to litter growth, pre-weaning mortality and subsequent reproductive performance of the sow. Two hypotheses were tested: (1) that feeding a marine oil-based supplement rich in protected n-3 LCPUFAs to gilts in established gestation would improve the growth performance of their litters; and (2) that continued feeding of the supplement during lactation and after weaning would offset the negative effects of lactational catabolism induced, using an established experimental model involving feed restriction of lactating primiparous sows. A total of 117 primiparous sows were pair-matched at day 60 of gestation by weight, and when possible, litter of origin, and were allocated to be either control sows (CON) fed standard gestation and lactation diets, or treated sows (LCPUFA) fed the standard diets supplemented with 84 g/day of a n-3 LCPUFA rich supplement, from day 60 of first gestation, through a 21-day lactation, and until euthanasia at day 30 of their second gestation. All sows were feed restricted during the last 7 days of lactation to induce catabolism, providing a background challenge against which to determine beneficial effects of n-3 LCPUFA supplementation on subsequent reproduction. In the absence of an effect on litter size or birth weight, n-3 LCPUFA tended to improve piglet BW gain from birth until 34 days after weaning ( P 5 0.06), while increasing pre-weaning mortality ( P 5 0.05). It did not affect energy utilization by the sow during lactation, thus not improving the catabolic state of the sows. Supplementation from weaning until day 30 of second gestation did not have an effect on embryonic weight, ovulation rate or early embryonic survival, but did increase corpora lutea (CL) weight ( P 5 0.001). Eicosapentaenoic acid and docosahexaenoic acid (DHA) levels were increased in sow serum and CL ( P , 0.001), whereas only DHA levels increased in embryos ( P , 0.01). In conclusion, feeding n-3 LCPUFA to gilts tended to improve litter growth, but did not have an effect on overall subsequent reproductive performance.

“…Arachidonic acid (ARA; c20:4 n-6), eicosapentaenoic acid (EPA; c20:5 n-3) and docosahexaenoic acid (DHA; c22:6 n-3) are long-chain polyunsaturated fatty acids (LC-PUFA) and well known to play important regulatory functions in the immune, nervous and cardiovascular system (Innis, 2007;Calder, 2009;Calder and Yaqoob, 2009;Russo, 2009). The n-6 LC-PUFA can be synthesized from linoleic acid (LA; c18:2 n-6) and those of the n-3 family from a-linolenic acid (ALA; c18:3 n-3).…”

Section: Introductionmentioning

confidence: 99%

“…Changes in brain DHA concentrations have been demonstrated to be positively correlated with cognitive development (Innis, 2007). In addition, the dietary supplementation of DHA could improve the cognitive dysfunction due to aging (McCann and Ames, 2005;Cole and Frautschy, 2006).…”

Section: Introductionmentioning

confidence: 99%

Linoleic and α-linolenic acid as precursor and inhibitor for the synthesis of long-chain polyunsaturated fatty acids in liver and brain of growing pigs

Smink

Gerrits

Gloaguen

et al. 2012

Studies suggested that in human adults, linoleic acid (LA) inhibits the biosynthesis of n-3 long-chain polyunsaturated fatty acids (LC-PUFA), but their effects in growing subjects are largely unknown. We used growing pigs as a model to investigate whether high LA intake affects the conversion of n-3 LC-PUFA by determining fatty acid composition and mRNA levels of D5-and D6 desaturase and elongase 2 and -5 in liver and brain. In a 2 3 2 factorial arrangement, 32 gilts from eight litters were assigned to one of the four dietary treatments, varying in LA and a-linolenic acid (ALA) intakes. Low ALA and LA intakes were 0.15 and 1.31, and high ALA and LA intakes were 1.48 and 2.65 g/kg BW 0.75 per day, respectively. LA intake increased arachidonic acid (ARA) in liver. ALA intake increased eicosapentaenoic acid (EPA) concentrations, but decreased docosahexaenoic acid (DHA) (all P , 0.01) in liver. Competition between the n-3 and n-6 LC-PUFA biosynthetic pathways was evidenced by reductions of ARA (.40%) at high ALA intakes. Concentration of EPA (.35%) and DHA (.20%) was decreased by high LA intake (all P , 0.001). Liver mRNA levels of D5-and D6 desaturase were increased by LA, and that of elongase 2 by both ALA and LA intakes. In contrast, brain DHA was virtually unaffected by dietary LA and ALA. Generally, dietary LA inhibited the biosynthesis of n-3 LC-PUFA in liver. ALA strongly affects the conversion of both hepatic n-3 and n-6 LC-PUFA. DHA levels in brain were irresponsive to these diets. Apart from D6 desaturase, elongase 2 may be a rate-limiting enzyme in the formation of DHA.