supplementation and so the control diet has been balanced for nitrogen content by the addition of alanine. This study was designed to look at the effects of global protein supplementation and so sows were fed 16.3 percent protein as opposed to the control diet which contained 12.3 percent protein. Therefore, nitrogen content is clearly increased in the supplemented diet. In addition, as with fat supplementation, not all macronutrient components could stay the same to maintain energy content and health of the sow. As a result, protein supplemented sows received 1.2 percent more fat and 1.4 percent less fibre than those fed the control diet and this may influence postnatal mortality.
It is also important to consider the differences in the time course for protein supplementation between these experiments. This is the only study to investigate the effects of supplementation throughout the majority of the gestational period. In addition, the only other study in pigs, which supplemented arginine from the first day of gestation, produced negative effects, shown by a reduction in litter size at 25 days when pregnancy was terminated (Li et al., 2010). Therefore, it may be, the long-time period of protein supplementation, particularly early in gestation, the increased protein or fat content, or the reduction in fibre content which causes the high piglet mortality rates seen in this study.
3.4.3 Conclusions
In conclusion, this study has demonstrated that fat supplementation throughout pregnancy, reduces maternal glucose tolerance towards term and decreases the survival rate of piglets after birth, possibly due to the development of hypoglycaemia in these offspring. Furthermore, supplementing the maternal diet with protein also increased the incidence of postnatal mortality. These findings may have consequences for the pig industry where reducing piglet mortality is of key economical importance and where fat and protein supplementation were previously considered to be beneficial practice (Pettigrew, 1981, Wu et al., 2010). In addition, glucose intolerance in the mother is thought to be a risk factor for development of metabolic disease in the offspring (Chapter 1.3.1) (Boney et al., 2005, Franks et al., 2006), and so the aim of next chapter is to follow up the effects of maternal fat supplementation by observing the outcomes of the offspring.
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Chapter 4 - The effect of maternal fat supplementation
on offspring development
4.1 Introduction
The consequences of supplementing the pig diet with fat during pregnancy on the programming of piglet development have thus far not been investigated. Studies have instead focussed on changing the fatty acid profile of the offspring by altering the polyunsaturated fatty acid content of the maternal diet (Chapter 1; Section 1.6.3.2.1) (Rooke et al., 1998, Rooke et al., 2001a, Rooke et al., 2001b). Or, on the supposed beneficial effects of fat supplementation on increasing offspring survival rate, which is of key economical importance in the pig industry (Chapter 3) (Seerley et al., 1974, Pettigrew, 1981, Boyd et al., 1978, Seerley et al., 1981, Azain, 1993). Despite this, the present study has previously reported detrimental effects of fat supplementation during pregnancy on maternal glucose tolerance and neonatal mortality (Chapter 3). Briefly, fat supplementation caused a reduction in maternal glucose tolerance at term, perhaps leading to hypoglycaemia in the piglets, providing the link to the increase in neonatal mortality that was observed within the first 24 hours after birth.
4.1.1 Maternal fat supplementation and programming of offspring metabolism
It has been well documented that offspring born to mothers who develop gestational diabetes, often due to intake of a high fat diet and/or maternal obesity, have increased risk of developing metabolic complications such as obesity and impaired glucose tolerance at an early age (Chapter 1; Section 1.3.2) (Boney et al., 2005, Franks et al., 2006). However, these offspring are usually of very high-birth weight due to fetal macrosomia caused by hyperglycaemia in the mother (Jovanovic and Pettitt, 2001, Schmidt et al., 2001, Franks et al., 2006).
In addition, investigations into high-fat feeding during pregnancy in rats have demonstrated similar detrimental effects on the metabolism of the offspring, despite there being no effect on birth weight (Chapter 1; Section 1.3.2) (Khan et al., 2003, Khan et al., 2005, Taylor et al., 2005). These findings are similar to those seen in the offspring of maternal protein restricted or nutrient restricted rats and sheep (Chapter 1; Section
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1.2)(Langley-Evans et al., 1996, Langley-Evans et al., 1998, Bertram et al., 2001, Whorwood et al., 2001).Due to the similarities seen between the high-fat and low-protein models of developmental programming, which leads to a phenotype with features of the metabolic syndrome, it has been proposed that a there is a common underlying mechanism such as perturbed glucocorticoid (GC) activity and insulin resistance (Khan et al., 2003, Taylor et al., 2003). This is supported by the elevation in plasma corticosterone seen at 20 days of gestation in fat supplemented dams (Taylor et al., 2003). Furthermore, feeding a high- fat diet to non-pregnant rats leads to both basal and stress-induced activation of the hypothalamic pituitary adrenal (HPA) axis, thus elevating adrenal GC production (Pascoe et al., 1990, Tannenbaum et al., 1997). However, male offspring of coconut oil-fed dams, which is high in saturated fatty acids (Chapter 1; Section 1.6.1.3), show increased blood pressure but do not show evidence of altered HPA axis activation in the hypothalamus or liver (Langley-Evans, 1996), suggesting perhaps that another mechanism may be involved.
4.1.2 Birth weight and offspring development
Pigs exhibit the most severe naturally occurring intrauterine growth retardation (IUGR) of all livestock species (Wu et al., 2006). IUGR or ‘runt’ piglets are defined as weighing 1 kg or less, and less than 65 percent of the birth weight of the larger litter-mate controls (Hegarty and Allen, 1978). Studies have shown that the within-litter weight distribution seen at birth is already established by the end of the embryonic stage of pregnancy (day 35) (Van der Lende et al., 1990, Finch et al., 2002).
As previously reported in this thesis, low birth weight piglets have a higher incidence of mortality (Chapter 3). Those small piglets that do survive will grow more slowly than their heavier litter mates, often due to their inability to compete with larger piglets (McGlone et al., 2001, Gondret et al., 2006). Thus it is normal husbandry practice, as demonstrated in this study, to separate litters after weaning and group them according to birth weight (McGlone et al., 2001). It is then possible to feed these animals appropriately so that they achieve their target weight and body composition in the shortest time possible (McGlone et al., 2001). However, keeping pigs in groups based on body weight decreases their ability to