Abstract
Modifications in maternal nutrition during pregnancy can significantly disrupt fetal growth and subsequent post-natal health and survival. This study investigated the effects of undernutrition on fetal growth and the potential mechanisms involved. Tissue from pregnant ewes (n=27) was investigated on days 45, 90 and 135 of gestation (term = approximately 150 days). The thoracic girth (P<0.05) was greater in fetuses from nutrient restricted ewes on day 45 and there was also a trend towards an increased gut weight (P<0.08). By day 90, the fetal brain and thymus weight were lighter in underfed than in well-fed animals whilst the weight of the fetal ovaries was heavier (P<0.05). On day 135 the fetal heart, pancreas, thymus, gut and kidney weights were lighter in undernourished ewes (P<0.05). When expressed as a percentage of fetal body weight, significance was retained in the heart, pancreas and thymus (P<0.05). Bone growth was also affected. At day 90 the fetal femur and metatarsal were longer in underfed mothers (P<0.05). In contrast, the fetal humerus and scapula were shorter in underfed than in well-fed animals on day 135 (P<0.05) when the weight of the semitendinosus muscle (P<0.05) was also reduced. The fall in fetal glucose (P<0.1), insulin (P<0.01) and IGF-I (P<0.01) levels in underfed ewes on day 135 may have compromised fetal growth. Fetal plasma IGF binding protein-2 also increased between days 90 and 135 in underfed ewes (P<0.03), whilst levels were unaltered in well-fed animals. Although maternal and fetal plasma IGF-I levels increased with gestation (P<0.01) and the placentome morphology altered in all ewes (P<0.05), the fall in placental mass (P<0.05), amniotic and allantoic glucose concentrations (P<0.05) and maternal plasma glucose and insulin levels (P<0.05) in underfed ewes in late gestation may have compromised fetal substrate delivery. These perturbations in fetal development may have significant implications on adult health and carcass conformation, raising important health and economic issues in medical and agricultural sectors.
Highlights
Perturbations in maternal nutrition during pregnancy may ‘programme’ permanent structural and physiological modifications in fetal development. Whilst these adaptations may occur to sustain fetal development in utero, in extrauterine life they are believed to have important pathological implications. These include reduced neonatal viability (Alexander 1974), whilst in adult life an increased predisposition to cardiovascular, metabolic and endocrine disease has been observed in humans, with poor wool and carcass quality arising in sheep
Substrates such as glucose can promote fetal growth directly by providing energy and/or building blocks required for tissue growth (Fowden 1997)
The fetal origins hypothesis suggests that in humans poor nutrition in utero is associated with an increased predisposition to major illnesses in later life, in particular cardiovascular disease and non-insulin dependent diabetes
Summary
Perturbations in maternal nutrition during pregnancy may ‘programme’ permanent structural and physiological modifications in fetal development (review: Barker 1995, Robinson et al 1999, Symonds et al 2001). Whilst these adaptations may occur to sustain fetal development in utero, in extrauterine life they are believed to have important pathological implications (review: Barker & Clark 1997, McMillen et al 2001) At birth, these include reduced neonatal viability (Alexander 1974), whilst in adult life an increased predisposition to cardiovascular, metabolic and endocrine disease has been observed in humans (review: Barker & Clark 1997, Godfrey 1998), with poor wool and carcass quality arising in sheep (review: Black 1983, Bell 1992, Kelly et al 1996). Fetal growth depends upon the acquisition of substrate from diverse sites including: (i) the maternal compartment, via the placenta, as products of digestion or mobilised body reserves (McCrabb et al 1992); (ii) the placental compartment (Chung et al 1998); (iii) amniotic fluid (Ross & Nijland 1998) or (iv) from endogenous reserves within the fetus itself (Fowden 1997). Other substrates act indirectly, regulating factors such as insulin to promote tissue accretion or insulin-like growth factor (IGF-I) to exert metabolic, mitogenic and differentiative activities (Fowden 1995, Harding & Johnston 1995)
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