Nutritional regulation of fetal growth and implications for productive life in ruminants

Abstract

The maternal nutritional and metabolic environment is critical in determining not only the reproductive success but also the long-term health and viability of the offspring. Changes in maternal diet at defined stages of gestation coincident with different stages of development can have pronounced effects on organ and tissue function in later life. This includes adipose tissue for which differential effects are observed between brown and white adipose tissues. One early, critical window of organ development in the ruminant relates to the period covering uterine attachment, or implantation, and rapid placental growth. During this period, there is pronounced cell division within developing organelles in many fetal tissues, leading to their structural development. In sheep, a 50% global reduction in caloric intake over this specific period profoundly affects placental growth and morphology, resulting in reduced placentome weight. This occurs in conjunction with a lower capacity to inactivate maternal cortisol through the enzyme 11b-hydroxysteroid dehydrogenase type 2 in response to a decrease in maternal plasma cortisol in early gestation. The birth weight of the offspring is, however, unaffected by this dietary manipulation and, although they possess more fat, this adaptation does not persist into adulthood when they become equally obese as those born to control fed mothers. Subsequently, after birth, further changes in fat development occur which impact on both glucocorticoid action and inflammatory responses. These adaptations can include changes in the relative populations of both brown and white adipocytes for which prolactin acting through its receptor appears to have a prominent role. Earlier when in utero nutrient restricted (i.e. between earlyto-mid gestation) offspring are exposed to an obesogenic postnatal environment; they exhibit an exaggerated insulin response, which is accompanied by a range of amplified and thus, adverse, physiological or metabolic responses to obesity. These types of adaptations are in marked contrast to the effect of late gestational nutrient restriction, which results in reduced fat mass at birth. As young adults, however, fat mass is increased and, although basal insulin is unaffected, these offspring are insulin resistant. In conclusion, changes in nutrient supply to either the mother and/or her fetus can have profound effects on a range of metabolically important tissues. These have the potential to either exacerbate, or protect from, the adverse effects of later obesity and accompanying complications in the resulting offspring.

An evolving scientific basis for the prevention and treatment of pediatric obesity

“…54 These processes can be manipulated by environmental challenges to the fetus and/or neonate, which offer the potential to promote BAT function in the newborn as well as into later life. 55 The potential influence of maternal body weight and glycemic status on BAT remains to be described, 56 as does the substantial change in dietary and activity patterns over the past two decades, coincident with the obesity epidemic. 57 …”

Enhanced or Reduced Fetal Growth Induced by Embryo Transfer into Smaller or Larger Breeds Alters Post-Natal Growth and Metabolism in Pre-Weaning Horses

“…In production animals, the Developmental Origins of Health and Disease (DOHaD) are of interest for their role in programming characteristics linked to commercial benefits, such as offspring survival, growth rate, body composition, fleece, milk and meat qualities and reproductive function [16], [17]. Alterations in the fetal environment could also limit future health and athletic performance of the horse [18].…”

The Ontogeny of Brown Adipose Tissue

“…The mismatch is important because the metabolic environment in which twins grow and develop is very different from that experienced by singletons (117), and this can have a pronounced effect on later fat deposition in sheep (46). In studies that have been undertaken in sheep where fetal number is fixed between groups, the timing of any maternal intervention has been shown to be critical in determining the outcome in the newborn (123). This is not unexpected in view of the different stages of adipose tissue development targeted in different studies (see Figure 7).…”