Dam-Foetus Interaction: History
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Dam-foetus interaction through the placenta guarantees the survival of the foetus.

  • calf immunology
  • colostrum
  • dam-foetus interaction
  • growth
  • gut health
  • puberty

1. Introduction

Development from conception to puberty progresses through well-regulated stages at molecular, cellular and animal level. For the neonate, passive transfer of immunity is a key primary defence mechanism against infections. Calf immunity, growth and puberty are critical factors influencing productivity of heifers. Some studies focused on these factors individually, rather than their integrations. Recently, considering the interactions between these vital physiological processes has become important to optimize calf survival. During gestation, the placenta supports foetal development and prepares it for extra-uterine survival [1]. After birth, colostrum transfers immune molecules [2][3] which, in case of failure, causes increased susceptibility to infections that lowers survival [4][5]. Colostrum also provides many growth factors such as insulin-like growth factor I (IGF-I) [6], a key factor regulating growth and immune response in calves [7].

Acquiring growth factors improves calf immunity because these factors modulate development and differentiation in-utero [8][9] as well as after birth. Colostrum stimulates gastrointestinal development and function through the absorption of growth factors and other immune components [10]. Therefore, good colostrum management is important to promote growth and daily weight gain [11][12] as well as facilitate early attainment of puberty.

A better understanding of the interrelationship of the factors involved in immune function, growth and reproduction is needed. The objective of this review is to discuss calf physiology and the interactions that enhance calf survival and to offer an insight into strategies adopted at these life stages to optimise production.

2. Dam-Foetus Interaction and Ante-Natal Development

Dam-foetus interaction through the placenta guarantees the survival of the foetus. During pregnancy, maternal metabolic adjustment to promote foetal development and growth occurs through two pathways: one represented by nutritional partitioning, and the other by increased placental development leading to improved nutrient transfer and hormonal production. Nutrient availability is also supported by appetite changes of the dam in order to support the growing foetus. It is thought that there are no negative effects of dietary protein content on any of the reproductive measures such as days to conception, calving interval [13]. However, diets containing balanced metabolizable energy and protein that satisfy both maintenance and growth requirements of the dam and conceptus growth are fundamental for optimal foetal development. Additionally, the placenta not only provides nutrients to the foetus, but it also regulates maternal cortisol levels that has a negative impact on foetal growth. Furthermore, these actions signal the placenta to alter foetal phenotype according to the current micro-uterine environment as an adaptive response (prenatal programming) [14]. In animal and biomedical science, there is growing evidence that foetal programming can alter postnatal development, growth, and disease susceptibility of the offspring [14]. Key times during which foetal programming can be altered are thought to be during placentation, immune system development and muscle and fat development.

2.1. Placentation

While most foetal growth occurs during late gestation [15], inadequate nutrition during early gestation can have profound effects on placental development, vascularization, and embryo organogenesis [16]. The placenta is a transient unique organ of pregnancy that provides an interface for metabolic exchange between the dam and the foetus [17]. It is a metabolically and immunologically active tissue that develops after maternal recognition of pregnancy in mammals [18], and it is fully developed by 40 days in cattle [17]. Placental surface growth, vascularisation and secretion of growth factors are maintained throughout gestation to meet increasing foetal demands. Thus, any nutrient restrictions during this phase can dramatically impair placentation and embryo development [19]. In fact, it was observed that nutrient restriction during early gestation, followed by adequate feeding during day 125 to 250 impaired placental angiogenesis and resulted in underdevelopment of placentomes [20]. Uteroplacental blood flow is central in programming foetal growth as it affects the transport of nutrients through the placenta. In fact, in large animal models it has been demonstrated that nutrients transport increases throughout gestation primarily because of increased uteroplacental blood flow rather than increased nutrient extraction from each unit of blood [21].

2.2. Immune System Development

The immune system of mammalian embryos starts developing early in gestation and continues to mature after birth [22][23]. Although the ruminant immune system forms during foetal development, the passive transfer of immunity depends mainly on quality and quantity of colostrum available and on the absorption capacity of the new-born [24][25][26][27]. However, research has demonstrated that the ability of the offspring to acquire immunoglobulins G (IgG) seems to be affected by the nutrition of the dam during late gestation [28]. In fact, a decrease in protein intake during the last trimester of gestation results in impaired serum IgG concentration in the calf. Furthermore, calves born to cows fed balanced diet, but fed colostrum from dams fed restricted diets have less serum IgG concentrations at 24 h of life than the calves receiving colostrum from well-nourished cows [28]. Nutrient-restricted cattle have decreased colostrum tri-iodothyronine concentration which plays an important role on IgG absorption at calf intestinal level [29][30].

2.3. Growth and Attainment of Puberty

Insulin growth factors (IGFs) influence maternal metabolism, thereby controlling nutrient availability for foetal growth. IGFs also regulate placental morphogenesis, substrate transport and hormone secretion. Increased IGF-I, secondary to maternal GH treatment in early pregnancy, increases maternal nutrient concentrations and sometimes increases foetal weight at the expense of maternal tissue mass [31]. The effects of the IGFs on foetal growth must occur indirectly either affecting maternal metabolism and nutrient partitioning, and/or placental development and function, since IGFs and GH do not cross the placenta in significant quantities [32].

The major factors controlling the onset of puberty are body weight and growth rather than age [33]. Some studies have demonstrated the importance of dam nutrition on growth, attainment of puberty and reproductive performance of the offspring. For instance, although heifers born to dams supplemented with protein during the last third of pregnancy had similar birthweight to calves born to unsupplemented dams, when mature these animals had higher pregnancy rates [34]. Restricted nutrition in beef cattle decrease birth weights and reduces postnatal growth [35]. Although the effect of global nutrients restrictions and /or excess has been extensively investigated, individual nutrients hinder offspring wellbeing if deficient. For example, methionine supplementation in Holstein cows changes the transcriptome of flushed embryos, including genes involved in embryonic development and immune responses [36]. Recent, research focusing on the effect of maternal nutrition on the neuroendocrine system function concluded that maternal nutrition modulates the hypothalamic pathways controlling GnRH release, and therefore affects the programming of puberty in the female offspring [37][38]. In cattle, little is known about the effects of dam nutrition on the neonate neuroendocrine system. Any nutritional and metabolic change occurring from foetal life to puberty, can impact the hypothalamic pathways controlling GnRH secretion and pubertal maturation [39].

In fact, maternal nutrition meeting the animal requirements during gestation, together with high body weight gain rates during early postnatal development, results in increased circulating levels of leptin, insulin, and IGF1; reduced neuropeptide Y (NPY) mRNA abundance and NPY (inhibitory) inputs to GnRH neurons. These endocrine and neuroendocrine changes, some of which will be discussed in Section 3.3.6, contribute to promoting early puberty.

2.4. Muscle and Fat Development

Skeletal muscle development is initiated in the embryonic stage, during the first trimester of pregnancy, when primary myogenesis occurs with formation of primary myofibers [40]. During this phase, maternal nutrition has negligible effects on foetal skeletal muscle development. In cattle the majority of muscle fibres form between the 2nd and 7th/8th months of gestation, period that corresponds to the secondary myogenesis [41]. This period is crucial because there will be no net increase in the number of muscle fibres after birth [42][43].

Post-natal muscle growth occurs mainly due to an increase in muscle fibre size rather than new muscle fibre formation [43][44]. Adipogenesis is initiated around mid-gestation [45], overlapping with the period of secondary myogenesis. The amount of intramuscular fat is determined by the number and size of intramuscular adipocytes within foetal skeletal muscle. Skeletal muscle and fat are less of a priority in terms of nutrient partitioning during foetal development when compared with organs such as the brain, heart, and liver. As a result, skeletal muscle development is particularly vulnerable to nutrient availability [46].

It has been reported that calves from nutrient restricted beef cows have decreased average daily gain and fatter carcasses at 30 months of age [47][48]. However, in beef calves from dams fed nutrient restricted diets during early pregnancy, but that were realigned during late gestation; muscle fibre size and muscle progenitor cell numbers could be rescued [49]. Furthermore, it has been reported that improving the dams’ diet by either increasing forage quality or exceeding their energy requirements during mid to late gestation, resulted in calves that were leaner and had better yielding carcasses compared to offspring from dams fed a negative energy diet [50][51].

This entry is adapted from the peer-reviewed paper 10.3390/ani11051212

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