Plane of nutrition affects growth rate, organ size and skeletal muscle satellite cell activity in newborn calves

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In utero growth restriction (IUGR) can manifest as long‐term health consequences in adults, a concept referred to as foetal programming (Tamashiro and Moran, 2010). Early life insults on the foetus from the environment, maternal nutrition and stress can predispose the offspring to neurocognitive deficits, cardiovascular disease and diabetes (Padmanabhan et al., 2016). Metabolic programming of the foetus is not limited to gestational undernutrition as maternal over nutrition also can lead to adverse health outcomes in adult humans (Lau and Rogers, 2004), rodents (Burton and Fowden, 2012) and other species (Reynolds and Caton, 2012). The effects of insufficient nutrition on neonates exhibiting a normal birthweight are poorly described and often linked to a pre‐existing disease, trauma or infection (Luyckx and Brenner, 2015).
Modern dairy calf husbandry frequently involves placing the newborn on milk replacer (MR) diets. The amount of MR and subsequent nutrient intake directly affects growth trajectory (Hengst et al., 2012), body composition (Bartlett et al., 2006), endocrine profiles (Daniels et al., 2008) and immune function (Obeidat et al., 2013; Ballou et al., 2015). Neonatal calves restrict fed MR to promote the grain consumption exhibit smaller body weights, smaller frames and reduced average daily gains than calves fed at higher caloric intakes (Khan et al., 2011). Intensified MR diets contain a greater amount of crude protein (CP) and a higher CP:fat ratio. The improved plane of nutrition leads to greater body weights, feed efficiency and health status during the neonatal period that may translate into greater product yields as adults (Davis Rincker et al., 2011). The added nutrient intake in animals reared on the intensive diets leads to a greater amount of muscle protein deposition with carcass composition affected primarily by the level of dietary fat intake (Hill et al., 2008).
Post‐natal skeletal muscle growth is facilitated by satellite cells, a heterogeneous population of muscle stem and progenitor cells. During periods of muscle hypertrophy in mammals, satellite cells fuse to the existing fibres to increase myonuclei numbers and thus, the transcriptional machinery necessary for efficient contractile protein synthesis (Allen et al., 1999). Satellite cells are typically found in a quiescent state but become mitotically active, proliferate and differentiate when needed for growth, repair and regeneration (Wang et al., 2014). Satellite cell myogenesis can be altered by age, disease, hormonal status and exercise. Of note, adults with type II diabetes and suffering from obesity demonstrate reductions in muscle strength, myokine activity and satellite cell myogenesis (Scheele et al., 2012; Lee et al., 2015; Fu et al., 2016). The impact of early neonatal nutrition on satellite cell bioactivity remains poorly understood.
The objective of the experiment was to examine the effect of plane of nutrition on parameters of tissue and organ growth and skeletal muscle size and satellite cell activity.
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