Abstract
Piglets with low birth weight present low vitality after farrowing, often leading to impaired weight gain during lactation. A recessive missense variant (C > T) for increased appetite and fatness in the porcine leptin receptor gene (rs709596309) causes a negative maternal effect on the weight of piglets at weaning. However, it is not known whether this variant already exerts an effect on the birth weight and vitality of newborn piglets and on their growing capacity during lactation. An experiment was conducted using 668 purebred Duroc piglets (131 CC, 311 CT, and 226 TT) from 74 multiparous sows (9 CC, 43 CT, and 22 TT) and 14 boars (1 CC, 10 CT, and 3 TT). All piglets were individually weighed at birth and tested for vitality, which was assessed on a scale from 1 (low vitality) to 3 (high vitality) based on behavioral observations, including the status of the piglet immediately before the test. Only non-adopted piglets were considered for piglet performance at weaning. Inferences on the effect of the genotype on birth and weaning traits were done on a Bayesian setting based on 2-trait bivariate models including the effects of the piglet and the litter, as well as the genotype of the sow and the piglet, the sex of the piglet, and the parity number. Vitality and the status of the piglet before the test were analyzed using a liability threshold (probit) model. As compared to other genotypes, TT newborn piglets were 28 g heavier, were more vital (the probability of being scored as highly vital was 6.5% higher) and were more often found suckling before the test (the probability of being suckling at test was 6.5% higher). As a result, they grew more during lactation (153 g) and were heavier at weaning (169 g) than littermates of the two other genotypes, thus partly compensating for the limited maternal capacity of TT sows. Our findings provide evidence that appetite-influencing genes, such as the leptin receptor gene, have developmental implications from very early life stages.