Effects of prenatal transportation stress on liver gene expression in male and female Brahman calves

Le résumé fourni par la source

The liver is a central regulator of metabolic and endocrine functions that support fetal growth and postnatal development. Prenatal stress can reprogram hepatic development in the offspring, potentially causing long-term changes in metabolism and production efficiency. However, the influence of prenatal stress on hepatic molecular function and resulting phenotypes in beef cattle remains poorly understood. Therefore, the objectives of this study were to evaluate phenotypic traits and liver tissue gene expression in Brahman heifer and bull calves from prenatal transportation stress (PNS) and control (Control) treatment groups. One group of pregnant Brahman cows were transported for a 2-h period every 20 (±5) d from 60 to 140 days of gestation. Another group of pregnant Brahman cows served as Control. Thirty-two calves, eight heifer and eight bull calves from the PNS and Control groups, respectively, were utilized. Calves were weighed at approximately 25 (±2) d of age. The following day, calves were euthanized, and liver tissues were harvested. Phenotypic traits evaluated include birth weight, harvest weight, liver weight, pen score, and liver weight:harvest weight. Interaction of sex and treatment did not explain substantial variation for any trait ( P > 0.28). Sex influenced birth weight, harvest weight, liver weight ( P < 0.05), and treatment influenced liver weight:harvest weight ( P < 0.10). Linear regression coefficients of traits on calf age as a linear covariate were not different from 0 ( P > 0.41). Controlling false discovery rate at 0.10, there were no differentially expressed genes for PNS relative to Control and 13 differentially expressed genes for male relative to female comparisons. No genes were found to be differentially expressed across all comparisons. It is possible that the few differences between sexes and treatments may be due to relatively small sample sizes or to an unknown adaptation mechanism to the stress prenatally induced by this young age. Heightening the severity of prenatal transportation stress through increased duration or frequency of transportation may result in more differentially expressed genes.

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