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International audience; Maternal aging, excluding extreme ages, is associated with increased foal weight/size and heavier/more voluminous placenta. Maternal parity is a confounding factor as it is often strongly correlated with maternal age. The aim of this study was to analyze the effect of mare age, while excluding a parity effect, on placental structure and gene expression and foal growth and health.Placentas from 10 young (6-year-old, YM) and 12 older (>10-year-old, OM) multiparous mares of similar parity were recovered, measured and weighted after foaling. Placental structure was analyzed by stereology on HES stained histological slides. Paired-end RNA-sequencing was performed on 6 placentas/group (Illumina, NextSeq500). Differential expression was analyzed (DESeq2) using a false discovery rate

International audience; INTRODUCTION:Obesity is a growing concern in horses. The effects of maternal obesity on maternal metabolism and low-grade inflammation during pregnancy, as well as offspring growth, metabolism, low-grade inflammation, testicular maturation and osteochondrotic lesions until 18 months of age were investigated.MATERIAL AND METHODS:Twenty-four mares were used and separated into two groups at insemination according to body condition score (BCS): Normal (N, n = 10, BCS ≤4) and Obese (O, n = 14, BCS ≥4.25). BCS and plasma glucose, insulin, triglyceride, urea, non-esterified fatty acid, serum amyloid A (SAA), leptin and adiponectin concentrations were monitored throughout gestation. At 300 days of gestation, a Frequently Sampled Intravenous Glucose Tolerance Test (FSIGT) was performed. After parturition, foals' weight and size were monitored until 18 months of age with plasma SAA, leptin, adiponectin, triiodothyronine (T3), thyroxine (T4) and cortisol concentrations measured at regular intervals. At 6, 12 and 18 months of age, FSIGT and osteoarticular examinations were performed. Males were gelded at one year and expression of genes involved in testicular maturation analysed by RT-qPCR.RESULTS:Throughout the experiment, maternal BCS was higher in O versus N mares. During gestation, plasma urea and adiponectin were decreased and SAA and leptin increased in O versus N mares. O mares were also more insulin resistant than N mares with a higher glucose effectiveness. Postnatally, there was no difference in offspring growth between groups. Nevertheless, plasma SAA concentrations were increased in O versus N foals until 6 months, with O foals being consistently more insulin resistant with a higher glucose effectiveness. At 12 months of age, O foals were significantly more affected by osteochondrosis than N foals. All other parameters were not different between groups.CONCLUSION:In conclusion, maternal obesity altered metabolism and increased low-grade inflammation in both dams and foals. The risk of developing osteochondrosis at 12 months of age was also higher in foals born to obese dams.

Obesity is a growing concern in horses. The effects of maternal obesity on maternal metabolism and low-grade inflammation during pregnancy, as well as offspring growth, metabolism, low-grade inflammation, testicular maturation and osteochondrotic lesions until 18 months of age were investigated. Twenty-four mares were used and separated into two groups at insemination according to body condition score (BCS): Normal (N, n = 10, BCS = 4.25). BCS and plasma glucose, insulin, triglyceride, urea, non-esterified fatty acid, serum amyloid A (SAA), leptin and adiponectin concentrations were monitored throughout gestation. At 300 days of gestation, a Frequently Sampled Intravenous Glucose Tolerance Test (FSIGT) was performed. After parturition, foals' weight and size were monitored until 18 months of age with plasma SAA, leptin, adiponectin, triiodothyronine (T3), thyroxine (T4) and cortisol concentrations measured at regular intervals. At 6, 12 and 18 months of age, FSIGT and osteoarticular examinations were performed. Males were gelded at one year and expression of genes involved in testicular maturation analysed by RT-qPCR. Throughout the experiment, maternal BCS was higher in O versus N mares. During gestation, plasma urea and adiponectin were decreased and SAA and leptin increased in O versus N mares. O mares were also more insulin resistant than N mares with a higher glucose effectiveness. Postnatally, there was no difference in offspring growth between groups. Nevertheless, plasma SAA concentrations were increased in O versus N foals until 6 months, with O foals being consistently more insulin resistant with a higher glucose effectiveness. At 12 months of age, O foals were significantly more affected by osteochondrosis than N foals. All other parameters were not different between groups. In conclusion, maternal obesity altered metabolism and increased low-grade inflammation in both dams and foals. The risk of developing osteochondrosis at 12 months of age was also higher in foals born to obese dams.

Human and animal model studies have shown that the adult phenotype of an individual can be modulated by maternal environment. In horses, moderate maternal undernutrition in late gestation does not affect the foal’s birth weight as the placenta appears to compensate for maternal restriction but alters the metabolism of the growing foal and results in delayed testicular maturation at 12 months of age and bone development from 19 months of age. Moreover, excess nutrition of these foals between 20 and 24 months of age largely modifies the regulation of their carbohydrate metabolism, which can subsequently lead to decreased athletic performances. On the other hand, feeding mares with cereals in late gestation increases the risk for the foal to develop osteochondrosis. These effects could possibly be reduced by feeding meals throughout the day, for instance through the use of an automatic feeder. Thus, the quality of the nutrition of both mares and foals is essential to optimize chances of athletic and reproductive performance in adulthood.; Le rôle de l’environnement maternel pour le développement du phénotype adulte est bien connu chez l’homme et les animaux modèles. Dans l’espèce équine, la sous-nutrition modérée de la jument gestante n’entraîne pas d’effet sur le poids de naissance du poulain car le placenta semble compenser cette sous-nutrition. Cependant, on observe un retard de maturation testiculaire à 12 mois et de développement osseux à partir de 19 mois. De plus, une surnutrition des poulains entre 20 et 24 mois altère l’intégralité de leur système de régulation du métabolisme glucidique, pouvant entraîner par la suite des effets négatifs sur leurs performances sportives. D’autre part, la supplémentation des juments avec des céréales en fin de gestation augmente le risque pour le poulain de développer des lésions d’ostéochondrose. Ces effets pourraient peut-être être réduits par une alimentation fractionnée des poulains dans la journée (utilisation d’un distributeur automatique). Une alimentation de qualité chez la jument gestante et son poulain en croissance est donc essentielle pour optimiser les chances de performances sportives et reproductives à l’âge adulte.

International audience