Abstract
Obesity is a major health issue in the horse industry, often associated with insulin resistance. This study aimed to analyse effects of maternal obesity at insemination and insulin resistance during late gestation on term placenta and foals at term. A total of 24 multiparous saddlebred mares were allocated to 1 of 2 groups at insemination: group obese (O) had a body condition score (BCS, French scale 1–5) >4 (N = 15), and group normal (N) had a BCS = 4 (N = 9). From insemination until the sixth month of gestation, all the mares had access to pasture. From wintering, they were housed in box stalls and fed the same amount of energy, proteins, and fibre as a percentage of their body weight. During all the gestation, BCS, basal blood glucose, insulin, triglycerides, and nonesterified fatty acid plasma concentrations were measured each month. At 300 days of gestation, a frequent sampling glucose tolerance test, enabling the simultaneous evaluation of insulin sensitivity (IS) and glucose tolerance, was performed. At birth, placentas and foals were measured. Placentas were sampled around the umbilical cord to perform structural and functional analyses by stereology and RT-qPCR. Results were analysed using a type 3 ANOVA taking into account mare group and foal sex. Effects were considered significant when P < 0.05. At 300 days of gestation, the frequent sampling glucose tolerance test indicated that half of the O mares were insulin resistant (IS <1; N = 8), whereas the other half were insulin sensitive (IS >1; N = 7). Based on these results, O mares were subdivided in 2 groups: obese resistant and obese sensitive (OS). Obese resistant mares were 61% less insulin sensitive than N mares and 59% less insulin sensitive than OS mares (P < 0.0001, P < 0.01, respectively). There was no difference for IS between N and OS mares. All analyses were thus performed comparing the 3 groups. In the N group, 3 mares were insulin resistant (one-third of the mares of the N group). Feed intake during wintering was not different between groups. Mares of both O groups maintained a high BCS (>4) during pregnancy, whereas N mares lost BCS down 2.75 at birth (<0.001). Basal glucose, insulin, triglycerides, and nonesterified fatty acid plasma were not different during gestation. At birth, no difference was observed for placental weight, surface and volume, nor for foal weight and withers height. The volume of allantoic vessels was reduced in placentas of OS mares compared with those of OR (P = 0.03; 78%) and N mares (P = 0.005; 65%). Moreover, placentas from OS mares had an increased volume of haemotrophic trophoblast (P = 0.03) and microcotyledonary vessels (P = 0.03) compared with N mares. No difference of expression was observed for 11 genes related to nutrient transfer, vascularization, growth, and development. Mare that are obese at insemination and insulin sensitive in late gestation appear to develop placental structural adaptations during gestation, possibly to increase fetoplacental exchanges, compared with obese, insulin resistant mares and lean mares. The monitoring of foal development (growth, metabolism, and osteoarticular status) is ongoing.
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