Data from: Maternal obesity increases insulin resistance, low-grade inflammation and osteochondrosis lesions in foals and yearlings until 18 months of age

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) 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. 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, SAA plasma 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.

马匹肥胖问题已日益受到学界关注。本研究探讨了妊娠期母马肥胖对母体代谢、低度炎症状态的影响，以及对子代生长发育、代谢水平、低度炎症、睾丸成熟直至18月龄时的骨软骨病变的影响。本研究选用24匹母马，在配种时根据体况评分（Body Condition Score, BCS）分为两组：正常组（N组，n=10，BCS≤4）与肥胖组（O组，n=14，BCS≥4.25）。整个妊娠期监测各组母马的体况评分以及血浆葡萄糖、胰岛素、甘油三酯、尿素、非酯化脂肪酸、血清淀粉样蛋白A（Serum Amyloid A, SAA）、瘦素与脂联素浓度。妊娠第300天时，对母马实施频繁取样静脉葡萄糖耐量试验（Frequently Sampled Intravenous Glucose Tolerance Test, FSIGT）。分娩后，监测驹马的体重与体尺直至18月龄，并定期检测其血浆SAA、瘦素、脂联素、三碘甲状腺原氨酸（Triiodothyronine, T3）、甲状腺素（Thyroxine, T4）与皮质醇浓度。在驹马6、12及18月龄时，实施FSIGT与骨关节检查。对1岁龄的公驹进行去势，并通过实时定量聚合酶链式反应（Real-time Quantitative PCR, RT-qPCR）分析与睾丸成熟相关的基因表达情况。整个实验期间，肥胖组母马的体况评分均高于正常组。妊娠期内，肥胖组母马的血浆尿素与脂联素浓度降低，而SAA与瘦素浓度升高；此外，肥胖组母马的胰岛素抵抗程度更高，葡萄糖效能也更强。产后阶段，两组驹马的生长情况无显著差异。但直至6月龄，肥胖组母马所产驹马的血浆SAA浓度均高于正常组，且该组驹马始终表现出更高的胰岛素抵抗程度与更强的葡萄糖效能。12月龄时，肥胖组驹马的骨软骨病发病率显著高于正常组。其余各项检测指标在两组间均无显著差异。综上，母马肥胖可改变母体代谢水平，并升高母马及其子代的低度炎症水平；肥胖母马所产驹马在12月龄时患骨软骨病的风险也更高。