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.Mares measurements and metabolism during pregnancyMeasurements (BCS=Body Condition Score and body weight (kg)) and plasma concentrations of metabolic factors (basal leptin (ng/mL), adiponectin (ng/ml), glucose (mg/dL), insulin (mUI/L), urea (mmol/L), triglycerides (mmol/L), NEFA=Non Esterified Fatty Acid (mmol/L) and SAA= Serum Amyloid A (microg/mL)) of mares during the year before insemination, during gestation and during lactation.Mares_Longitudinal.xlsxNutritional data of pregnant maresEnergy (HFU=Horse Feed Unit (1HFU=2250kcal)), proteins (HDCP=Horse Difestible Crude Proteins), Fibres (RC=Raw Cellulose), calcium (Ca), phosphorus (P) and calcium to phosphorus ration (Ca_P) ingested by mares between 180 and 330 days of gestation.Mares_Nutrition.xlsxMares FSIGTData from the Frequently Sampled Intravenous Glucose Tolerance Test (FSIGT) performed in mares at 300 days of gestation. AIRg=Acute pancras response, DI=Disposition index, SI=Insulin sensitivity, Sg=Glucose effectivness, GB=Basal glucose, IB=Basal insulin.Mares_FSIGT_300days.xlsxMeasurements and metabolism in growing foalsMeasurements (body weight (kg), WH=wither's height (cm), TP=thoracic perimeter (cm), BCS=Body Condition Score), plasma concentrations of metabolic factors (leptin (ng/mL), adiponectin (ng/mL), SAA=Serum Amyloid A (ng/mL), T3=Triiodothyronin (ng/mL), T4=thyroxin (ng/mL)) and serum concentrations of cortisol (ng/mL) in growing foals between birth and 690 days of age.Foals_Longitudinal .xlsxFoals FSIGTData from the Frequently Sampled Intravenous Glucose Tolerance Test (FSIGT) performed in growing foals at 180, 360 and 540 days of age. AIRg=Acute pancras response, DI=Disposition index, SI=Insulin sensitivity, Sg=Glucose effectivness, GB=Basal glucose, IB=Basal insulin.Foals_FSIGT.xlsxTesticular function in foals at 12 months of ageExpression (arbitrary unit) of genes markers of testicular maturity (Cyp19, Cx43=Connexin 43, AR, STAR), testicular immaturity (AMH) and genes involved in the etablishment of the blood-testis barrier (Occludin, N Cadherin).Foals_Testis.xls