Presented at the Neonatal Society 2006 Widdowson Meeting.

Ousey JC¹, Fowden AL², Wilsher S¹, Allen WR¹

¹ University of Cambridge Equine Fertility Unit, Newmarket, UK
² Department of Physiology, Developmental Neuroscience, University of Cambridge, Cambridge, UK

Introduction: In many species variations in maternal nutrient intake during pregnancy alter pancreatic and hypothalamo-pituitary-adrenal (HPA) axis function in the offspring both before and after birth (1). Previous studies in horses have shown that increasing or decreasing fetal nutrient availability induced by altering placental size, affect pancreatic β cell and HPA function, respectively, in newborn foals (2,3). However, little is known about the effects of maternal nutrition per se on equine postnatal endocrine function despite the fact that many broodmares are obese and fed high energy rations during pregnancy.

Aim: To identify the effects of maternal nutritional status throughout gestation on pancreatic β cell and HPA function in neonatal Thoroughbred (TB) foals.

Maaterials & Methods: Ten primiparous TB mares were fed either a maintenance (Moderate, n=5) or 2.5-3 x maintenance diet (High, n=5) throughout pregnancy. At the end of the first trimester, all the mares experienced acute undernutrition when they inadvertently became infected with Streptococcus equi and lost approximately 10 % of their body mass. The mares were weighed and bled weekly. The foals were weighed at birth and starting on Day 1, an adrenocorticotrophic hormone (ACTH) stimulation test (0.125 mg Synacthen, im), a glucose tolerance test (GTT, 0.5 mg/kg, 40% w/v iv ) and insulin sensitivity test (0.05 IU/kg iv) were performed at > 24 h intervals. Blood samples were collected during (-30 to +120 min) the challenge tests. The foals were fed by their dams except during the GTT and insulin tests when they were muzzled. Blood samples were analysed for insulin, glucose (mares and foals) and cortisol concentrations (foals only). This study was performed in accordance with the Animal (Scientif ic Procedures) Act (1986).

Results: Maternal insulin concentrations (both groups), and glucose concentrations (Moderate), during illness decreased (P<0.05) from pre-infection levels. Insulin concentrations were higher (P<0.05) in the High than Moderate mares before, during and after infection. All the mares recovered and foaled normally. High mares weighed (P<0.05) more at birth than the Moderate mares. All foals were healthy and body weights were similar between the two nutrition groups, although their overall mean body weight was (P<0.05) lower than that obtained previously in foals from healthy, primiparous mares. Plasma cortisol concentrations were similar in both groups during the ACTH test but elevated (P<0.05) compared to previously published values (3). Glucose concentrations were similar for both GTT and insulin sensitivity test. Insulin concentrations and area under the curve following GTT were greater (P<0.05) in the Moderate than High foal group but levels in the High group were equivalent to those reported previously for foals from uninfected, well-fed mares (2), suggesting that the foals from the Moderate nutrition group had enhanced β cell responses to glucose. These data indicate that an acute nutrient restriction in mid gestation caused by maternal illness and inappetence, superimposed on a Moderate feed intake throughout pregnancy, enhanced insulin secretion during GTT in neonatal foals. Moreover, foals from both groups may have been stressed in utero leading to low birth weights and high cortisol levels.

Conclusion: Acute undernutrition caused by illness in mares during pregnancy may reprogramme the endocrine pancreas and HPA axis in the foals after bir th. Nutritional programming of the β cells, but not the HPA axis, appears to depend on the level of nutrition before and after the insult.

References
1. Hoet JJ & Hanson MA J Physiol 1999; 514:617-627.
2. Forhead AJ et al. J Endocrinol 2004; 181:459-467.
3. Ousey JC et al Equine vet. J 2004; 36:616-621.