Effects of maternal dexamethasone treatment on pancreatic [beta] cell function in the pregnant mare and post natal foal

Summary Reasons for performing study Synthetic glucocorticoids are used to treat inflammatory conditions in horses. In other pregnant animals, glucocorticoids are given to stimulate fetal maturation with long-term metabolic consequences for the offspring if given preterm. However, their metabolic effects during equine pregnancy remain unknown. Objective Thus, this study investigated the metabolic effects of dexamethasone administration on pregnant pony mares and their foals after birth. Study design Experimental study. Methods A total of 3 doses of dexamethasone (200 µg/kg bwt i.m.) were given to 6 pony mares at 48 h intervals beginning at [asymptotically =]270 days of pregnancy. Control saline injections were given to 5 mares using the same protocol. After fasting overnight, pancreatic [beta] cell responses to exogenous glucose were measured in the mares before, during and after treatment. After birth, pancreatic [beta] cell responses to exogenous glucose and arginine were measured in the foals at 2 and 12 weeks. Results In mares during treatment, dexamethasone but not saline increased basal insulin concentrations and prolonged the insulin response to exogenous glucose. Basal insulin and glucose concentrations still differed significantly between the 2 groups 72 h post treatment. Dexamethasone treatment significantly reduced placental area but had little effect on foal biometry at birth or subsequently. Foal [beta] cell function at 2 weeks was unaffected by maternal treatment. However, by 12 weeks, pancreatic [beta] cell sensitivity to arginine, but not glucose, was less in foals delivered by dexamethasone- than saline-treated mares. Conclusions Dexamethasone administration induced changes in maternal insulin-glucose dynamics, indicative of insulin resistance and had subtle longer term effects on post natal [beta] cell function of the foals. The programming effects of dexamethasone in horses may be mediated partially by altered maternal metabolism and placental growth.