431 - Effects of Exogenous Glucocorticoid Administration on Appetitic Center Brain Development in Dairy Bull Calves

The objective of study was to determine the effects of exogenous cortisol on leptin concentrations and appetitic center development of perinatal dairy bull calves. Holstein bull calves (n = 27) were weighed and randomly assigned to treatments within 4h of parturition (d0). Each calf was intravenously infused with either a low cortisol (LC; n = 9, 3.5 ug/kg of BW), high cortisol (HC; n = 9, 7.0 ug/kg of BW), or a sham infusion control (CON; n = 9, similar volume of saline). Each calf was administered a second infusion (half dose) of its respective treatment 24h postpartum. All calves were housed similarly and fed milk replacer (28% CP, 20% fat) three times daily. Blood was collected via jugular venipuncture before infusion and from d0–5 of age. At 5d of age, calves were euthanized via sodium pentobarbital overdose. Cerebral-spinal fluid (CSF) from the third ventricle of the brain, hypothalamus, and adipose tissue (AT; omental, perirenal, and mesenteric) were collected. Blood and CSF samples were analyzed for leptin concentrations via a validated RIA. Adipose tissue samples were analyzed via western blotting for leptin and glucocorticoid receptor (GR) expression and normalized to glyceraldehyde 3-phosphate dehydrogenase (GAPDH) expression. Hypothalamus samples were analyzed via qRT-PCR for genes associated with neuronal growth factors and normalized to the average of two housekeeping genes. All data were analyzed via ANOVA or repeated measures analysis using appropriate models (SAS Institute Inc., Cary, NC). Serum and CSF leptin concentrations were decreased (P < 0.013) in HC and LC compared to CON. Leptin protein expression was decreased (P < 0.044) in perirenal and omental AT of LC calves compared to CON. Hypothalamic expression of BDNF, FGF1, and FGF2 were decreased (P < 0.006) in HC and LC compared to CON. In summary, exogenous cortisol administered to calves at birth reduced leptin concentrations and altered appetitic control center development of the brain.