A generalized non-specific response to stress is the elevation of circulating corticosteroid levels in animals. In teleosts, cortisol is the primary corticosteroid, and the stressor-mediated elevation of this hormone leads to an increase in plasma glucose levels. Cortisol action is mediated by its binding to either the glucocorticoid receptor (GR) and/or the mineralocorticoid receptor (MR), both of which are ligand-bound transcription factors. Chronic cortisol exposure has been shown to reduce feed intake, but the mechanisms are far from clear. The objective ofthis thesis was to investigate the possible mechanisms leading to cortisol-mediated appetite suppression in fish. The hypothesis was that elevated plasma glucose levels in response to stressor-mediated cortisol elevation inhibits feeding by activating the brain glucose sensing mechanisms. Indeed, elevated blood glucose levels suppressed food intake by inhibiting AMP-activated protein kinase (AMPK) expression in the zebrafish (Danio rerio) brain. However, the suppression of feeding associated with cortisol was not due to elevated glucose levels, as the brain glucose uptake capacity and the expression of AMPK remained unchanged. Instead,cortisol stimulation reduced the expression of protein kinase B (Akt) and the mammalian targetof rapamycin (mTOR), while increasing the transcript abundance of regulated in development and DNA damage responses 1 (redd1), a marker of protein breakdown, in the zebrafish brain. Interestingly, the loss of GR did not rescue the cortisol-mediated suppression in feeding or the inhibition of brain Akt expression. However, lack of GR increased brain glucose uptake and rescued the brain mTOR expression, along with a reduction in redd1 transcript levels. The resultsindicate that GR activation by elevated cortisol levels restrict glucose uptake and increase thecapacity for protein breakdown in the zebrafish brain. The cortisol-mediated suppression of feeding was not rescued in the absence of GR, suggesting a possible role for MR in the feeding regulation. Overall, the results suggest that both GR and MR activation may contribute to the cortisol-mediated energy substrate repartitioning in the brain, leading to feed inhibition during stress in fish.