Autism spectrum disorder (ASD) is a neurodevelopmental disorder affecting roughly 1% of the global population. Aberrant food selectivity (AFS) is a common comorbid symptom of ASD which can result in nutritional deficiencies, increased parental stress and reduced quality of life. However, alarmingly little research has been conducted investigating the nature and the underlying neurophysiological mechanisms of AFS in ASD. This study attempts to determine whether the VPA rat model of ASD exhibits AFS when presented with various diet types. These include standard chow and water, palatable sweet tastants (sucrose, saccharin and complex liquid diet) and finally palatable high fat milks. The mRNA expression levels of oxytocin, oxytocin receptor, dynorphin and kappa-opioid receptor were then determined. These genes have previously demonstrated to be involved in both feeding and social behaviours. The VPA rats were found to consume less standard chow and water, yet increased intake of the sweet tastants was observed. Additionally, in the VPA rats’ oxytocin expression in the hypothalamus was increased, as was dynorphin expression in the hypothalamus and brainstem. Increased expression of the anorexigenic oxytocin may have resulted in the decreased intake of chow and water, and could potentially be a result of increased leptin or melanocortin levels. However, increased dynorphin expression may be responsible for the increased intake of the palatable sweet tastants, via inhibition of proopiomelanocortin or neuropeptide S. The development of effective treatments for AFS in ASD requires an understanding of the underlying neurological mechanisms. This research provides the first evidence of AFS and elevated oxytocin and dynorphin expression in the VPA rat model of ASD, thus paving the way for further research in this area.