Poster only 3rd Metabolic Diseases; Breakthrough Discoveries in Diabetes & Obesity 2022

INVESTIGATING THE ROLE OF OREXIN IN A MOUSE MODEL OF FEMALE “EMOTIONAL” STRESS-INDUCED BINGE EATING (#108)

Mia O'Shea 1 2 , Muthmainah Muthmainah 2 3 , Robyn Brown 1 2 , Roberta Anversa 1 2 , Leigh Walker 2 3 , Andrea Gogos 2 , Priya Sumithran 4
  1. Department of Biochemistry and Pharmacology, University of Melbourne, Parkville, Vic, Australia
  2. Florey Institute of Neuroscience and Mental Health, Parkville, Vic, Australia
  3. Florey Department of Neuroscience and Mental Health, University of Melbourne, Parkville, Vic, Australia
  4. Department of Medicine (St Vincent's), University of Melbourne, Melbourne, Vic, Australia

Introduction

It is well established that stress and negative affect (e.g. sadness, anger) trigger overeating. This form of maladaptive eating behaviour, commonly referred to as “emotional eating”, is particularly common in women, and is associated with binge eating and higher risk of obesity. The neural mechanisms that underpin this form of dysregulated eating are yet to be elucidated but likely implicate neuronal substrates involved in both homeostatic and hedonic feeding. The orexin system (or hypocretin) represents a distinct population of lateral hypothalamic neurons, that has been previously implicated in reward, stress and feeding. Thus, we aim to investigate the role of the orexin system in stress-induced binge eating in females.

Methods 

To do so, a mouse model was employed that used a mild, psychological stressor and intermittent access to highly palatable food to induce binge eating in test mice. Mice exposed to the frustrative stressor and food reward consumed significantly more than control mice exposed to the food reward only. Immunohistochemistry for neuronal activity marker Fos was used to assess the recruitment of lateral hypothalamic neurons, including orexin during this behaviour. 

Results

Statistical analysis of cell counts has revealed significant activation in neurons throughout the lateral hypothalamus of stress-induced binge eating mice (p < .05). Early analysis of orexin data is indicative of a trend toward significant neuronal activation; however, full quantification of orexin data is ongoing. We hypothesize that orexin neurons will be significantly activated as a result of stress-induced binge eating compared to control.

Conclusions

Our preliminary evidence indicates a significant role for neurons of the lateral hypothalamus in female stress-induced binge eating, and a potential role for the orexin system. Investigation into the extent of orexin’s involvement remains ongoing. When completed, the results of this study will provide insight into the neurobiological processes underlying stress-driven binge eating.