Oral Presentation ANZOS Annual Scientific Meeting 2021

Intermittent access to high-fat high-sugar food is sufficient to induce compulsive-like eating, increases in visceral fat and glutamatergic dysfunction in the dorsal striatum (#80)

Diana Sketriene 1 , L Jarillas 1 , N Kraiwattanapirom 2 , C Mao 1 , AJ Lawrence 1 , RM Brown 1 3
  1. The Florey Institute, The University of Melbourne, Melbourne, VIC, Australia
  2. Mahidol University, Bangkok, Thailand
  3. Department of Biochemistry and Pharmacology, University of Melbourne, Parkville, VIC

Background: Occasional consumption of junk food is very common and is not usually considered to be harmful, particularly when normal body weight is maintained.  Interestingly, intermittent schedules of access are routinely used in the drug addiction field to induce escalation of drug intake and compulsive patterns of use. Compulsive reward seeking behaviour is a hallmark feature of addiction and can explain why so many people find it difficult to restrain from unhealthy food despite known negative consequences. There is increasing evidence that a compulsive reward-seeking behaviour reflects dysregulation in mesocorticolimbic circuitry in the brain. This study investigated the possibility that intermittent access to junk food may induce brain changes which facilitate unhealthy eating patterns.

Aim: To investigate whether occasional versus continuous access to high-fat high-sugar (HFHS) can induce compulsive-like eating and glutamatergic dysfunction in the striatum, a region of the brain associated with compulsive reward-seeking behaviour.

Methods: Rats were given either continuous access or intermittent access (IA; 1hx3 per week) to junk food (4.7kcal/gr, 30% fat) for at least 9 weeks. A control group was given access to standard chow only. Compulsive-like eating was assessed using a conditioned suppression paradigm. Membrane bound levels of target proteins (GluN2B, GluA1, GLT1 and xCT) in the dorsal striatum was measured by Western blot and recordings were made from dorsal striatum using whole cell patch clamp electrophysiology.

Results:  Total food intake and body weight were similar in IA and control groups, however IA had more visceral fat. IA rats showed compulsive-like behaviour towards HFHS compared to other groups, as well as increased levels of GluN2B, GluA1 in the dorsal striatum. Electrophysiology analysis is ongoing (results will be presented at meeting).

Conclusion: These findings suggest that even occasional exposure to HFHS causes glutamatergic changes in dorsal striatum which are sufficient to promote compulsive eating behaviour.