Dopamine and insulin in the amygdala curb compulsive junk food eating, mouse study finds
Feb 27th 2026
A Molecular Psychiatry study in male mice shows dopamine D2 receptors and insulin receptors in the central amygdala work together as a biological brake on compulsive consumption of sugary and fatty foods, with receptor loss weakening that control.
- Dopamine D2 receptors and insulin receptors co-locate in the central amygdala and interact to limit persistent food-seeking behavior.
- Mice lacking D2 receptors or lacking insulin receptors on D2 cells continued to press for sugary pellets despite mild foot shocks, showing compulsive-like eating.
- Removing D2 receptors reduced insulin receptor levels in the central amygdala by about 60 percent and impaired insulin signaling in those cells.
- Stimulating D2 receptors boosted insulin receptor activation, while silencing D2-expressing neurons increased consumption of sugary and fatty food.
- Results come from controlled genetic and neural-manipulation experiments in male mice, so translation to human behavior will require further research.