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Dopamine D2 receptor modulation of insulin receptor signaling in the central amygdala: implications for compulsive-like eating behavior
Compulsive eating behavior, defined as the excessive consumption of palatable, high-sugar, high-fat foods despite negative consequences, may be linked to dysfunction in the dopamine system, particularly involving dopamine D2 receptors (D2Rs). This research demonstrates that D2Rs regulate insulin receptor (InsR) signaling in the central amygdala (CeA), a mechanism crucial for the persistence of compulsive-like food-seeking behavior.
Specifically, the targeted ablation of D2Rs in the CeA significantly exacerbates compulsive-like eating behaviors, even in the face of adverse consequences. The study reveals notable colocalization of D2Rs and InsRs in the CeA, where the absence of D2Rs reduces InsR expression and compromises insulin signaling. Furthermore, pharmacological activation of D2Rs has been shown to enhance InsR phosphorylation and promote insulin signaling, indicating a pivotal modulatory role of D2Rs in InsR function.
These findings emphasize the critical interaction between D2Rs and InsRs in the CeA, which is essential for regulating brain insulin sensitivity and influencing both normal and maladaptive eating patterns. This research provides novel insights into the relationship between dopamine and insulin signaling, with significant implications for understanding neurological disorders associated with metabolic and reward dysregulation. [NPID: Dopamine, reward, highly-palatable, ultraprocessed, addiction, insulin signaling]
Year: 2026
