<p>Type 2 diabetes mellitus (T2DM) is a systemic metabolic disorder increasingly implicated in central nervous system (CNS) dysfunction, yet the molecular substrates underlying diabetes-induced dopaminergic (DAergic) dysregulation remain poorly defined. This study evaluated region-specific alterations in DAergic neurotransmission within the hippocampus, striatum, and prefrontal cortex, and their association with social behavioral deficits in diabetic mice. According to the weight and age of the animal, two groups were designated as the control group and the diabetes group. The control group was designated as group 1, and the diabetic group was designated as group 2. In group 2, diabetes was caused by injecting 50&#xa0;mg/kg of streptozotocin for five consecutive days in them. The behavioural tests were performed after eight weeks of inducing diabetes. On the 60th day, from the striatum, hippocampus, and cortex, total RNA was taken out after the dissection. Real-time polymerase chain reaction was used to carry out expression analysis. STZ-induced diabetic mice showed normal sociability and social novelty preference but exhibited a marked decline in social recognition memory, indicating selective impairment of long-term social cognition. Region-specific dysregulation of dopaminergic signaling was evident, particularly in the striatum and cortex. These transcriptional alterations likely represent compensatory neuroadaptive mechanisms responding to oxidative and neuronal stress induced by diabetes, suggesting that T2DM-driven dopaminergic imbalance contributes to cognitive and neurobehavioral dysfunction. T2DM induces differential dysregulation of dopaminergic signaling across cortical and subcortical regions, contributing to selective deficits in social cognition. These findings highlight potential therapeutic targets for mitigating diabetes-associated neurobehavioral dysfunction.</p> Graphical Abstract <p></p>