Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder marked by hyperglycemia, hyperinsulinemia, and altered insulin signaling. Current investigations propose that insulin not only participates in general metabolic processes but also exerts influence over brain functions. Also, altered insulin signaling is observed in conditions like Alzheimer's Disease and Obsessive-Compulsive Disorder. Despite evidence, current treatments targeting insulin signaling lack validation for mental disorders. Understanding insulin's role in concurrent mental and somatic disorders may reveal strategies for prevention and treatment. We previously confirmed the association between metabolic and cognitive alterations in a mouse model of T2DM (TALLYHO/JngJ, TH), which spontaneously exhibits hyperglycaemia and insulin resistance, together with deficits in attention and perseveration. The objective of this study was to explore the therapeutic potential of a primary antidiabetic agent, metformin, as a strategy to mitigate both mental and somatic abnormalities. Subchronic administration of metformin (300 mg/kg/day) commenced at 17 weeks of age for male TH mice and their controls. Via fully automated metabolic cages, we evaluated lipid and carbohydrate metabolism, locomotion, energy expenditure, and food and water intake. We then assessed memory, attention and compulsivity-related deficits via validated behavioural test paradigms. Metformin administration regulated weight gain and contrasted baseline hyperglycaemia in TH mice while also mitigating deficits in attention and spatial memory. This study supports the hypothesis that metformin administration can counteract both somatic and mental impairments, thus strengthening its therapeutic potential in T2DM-associated comorbidities. This project was funded by the EU Horizon 2020 research and innovation programme (grant N. 847879).