Cellular metabolism is a key determinant of macrophage activation, thereby fundamental to their diverse functions in regulating tissue homeostasis, inflammation and clearing invading pathogens. The intracellular parasite Leishmania is dependent on its host macrophage for all nutrient and energy resources and interventions that modulate macrophage metabolism and boost pro-inflammatory functions are emerging as an attractive alternative therapeutic. Here, we have repurposed the common oral anti-diabetic drug Metformin and determined its effect on cutaneous infection with Leishmania. Leishmania-susceptible Balb/c mice were infected intradermally with L. mexicana and administered metformin (1.0 and 0.15 mg/kg/day) in drinking water for the duration of the experiment. Compared to controls, metformin-treated mice exhibited milder cutaneous lesions indicating a reduced persistence of disease. We next generated a L. mexicana strain expressing TurboRFP (TurboRFP-L. mexicana) to quantify parasite infection in vitro by flow cytometry. Bone-marrow derived macrophages (BMDM) were then infected with TurboRFP-L. mexicana in the presence of Metformin. In line with in vivo results, Metformin treatment was deleterious to parasite growth and further augmented parasite clearance in the presence of pro-inflammatory cues lipopolysaccharide (LPS) and interferon-gamma (IFN-γ). However, this was not associated with increased macrophage production of nitric oxide, a potent anti-leishmanial, and instead Seahorse extracellular flux assays pointed towards mechanisms involving mitochondrial function and ROS production. Overall this work establishes Metformin as a potential host-based anti-leishmanial intervention.