Both obesity and type 2 diabetes (if co-existent also referred to as diabesity) can suppress the hypothalamic-pituitary-testicular (HPT) axis at multiple levels, and men with diabesity commonly present with a lowered testosterone. Such men commonly have non-elevated gonadotrophins. However, there is evidence, both pre-clinical and to a lesser extent from clinical studies in men, that diabesity can interfere with Leydig cell function via multiple mechanisms. These include disordered adipokine signalling (leptin, adiponectin), inflammation and reactive oxidative stress, and disordered micro-RNA signalling. From a therapeutic perspective, lifestyle measures (or medical/surgical weight loss interventions) with focus on achieving a healthy body weight and optimisation of diabetic control is the logical treatment, and, if successful, can restore HPT axis suppression. If these first-line approaches fail or are not sufficient, testosterone treatment can replace Leydig cell testosterone secretion but does not restore and might even reduce fertility. However, in contrast to organic hypogonadism, the risk-benefit ratio of testosterone treatment for patient-important health outcomes in men with diabesity-related HPT axis suppression remains uncertain.