Although insulin is a well-known cause of body weight gain, it is not clear whether it is due to the accumulation of fat or lean mass. We performed a 3 months Body-Impedance Analysis follow-up in 72 diabetic patients in a wide range of insulin indications: insulin introduction in young inaugural type 1 diabetics (n = 12), late-onset type 1 (n = 12), type 2 affected by intercurrent diseases (n = 12) or microangiopathic complications (n = 12), type 2 with failure of oral antidiabetic agents (n = 12), and insulin withdrawal in type 2 (n = 12). In type 1 patients, insulin led to the most important weight gain, but it was fat-free, with a major benefit on HbA1C. Type 2 patients affected by intercurrent diseases or microangiopathic complications had a mild, also fat-free weight gain, with a clear benefit on HbA1C. In type 2 patients with failure of oral agents, HbA1C declined less, weight gain was intermedia, but predominantly fat, mirrored by a predominant fat loss in type 2 patients whose insulin was stopped (without significant change in HbA1C). Both fat and lean mass contributed to insulin-induced body weight gain, but a significant negative relationship existed between their respective evolution in our patients (r = -0.23, p < 0.05 by linear regression analysis between delta fat mass and delta lean mass). Insulin-induced body weight gain is not univocal: insulin restaures or protects lean mass in its less controversial indications, whereas it leads to fat accumulation in type 2 patients with isolated failure of oral agents.