Several studies of ATM deficiency in a mouse model have been carried out. Atm −/− mice display an early defect in glucose-stimulated insulin release and later develop hyperglycaemia, and insulin resistance[1]. Unpublished data from the McCrimmon Group at University of Dundee suggest that mice heterozygous for ATM deficiency have impaired fasting glucose, but demonstrated a marked improvement in fasting glucose with metformin. A Cell Reports paper, detailing a mouse model of ATM deficiency, demonstrates insulin resistance in ATM deficient mice, with a lipodystrophic phenotype[2]. This phenotype (paucity of subcutaneous fat, and increased visceral fat) was attenuated by metformin and thiazolidinedione (TZD) use.