Following the well-established relationship between congenital IGF-1 deficit and onset of cardiovascular and metabolic diseases in humans [18] along with the radiation-induced IGF-1 signaling deterioration observed in radiotherapy patients and in preclinical models of radiation injury [42,43,45], we attempted to begin establishing a large animal model to study the late effects of radiation, specifically one that could mimic IGF-1 deficiency and its associated development of cardio-metabolic abnormalities after exposure to relatively low doses of radiation. This evidence concerns the gene IGF1 and Other metabolic disease.