Epidemiological studies have revealed strong and reproducible links between indices of poor fetal growth and susceptibility to the development of glucose intolerance and insulin resistance syndrome in adult life. To explain these associations, the thrifty phenotype hypothesis has been proposed. Mitochondrial DNA abnormalities have been known to cause insulin deficiency, insulin resistance and diabetes mellitus. In this review, we propose that mitochondrial dysfunction is a link between malnutrition during early life and disease in adult life. The potential mechanism for mitochondrial dysfunction will be focused on availability of the taurine and nucleotides, and imprinting on the genes.