We therefore hypothesize that diabetes-predisposing variants at this locus may increase levels of circulating glucose in pregnant mothers (i.e. which would tend to increase intrauterine growth and offspring birth weight), but simultaneously act to decrease offspring birth weight when the same alleles are transmitted to the fetus (e.g. by impairing beta cell function and therefore fetal insulin secretion). The gene discussed is INS; the disease is diabetes mellitus.