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Metabolic diseases are complex, multi-factorial disorders caused by genetic and environmental factors, where the prenatal environment also plays a prominent role. Not only is maternal diabetes associated with increased risks of complications during pregnancy, but a hyperglycemic environment in utero increases the child’s risk of long-term adverse health including abnormal glucose tolerance and development of metabolic disease. The interplay between genetic and environmental factors can alter the phenotype of the developing fetus but this area is largely unexplored. Telomeres are noncoding repeats that protect the ends of our chromosomes and they shorten during each replication cycle. The dynamics of telomeres appear to play a role in progression of metabolic disease, and the intrauterine environment may contribute to the establishment of shorter telomeres in the child.
Using a Danish cohort of children of women with or without GDM (n=1234), the aim of this study was to investigate if diabetes in pregnancy may affect the telomere lengths of the child´s DNA, and thereby affect the child´s risk of metabolic disease later in life. We measured telomere length in blood cell DNA from 9-16-year-old GDM offspring and controls. We found that in utero exposure to GDM is associated with shortened telomere length in girls, and that telomere length was negatively associated to insulin levels and HOMA-IR in the girls only. These results suggest that GDM has sex-specific long-term effects on offspring telomere length. The shortened telomere length in blood cells of GDM offspring might contribute to and/or predict risk of metabolic disease in the GDM offspring.