Thus, it cannot be excluded that obesity development in O-GDM and O-T1DM may have been initiated by subtle impairments of adipose tissue leptin production due to increased LEP DNA methylation causing impaired appetite suppression, adiposity, and eventually a new balanced/compensated metabolic state with normal or increased plasma leptin levels in the face of decreased tissue gene expression levels. The gene discussed is LEP; the disease is type 1 diabetes mellitus.