Additionally, the chronic exposure of isolated human islets to leptin, an adipokine also increased during GDM, blunted on one hand the production of the IL-1 receptor antagonist (IL-1Ra), that inhibits IL-1β signaling, and on the other hand induced IL-1β release leading to impaired β-cell function, caspase-3 activation and apoptosis [70]. This evidence concerns the gene LEP and gestational diabetes.