29, 30 However, premature activation of the gluconeogenic pathway, especially an increase in expression of Hnf4α and Pck1/Pck2, in fetuses exposed in utero to dexamethasone or to maternal HFD, has been associated with adulthood diabetic symptoms in both rodents and monkeys.9, 31, 32 This suggests that gluconeogenic gene activation before birth may be a common underlying mechanism for fetal programming of adult metabolic diseases. The gene discussed is HNF4A; the disease is metabolic disease.