SummaryTriamcinolone (20 μg per fetus) administeredin uteroto term rat fetuses (day 21 of gestation) increases the activities of renal G-6-Pase and PEPCK. The absence (or marked decrease) of circulating corticosteroids in fetuses from adrenalectomized, metopirone-treated mothers has, however, no clear effect on the enzyme activities. Therefore, it is doubtful that corticosteroids play a role in the development of G-6-Pase and PEPCK activities during the fetal period of life.In 21-day-old fetuses entirely decapitated on day 18, both enzyme activities are lower than in intact fetuses of the same litter (G-6-Pase, −48%; PEPCK, −36%). In partially decapitated fetuses, the activity of G-6-Pase remains at the control level, whereas the PEPCK activity is clearly reduced (-39%). These results strongly suggest that on the last days of gestation the hormone group of parathormone, calcitonine, or thyroxine controls the G-6-Pase activity, whereas the hypothalamo-hypophysis system is implied in the development of PEPCK activity.Parathormone (1 unit per fetus) administered to decapitated fetuses completely restores the G-6-Pase activity. Neither rat growth hormone, synacthene, nor arginine vasopressin has significant effects on the activity of PEPCK in the kidneys of decapitated fetuses.The administration of 0.5 μmole of dibutyryl-cAMP or cyclic adenosine 3′5′-monophosphate (cAMP) to decapitated fetuses completely restores the activity of renal PEPCK, suggesting that the development of PEPCK is controlled by cAMP-dependent hormone. The same dose of dibutyryl-cAMP has no effect on the activity of G-6-Pase; cAMP produces a slight but significant increase of this enzyme activity.SpeculationThe development of renal gluconeogenesis during the fetal period is probably controlled by several hormonal factors which do not include corticosteroids.