Hormonal control of glucose-6-phosphatase and phosphoenolpyruvate carboxykinase activities in the fetal rat kidney

Abstract

Triamcinolone (20 μg per fetus) administered hi utero to 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, me- topirone-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 fimole 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. Speculation: The development of renal gluconeogenesis during the fetal period is probably controlled by several hormonal factors which do not include corticosteroids. © 1981 International Pediatric Research Foundation, Inc.