Evelyne Delaval

Renal Glycogen Content and Hormonal Control of Enzymes Involved in Renal Glycogen Metabolism

Summary: Fetal rat kidney showed glycogen deposition that reached a maximal value of 60 μ g·mg prot−1 on day 18 and declined thereafter. At birth glycogen concentration is reduced (20 μ g·mg prot−1) but higher than adult one (cortex, 2.2 μ g·mg prot−1 and medulla, 3.4 μ g·mg prot−1). From day 17 to the birth, glycogen synthetase and phosphorylase activities increased slowly except for acid glucosidase activity which increased rapidly between day 18 to the birth (3-fold). Corticosteroid deprivation had no effect upon glycogen content but fetal decapitation on day 16 reduced glycogen content in kidney of 19-day-old fetuses.

Development of ammonia and glucose productions from glutamine in foetal rat kidney; Effects of metabolic acidosis

Ammoniagenesis and gluconeogenesis have been studied in foetal rat kidneys during the five last days of gestation by measuring in vitro NH3 and glucose productions from glutamine and by assaying activities of soluble phosphoenolpyruvate carboxykinase (PEPCK) and glucose 6-phosphatase (G6Pase). These studies were carried out in normal (mean blood pH: 7.30) and acidotic (pH: 7.12) foetuses. In normal foetuses, NH3 production by kidney cortex slices remains constant throughout the studied period of development, at a level 10-fold lower than the maternal one. On day 20 of gestation, a low glucose production (20-fold lower than the maternal one) appears for the first time. This may be related to an increase of PEPCK and G6Pase activities which occurs between day 19 and 20. In 20 days old foetuses, NH4Cl induced acidosis stimulates NH3 production but has no effect on PEPCK activity and glucose production. A response of gluconeogenesis to acidosis is observed one day later (day 21).

Hormonal Control of Glucose-6-phosphatase and Phosphoenolpyruvate Carboxykinase Activities in the Fetal Rat Kidney

Summary: Triamcinolone (20 μg per fetus) administered in 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, 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.Speculation: The development of renal gluconeogenesis during the fetal period is probably controlled by several hormonal factors which do not include corticosteroids.

Effect of Maternal Hyperglycemia on NaK ATPase Activity in Fetal Rat Kidney

The effect of moderate hyperglycemia on renal ATP production and ATPase activity of rat fetus was investigated using the experimental procedure of maternal continuous infusion of glucose during the last 5 days of gestation. Glucose-infused mothers and their fetuses showed a high level of glycemia (8.8 and 5.5 mM, respectively) and a high level of insulinemia (3 times higher than in controls). No change in either ATP or ADP concentration was detectable but an increase in NaK ATPase activity occurred without any change in Mg ATPase activity. These modifications should be the result of an enhanced Na/glucose cotransport leading to an enhanced extrusion of Na at the basolateral membrane. These results indicate that immature kidney is able to increase NaK ATPase activity to maintain Na homeostasis.

Role of catecholamines in the control of newborn kidney adenine nucleotide content

During the 1st h of extrauterine life, the adenine nucleotide content of the rat kidney is modified: the ATP level increases (+30%) while ADP and AMP are lowered (-30 and -50%, respectively). This leads to a high value of energy charge in the newborn kidney (0.89 vs. 0.80 in the fetus). It was possible to obtain in utero a similar modification of ATP, ADP, AMP concentrations by injections to the fetuses of cAMP, dibutyryl cAMP, or isoprenaline. Conversely, the postnatal changes in adenine nucleotide content could be prevented by administration to the fetus, just before birth, of beta- or beta 1-adrenoreceptor antagonists. Therefore the rise of kidney energy charge following parturition appears to be under hormonal control. Glucagon had no effect on kidney adenine nucleotide content. It is strongly suggested that the catecholamines released at the time of parturition are the triggering factor of this evolution.