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

Abstract

Fetal rat kidney showed g l y c y deposition that reached a maximal value of 60 pg *mg prot on day I8 and declined thereafter. At birth glycogen concentration is reduced (20 ~m m g prot-') but higher than adult one (cortex, 2.2 p g a m g prot-a d medulla, 3.4 p g * m g prot-I). From day 17 to the birtb, gtycogen synthetase and phospborylase activities increased slowly except for acid glucosidase activity which inereased rapidly between day 18 to the birth (3-fold). Corticosterokl deprivation had no effect upon glycogen content but fetal decapitation on day 16 reduced glycogen content in kidney of 19day-old fetuses.In the adult kidney, the concentration of glycogen, which is mainly localized in collecting ducts (18,20) is extremely low compared with other organs such as liver, heart of muscle. Glywgen turnover rate is more rapid in the medulla than in the cortex (18). It has been observed in several species (2, 15,25) that the glycogen concentration in kidneys of newborn animaln is relatively high and as far as we know, no data are available in the fetus. In the rat, Dicker and Shirley (8) have made a correlation between the progressive disappearance of renal glycogen during the 2-3 wk after birth and an initially high rate of anaerobic glycolysis that subsequently decreases to levels found in the adult. According to these authors the major source of ATP in neonatal kidney is anaerobic glycolysis whereas aerobic glycolysis predominates in the adult. Consequently, an increased glucose requirement, which may be supplied by glycogen mobilization, may be expected in the kidney of young rats. The differentiation of rat kidney is known to take place a few days before birth (6,21). Assuming that renal glycogen may play an impurtant role in providing energy for difierentiation and maturation during the perinatal period, we studied the evolution of renal glycogen concentration in relationship to enzyme activities involved in glycogen metabolism in fetal and newborn rats. In addition an eventual endocrine control of glycogen metabolism was also investigated. MATERIALS AND METHODSThe female rats used in these experiments were of the Sherman strain whose length of gestation was 21 days. Fetuses between 1 6 21 days of gestation were used. EXPERIMENTAL PROCEDURESMaternal adrenalectomy and metopirone treatment. In order to suppress corticosteroids in fetal plasma, maternal adrenalectomy was associated with metopirone treatment as previously described (10). Maternal adrenalectomy was performed at days 15 or 16 of gestation. Pregnant rats were then injected subcutaneously with metopirone at a dose of 10 mg twice daily until (days 18 or 21). Metopirone, which has been kindly supplied by CIBA laboratory, is a steroid hydroxylase inhibitor crossing the placental barrier. The effectiveness of treatment was routinelv controlled bv verifying the enlargement of the fetal adrenal g&ds. Fetuses i f adrenalectomized-treated mothers were compared with "control" fetuses of sham-omrated mothers.Fetal decapitation. Hypothalamo-hypophyseal and ...

Role of Catecholamines in the Control of Newborn Kidney Adenine Nucleotide Content

“…In previous experiments, we had found that in postmature fetuses, where there is an important increase in plasma glu cagon level, the kidney EC remains low until delivery. Since, in addition, it has been es tablished by Delaval et al [8] that kidney glycogen stores are not utilized at birth, it seems clear that the scheme proposed by Sut ton and Pollack [4] to explain the EC rise in the newborn liver cannot be applied to the newborn kidney.…”

Glycogen and Enzymes of Glycogen Metabolism in Rat Embryos and Fetal Organs

“…In every tissue there is a shift to a marked preponderance of phosphory lase over synthase activity, compared with ratios that favor synthase in the developing organism (tables 1,2). This is true for the brain [Watanabe and Passonneau, 1973], liver [Khandewal et al, 1984[Khandewal et al, , 1985, kidney [Delaval et al, 1983] and heart [De Tata et al, 1983;Williams and Mayer, 1966].…”