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GTP-dependent protein(Gs) activity in preterm infants
C Marguet1, J P Basuyau, P Brunelle
1Developmental Biology Group Research, Hospital Charles Nicolle, Rouen, France.
Insights
This study investigated if immature stimulatory GTP-dependent protein (Gs) causes renal resistance to parathyroid hormone (PTH) in newborns. Results indicate Gs protein is not involved in early neonatal hypocalcemia or PTH resistance.
Area of Science:
- Neonatology
- Pediatric Endocrinology
- Molecular Physiology
Background:
- Previous research identified renal resistance to parathyroid hormone (PTH) in preterm infants during the first week of life, potentially explaining neonatal hypocalcemia.
- Renal resistance to PTH is known in pseudohypoparathyroidism type 1, linked to defects in the stimulatory GTP-dependent protein (Gs).
Purpose of the Study:
- To investigate the potential role of functional immaturity in the Gs protein in the pathophysiology of early renal resistance to PTH in newborns.
- To determine if Gs protein activity correlates with gestational age, birth weight, or the presence of hypocalcemia in neonates.
Main Methods:
- Studied 27 newborn infants (7 full-term, 20 preterm).
- Assessed biological activity of the Gs unit via bioassay on days 1, 3, and 10 postpartum.
- Analyzed correlations between Gs unit activity, gestational age, birth weight, and infant calcium levels.
Main Results:
- No correlation was found between Gs unit activity and gestational age or birth weight.
- Infants with hypocalcemia showed no difference in Gs unit activity compared to normocalcemic infants.
- Gs unit activity was present and measurable from 29 weeks of gestation.
Conclusions:
- The Gs protein does not appear to be implicated in the early renal resistance to PTH observed in preterm infants.
- Functional immaturity of the Gs protein is unlikely to be the cause of early neonatal hypocalcemia related to PTH resistance.
Abstract:
In a previous study, we showed a renal resistance to PTH in preterm infants during their 1st week of life. We proposed it could explain early neonatal hypocalcemia. Such renal resistance is well known in type 1 pseudohypoparathyroid patients and is explained by a defect of stimulatory GTP-dependent protein (Gs). To determine if functional immaturity in the Gs protein could be involved in PTH resistance, we studied 27 newborn babies: 7 full-term and 20 preterm babies. Biological activity of the Gs unit was determined on days 1, 3 and 10 after delivery by bioassay. No correlation was found between the Gs unit activity and either gestation or birth weight at these dates. Eight infants had hypocalcemia and their Gs unit activity did not differ from those with normocalcemia. Furthermore, we showed that the Gs unit is active from 29 weeks of gestation. We conclude that the Gs protein appears not to be involved in the pathophysiology of early renal resistance to PTH and therefore in early neonatal hypocalcemia.