Endocrine Abstracts

Aldosterone is the main steroid hormone controlling sodium homeostasis in human. During the neonatal period, full term newborns and more specifically premature infants, are subjected to an impaired renal capacity to reabsorb sodium, responsible for sodium loss and failure to thrive which could be linked to a renal aldosterone unresponsiveness at birth. A clinical prospective study on 50 newborns and their mothers, revealed high aldosterone and renin levels in umbilical blood s...

Renal and cardio-vascular complications of prematurity are well established, notably those associated with renal tubular immaturity, responsible for major salt loss at birth, as well as early hypertension in adulthood. However, the molecular underlying mechanisms remain poorly understood. Our objective was to investigate the impact of preterm birth on the ontogenesis of renal corticosteroid pathways, to evaluate its implication on perinatal complications and on the emergence o...

The Mineralocorticoid Receptor (MR), a hormone-activated transcription factor that mediates sodium-retaining action of aldosterone, is highly expressed in the distal nephron in which large variations in extracellular fluid tonicity are generated by the cortico-papillary gradient. However, mechanisms regulating MR expression remain sparse. We recently showed that extracellular tonicity modulates renal MR expression through posttranscriptional mechanisms (Viengchareun, Mol Endoc...

Sex differences have been demonstrated in various biological processes such as arterial blood pressure. However, the potential sex dimorphism of the renin-angiotensin-aldosterone system and, by extension, the mineralocorticoid receptor (MR) signaling pathway, major regulators of blood pressure, has only been poorly studied, notably in the kidney. Basal systolic blood pressure (SBP) and heart rate (HR) were measured in adult male and female mice. Renal gene expression studies o...

The Mineralocorticoid Receptor (MR, NR3C2) mediates sodium-retaining action of aldosterone. Recently, we have shown that the physiological sodium loss observed in newborns in their first days of life is due to a low renal MR expression. However, the underlying molecular mechanisms remain unknown to date. In the adult renal KC3AC1 cell line, we demonstrated that variations in extracellular tonicity, which exist in the nephron, modulate MR expression by posttranscriptio...

The 11-beta hydroxysteroid dehydrogenase (11βHSD) isozymes are well-known regulators of glucocorticoid hormone metabolism: 11βHSD2, mostly expressed in the distal nephron, converts cortisol [F] into cortisone [E] in humans or corticosterone into 11-dehydrocorticosterone in rodents (11-dehydro derivatives being inactive compounds), and 11βHSD1, ubiquitously expressed but predominantly in the liver, catalyzes the opposite reaction. Under pathophysiological conditi...