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Maturation of rat renal phosphate transport: effect of triiodothyronine
S Euzet1, M Lelièvre-Pégorier, C Merlet-Bénichou
1Unité de Recherches sur le Développement Normal et Pathologique des Fonctions Epithéliales, INSERM U.319, Université Paris 7, France.
Insights
Thyroid hormone (T3) precociously matures renal phosphate (Pi) transport in young rats. This study shows T3 administration enhances Pi reabsorption and transporter expression, suggesting its role in normal Pi transport development.
Area of Science:
- Endocrinology
- Nephrology
- Molecular Biology
Background:
- Weaning normally increases renal phosphate (Pi) transport affinity and plasma 3,5,3'-triiodothyronine (T3) levels between postnatal days 14-21.
- The role of T3 in regulating Pi transport maturation is not fully understood.
Purpose of the Study:
- To investigate the role of T3 in the maturation of renal phosphate (Pi) transport.
- To determine if exogenous T3 can induce precocious maturation of Pi transport in immature rats.
Main Methods:
- Clearance experiments and brush-border membrane vesicle studies were conducted on 14-day-old rats administered T3.
- Phosphate (Pi) excretion and reabsorption rates were measured.
- Na(+)-cotransported Pi uptake kinetics (affinity and Vmax) and Pi transporter (NaPi-2) expression were analyzed.
Main Results:
- T3 administration significantly reduced fractional Pi excretion and increased Pi reabsorption.
- Brush-border membrane vesicles showed increased carrier affinity (30%) and Vmax (46%) for Na(+)-cotransported Pi.
- Immunoreactive Pi transporter levels were elevated in T3-treated rats, while glucose transport remained unaffected.
Conclusions:
- Exogenous T3 administration induces precocious maturation of renal Pi transport in 14-day-old rats.
- Thyroid hormone (T3) is likely involved in the normal developmental maturation of renal Pi transport.
- T3 specifically affects Pi transport, not other Na(+)-dependent systems like glucose transport.
Abstract:
1. Prevention of weaning prevents the increase in the carrier affinity for Na(+)-cotransported phosphate (Pi) and the normal elevation of plasma 3,5,3'-triiodothyronine (T3) which occur between postnatal days 14 and 21. 2. This study examines the possible role of T3 in the control of the maturation process of Pi transport. Clearance experiments and brush-border membrane studies were performed on 14-day-old rats given T3. 3. The fractional excretion of Pi of T3-treated rats was 33% lower compared with controls (P < 0.01). After Pi perfusion, it remained at a lower level, and the amount of Pi reabsorbed per minute, corrected for the glomerular filtration rate (RPi/GFR), was higher. 4. The membrane vesicles from 14-day-old rats given T3 showed a 30% increase in carrier affinity for Na(+)-cotransported Pi. In addition to this maturational effect of T3, a 46% increase in Vmax was also observed. 5. The amount of immunoreactive Pi transporter, detected using anti-(NaPi-2) antiserum, was increased in T3-treated rats. 6. Glucose transport, another Na(+)-dependent transport system, was not altered by T3. 7. It is concluded that exogenous T3 given before the third postnatal week specifically induced precocious maturation of renal Pi transport in 14-day-old rats, suggesting that thyroid hormone is normally involved in this maturation.