Related Experiment Videos
Renal adaptation to phosphorus deprivation: characterization of early events
B S Levine1, L D Ho, K Pasiecznik
1Medical Service, Veterans Administration Wadsworth Medical Center, CA.
Insights
Early renal adaptation to low phosphorus (P) involves a rapid increase in phosphate (Pi) uptake, independent of parathyroid hormone and protein synthesis. This adaptation is signaled by a drop in serum P levels.
Area of Science:
- Nephrology
- Renal Physiology
- Nutritional Science
Background:
- Dietary phosphorus (P) intake significantly influences renal function.
- The kidney plays a crucial role in maintaining phosphorus homeostasis.
- Rapid adaptive mechanisms in the kidney are essential for nutrient balance.
Purpose of the Study:
- To investigate the early events and molecular mechanisms preceding renal adaptation to low dietary phosphorus.
- To characterize the time course of changes in renal phosphate transport.
- To determine the role of parathyroid hormone and protein synthesis in this adaptation.
Main Methods:
- Rats were fed either a high (0.6%) or low (0.03%) phosphorus diet.
- Renal brush border membrane vesicles were isolated at 1, 2, and 4 hours post-gavage.
- Na-dependent phosphate (Pi), glucose, and proline transport were measured; experiments included thyroparathyroidectomy and administration of actinomycin D or cycloheximide.
Main Results:
- Low dietary phosphorus led to a significant decrease in serum phosphorus levels within 1 hour.
- Renal Na-dependent Pi uptake increased by approximately 59% in the low phosphorus group at 4 hours.
- This adaptation was independent of parathyroid hormone and did not require de novo protein synthesis.
Conclusions:
- Early renal adaptation to low dietary phosphorus is a rapid process, occurring within 4 hours.
- The adaptation involves an increase in phosphate transport, potentially due to altered carrier availability or activity.
- The primary signal for adaptation may be the reduction in serum phosphorus or filtered phosphate load.
Abstract:
Renal adaptation to low dietary phosphorus (P) can occur within 4 h. To characterize events preceding adaptation, rats were gavaged with 0.6% P (+P) or 0.03% P (-P) diet and killed 1, 2, or 4 h later. Brush border membrane vesicles were prepared and Na-dependent phosphate (Pi), glucose, and 1-proline transport were measured. In intact rats, 1 h after gavage, serum P in +P was 8.0 +/- 0.5 and in -P, 6.1 +/- 0.4 mg/dl, p less than 0.01. One and 2 h after gavage, Pi uptake was similar between groups; at 4 h, 0.25 min Pi uptake was increased by 59.3% +/- 14.8 in -P, p less than 0.02, n = 11. In thyroparathyroidectomized rats, Pi uptake increased in -P by 40.1% +/- 7.4 compared to +P at 2.5 h after gavage, and by 51.3 +/- 9.3 at 4 h, p less than 0.025, n = 11. When actinomycin D or cycloheximide were administered both 16 h prior to and at gavage, 0.25 min Pi uptake 4 h after gavage was 59.1% +/- 14 and 60.6% +/- 19 higher in -P than +P, respectively, p less than 0.025. The adaptation was detected only when measured with an inward-directed Na-gradient. Na-dependent glucose and proline uptakes were not changed by -P diet. These studies demonstrate that early renal adaptation to low dietary P is preceded by a fall in serum P, is independent of parathyroid hormone, and does not require protein synthesis. Early adaptation may represent an increased rate of carrier movement or a change in availability of already synthesized carrier. The signal for adaptation may be the decrease in serum P, or filtered load of phosphorus.