Early increase in pulsatile growth hormone release after unilateral nephrectomy in adult rats.
Haramati. A A; Lumpkin. M D MD; Mulroney. S E SE
Key Findings
- Unilateral kidney removal caused a 3‑4× increase in pulsatile GH levels 24 hours after surgery.
- The GH surge was temporary, falling back toward baseline by 48 hours.
Practical Outcomes
- For most biohackers, this study offers limited direct use because it involves a surgical model in rats and a GH‑blocking drug, not a supplement you would take. It does suggest that short‑term spikes in GH can drive organ growth, which might be relevant when considering GH‑related interventions, but there’s no actionable protocol for humans from this data.
Summary
In rats that had one kidney removed, the body quickly released a lot more growth hormone (GH) for about a day, which helped the remaining kidney grow larger. When researchers gave the rats a drug that blocks the signal that makes GH release (a GRF‑1‑29 antagonist), the GH spike was reduced and the kidney didn't grow as much. The effect was short‑lived, dropping back toward normal after two days.
Abstract
Removal of one kidney results, within days, in accelerated growth of the remaining kidney. However, the mechanisms that underlie this compensatory renal hypertrophic response, particularly in the early time period following nephrectomy, are not understood. In this study we tested the hypothesis that removal of one kidney leads to a change in the pulsatile release of growth hormone (GH), which facilitates compensatory renal growth. Adult Wistar rats were implanted with Silastic cannulas in jugular veins and underwent either unilateral nephrectomy (UNX) or sham operation. Plasma levels of GH were determined 24 and 48 h after sham operation or UNX. Blood samples were taken every 20 min over a 6-h period from conscious, unrestrained animals. Pulsatile GH release was markedly elevated 24 h after UNX in both the amplitude of the surges as well as in the duration of release. Peak GH levels after 24 h were three- to fourfold higher in UNX rats compared with sham controls (417 +/- 75 vs. 119 +/- 23 ng/ml, P < 0.05). However, this enhanced release of GH appeared to be of short duration and began declining by 48 h post-UNX (peak level of 227 +/- 37 ng/ml, P < 0.05 vs. both 24 h UNX and sham controls). To examine whether this rise in GH release post-UNX contributed to the compensatory renal growth, rats underwent UNX and were immediately treated with an antagonist to GH-releasing factor (GRF-AN; i.e., [N-Ac-Tyr1,D-Arg2]GRF-(1-29) amide, 200 micrograms/kg twice daily), and the effects on GH release and renal growth were determined. Administration of GRF-AN significantly suppressed the increase in GH release post-UNX and was associated with a significant attenuation in renal growth 48 h post-UNX in GRF-AN-treated rats (8.7 +/- 2.6% vs. 22.7 +/- 3.0% in UNX controls, P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
Study Information
pubmed
1994
10.1152/ajprenal.1994.266.4.f628