Hexarelin, a growth hormone - releasing peptide, counteracts bone loss in gonadectomized male rats.
Sibilia. V V; Cocchi. D D; Pagani. F F; Lattuada. N N; Moro. G L GL; Pecile. A A; Rubinacci. A A; Muller. E E EE; Netti. C C
Key Findings
- Hexarelin sharply reduced urinary bone‑resorption markers (LP and HP) within a week in intact rats.
- In testosterone‑deficient (GDX) rats, hexarelin blocked the surge in bone‑resorption markers and the drop in bone‑formation enzyme (ALP).
- Hexarelin prevented the decline in bone mineral density at the lumbar spine and femoral metaphysis that normally occurs after gonadectomy.
Practical Outcomes
- For biohackers interested in bone health, hexarelin shows promise as a GH‑secretagogue that may also directly curb bone loss, especially in low‑testosterone or aging contexts. However, the data are from rats, the dosing (50 µg/kg twice daily) isn’t translated to humans, and safety/efficacy in people are untested, so any real‑world use would be experimental and should be approached with caution.
Summary
In a rat study, the peptide hexarelin (a strong growth‑hormone releaser) was given twice daily for a month. In normal rats it lowered markers of bone breakdown but didn’t change bone density. In rats that had their testes removed (a model of low testosterone and bone loss), hexarelin stopped the rise in bone‑resorption markers, kept bone‑formation activity up, and prevented the loss of bone density in the spine and thigh bone.
Abstract
The age-related decline in growth hormone (GH) secretion has been implicated in the pathogenesis of involutional bone loss. Whether restoration of GH secretion might be helpful in maintaining and/or improving bone mass during aging is still unsettled. The aim of the present study was to examine the effects of 30-day treatment with hexarelin (HEXA, 50 microg/kg subcutaneously b.i.d.), a highly effective GH-releasing compound, on bone metabolism and bone mineral density (BMD) in intact and osteopenic gonadectomized (GDX) mature male rats. Serum total alkaline phosphatase (ALP, bone formation marker) and bone resorption markers (lysylpyridinoline, LP and hydroxylysylpyridinoline, HP) were measured before and 7, 14 and 30 days after treatment. BMD was measured by dual-energy X-ray absorptiometry at lumbar vertebrae, femoral metaphysis and diaphysis before and at the end of the experiment. In intact rats, HEXA significantly (P<0.05) decreased LP (-36.3%) and HP (-22.8%) excretion at day 7, whereas it did not change serum ALP activity and BMDs. In GDX rats, HEXA completely prevented the significant (P<0. 01) increase in urinary excretion of both LP (+143.8%) and HP (+119. 4%), the early decrease in ALP activity (-26.5%) and the significant (P<0.05) decrease in BMDs in the femoral metaphysis (-7.9%) and lumbar vertebrae (-6.8%) caused by androgen deficiency. The bone-protective effects of HEXA could be attributed, at least in part, to its GH-releasing activity since chronic-treated rats maintained the GH response to an acute challenge with HEXA. The evidence that HEXA, unlike GH, inhibits bone resorption indicates that other mechanisms contribute to the bone sparing effect of HEXA.
Study Information
pubmed
1999
10.1054/ghir.1999.0105