Study summary · research use only
Ghrelin regulates proliferation and differentiation of osteoblastic cells
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this rat study, the authors evaluated ghrelin, the endogenous ligand of growth hormone secretagogue (GHS) receptors, on proliferation and activity of primary rat calvarial osteoblasts, comparing it with the synthetic GHS hexarelin (HEXA) and EP-40737. They report that ghrelin and HEXA (at 10(-10) M) increased osteoblast proliferation and raised alkaline phosphatase and osteocalcin production, whereas EP-40737 showed an antiproliferative action at 10(-9)-10(-8) M and did not stimulate these markers. GHS-R1a receptor mRNA and protein were detected in the osteoblasts. The authors conclude that ghrelin and synthetic GHS modulate osteoblast proliferation and differentiation, probably via this receptor.
Abstract
It has previously been reported that growth hormone secretagogues (GHS) may have a role in the regulation of bone metabolism in animals and humans. In this study we evaluated the effect of ghrelin, the endogenous ligand of GHS receptors, on the proliferation rate and on osteoblast activity in primary cultures of rat calvaria osteoblasts. In the same experiments, we compared the effects of ghrelin with those of hexarelin (HEXA) and EP-40737, two synthetic GHS with different characteristics. Both ghrelin and HEXA (10(-11)-10(-8) M) significantly stimulated osteoblast proliferation at low concentrations (10(-10) M). Surprisingly, EP-40737 demonstrated an antiproliferative effect at 10(-9)-10(-8) M, whereas lower concentrations had no effect on cell proliferation. Ghrelin and HEXA significantly increased alkaline phosphatase (ALP) and osteocalcin (OC) production. At variance with these peptides, EP-40737 did not significantly stimulate ALP and OC. The mRNA for GHS-R1a receptors and the corresponding protein were detected in calvarial osteoblasts by RT-PCR and Western blot respectively, indicating that ghrelin and GHS may bind and activate this specific receptor. We conclude that endogenous ghrelin and synthetic GHS modulate proliferation and differentiation of rat osteoblasts, probably by acting on their specific receptor.
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