The antiresorptive effect of GIP, but not GLP-2, is preserved in patients with hypoparathyroidism - a randomized crossover study
Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
Dokumenter
- The Antiresorptive Effect of GIP, But Not GLP-2, Is Preserved in Patients With Hypoparathyroidism—A Randomized Crossover Study
Forlagets udgivne version, 937 KB, PDF-dokument
Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-2 (GLP-2) are gut hormones secreted postprandially. In healthy humans, both hormones decrease bone resorption accompanied by a rapid reduction in parathyroid hormone (PTH). The aim of this study was to investigate whether the changes in bone turnover after meal intake and after GIP- and GLP-2 injections, respectively, are mediated via a reduction in PTH secretion. This was tested in female patients with hypoparathyroidism given a standardized liquid mixed-meal test (n = 7) followed by a peptide injection-test (n = 4) using a randomized crossover design. We observed that the meal- and GIP-, but not the GLP-2-induced changes in bone turnover markers, were preserved in the patients with hypoparathyroidism. To understand the underlying mechanisms, we examined the expression of the GIP receptor (GIPR) and the GLP-2 receptor (GLP-2R) in human osteoblasts and osteoclasts as well as in parathyroid tissue. The GIPR was expressed in both human osteoclasts and osteoblasts, whereas the GLP-2R was absent or only weakly expressed in osteoclasts. Furthermore, both GIPR and GLP-2R were expressed in parathyroid tissue. Our findings suggest that the GIP-induced effect on bone turnover may be mediated directly via GIPR expressed in osteoblasts and osteoclasts and that this may occur independent of PTH. In contrast, the effect of GLP-2 on bone turnover seems to depend on changes in PTH and may be mediated through GLP-2R in the parathyroid gland.
Originalsprog | Engelsk |
---|---|
Tidsskrift | Journal of Bone and Mineral Research |
Vol/bind | 36 |
Udgave nummer | 8 |
Sider (fra-til) | 1448-1458 |
Antal sider | 11 |
ISSN | 0884-0431 |
DOI | |
Status | Udgivet - 2021 |
Bibliografisk note
This article is protected by copyright. All rights reserved.
Antal downloads er baseret på statistik fra Google Scholar og www.ku.dk
ID: 260351297