2026-07-08 東北大学
図1. マウス頭蓋冠における骨吸収の比較
＜関連情報＞
- https://www.tohoku.ac.jp/japanese/2026/07/press20260708-04-liraglutide.html
- https://www.mdpi.com/1422-0067/27/12/5624
GLP-1受容体作動薬であるリラグルチドは、マクロファージのTNF-α発現を抑制することにより、LPS誘発性破骨細胞形成および骨量減少を軽減する Liraglutide, a GLP-1 Receptor Agonist, Mitigates LPS-Induced Osteoclastogenesis and Bone Loss by Downregulating Macrophage TNF-α Expression
Kou Murakami,Hideki Kitaura,Fumitoshi Ohori,Aseel Marahleh,Angyi Lin,Ziqiu Fan,Kohei Narita,Tomoko Ishiyama,Jin Hu,Huidan Zheng and Hiroyasu Kanetaka
International Journal of Molecular Sciences Published: 22 June 2026
DOI:https://doi.org/10.3390/ijms27125624
Abstract
Liraglutide, a glucagon-like peptide-1 (GLP-1) receptor agonist, restores hyperglycemic conditions in patients with type 2 diabetes and has recently shown promising anti-inflammatory properties. In this study, we explored its potential to suppress osteoclast formation and bone loss triggered by lipopolysaccharide (LPS), an inflammatory agent. In animal models, the co-administration of liraglutide with LPS on the calvaria regions in mice markedly reduced osteoclast numbers and bone resorption areas relative to treatment with LPS alone. Furthermore, the expression levels of receptor activators of the NF-κB ligand (RANKL) and tumor necrosis factor (TNF)-α mRNA were notably lower in the group receiving liraglutide and LPS compared to treatment with LPS alone. Moreover, in vitro tests revealed that liraglutide has no direct inhibitory effect on RANKL-induced osteoclastogenesis and TNF-α-induced osteoclastogenesis. In addition, liraglutide had no direct inhibitory effect on LPS-stimulated RANKL expression in osteoblasts. Moreover, liraglutide effectively suppressed TNF-α mRNA expression in macrophages stimulated by LPS. These findings suggest that liraglutide prevents inflammatory bone destruction not by targeting osteoclast formation directly but by inhibiting the production of TNF-α within macrophages.
