Loss of interleukin‐10 exacerbates early Type‐1 diabetes‐induced bone loss. Issue 3 (19th September 2019)

• Record Type: Journal Article
• Authors: Rios‐Arce, Naiomy D.; Dagenais, Andrew; Feenstra, Derrick; Coughlin, Brandon; Kang, Ho Jun; Mohr, Susanne; McCabe, Laura R.; Parameswaran, Narayanan
• Is Part Of: Journal of cellular physiology. Volume 235:Issue 3(2020:Mar.)
• Page Start: 2350
• Page End: 2365
• Publication Date: 2019-09-19
• Subjects: bone -- IL‐10 -- osteoblasts -- osteoporosis -- Type‐1 diabetes; Physiology -- Periodicals; Cell physiology -- Periodicals; 571.6
• DOI: 10.1002/jcp.29141
• Languages: English
• ISSNs: 0021-9541

Abstract

Abstract: Type‐1 diabetes (T1D) increases systemic inflammation, bone loss, and risk for bone fractures. Levels of the anti‐inflammatory cytokine interleukin‐10 (IL‐10) are decreased in T1D, however their role in T1D‐induced osteoporosis is unknown. To address this, diabetes was induced in male IL‐10 knockout (KO) and wild‐type (WT) mice. Analyses of femur and vertebral trabecular bone volume fraction identified bone loss in T1D‐WT mice at 4 and 12 weeks, which in T1D‐IL‐10‐KO mice was further reduced at 4 weeks but not 12 weeks. IL‐10 deficiency also increased the negative effects of T1D on cortical bone. Osteoblast marker osterix was decreased, while osteoclast markers were unchanged, suggesting that IL‐10 promotes anabolic processes. MC3T3‐E1 osteoblasts cultured under high glucose conditions displayed a decrease in osterix which was prevented by addition of IL‐10. Taken together, our results suggest that IL‐10 is important for promoting osteoblast maturation and reducing bone loss during early stages of T1D. Abstract : Type‐1 diabetes‐induced bone loss is exacerbated in interleukin‐10 deficient mice, especially early after disease induction.