PPARβ/δ Agonist Alleviates Diabetic Osteoporosis via Regulating M1/M2 Macrophage Polarization

Diabetic osteoporosis is a common complication in diabetic patients, leading to increased fracture risk and impaired bone healing. As a member of the peroxisome proliferator-activated receptor (PPAR) family, PPARβ/δ agonist is suggested as a therapeutic target for the treatment of metabolic syndrome...

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Autores principales:	Miao Chen, Weimin Lin, Rui Ye, Jianru Yi, Zhihe Zhao
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	PPARβ/δ diabetes mellitus diabetic osteoporosis macrophage polarization inflammation Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/785659e95fb1427e88550f87400afd8f
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spelling	oai:doaj.org-article:785659e95fb1427e88550f87400afd8f2021-12-01T07:04:56ZPPARβ/δ Agonist Alleviates Diabetic Osteoporosis via Regulating M1/M2 Macrophage Polarization2296-634X10.3389/fcell.2021.753194https://doaj.org/article/785659e95fb1427e88550f87400afd8f2021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fcell.2021.753194/fullhttps://doaj.org/toc/2296-634XDiabetic osteoporosis is a common complication in diabetic patients, leading to increased fracture risk and impaired bone healing. As a member of the peroxisome proliferator-activated receptor (PPAR) family, PPARβ/δ agonist is suggested as a therapeutic target for the treatment of metabolic syndrome, and has been reported to positively regulate bone turnover by improving osteogenesis. However, its regulatory role in diabetic osteoporosis has not been reported yet. Here, we explored the therapeutic effects and potential mechanisms of PPARβ/δ agonist to the osteoporotic phenotypes of diabetic mice. Our results indicated that the osteoporotic phenotypes could be significantly ameliorated in diabetic mice by the administration of PPARβ/δ agonists. In vitro experiments suggested that PPARβ/δ agonist treatment could alleviate the abnormal increase of osteoclast activity in diabetic mice by rectifying high glucose-mediated macrophage dysfunction instead of directly inhibiting osteoclast differentiation. Mechanistically, Angptl4 may act as a downstream target of PPARβ/δ to regulate macrophage polarization. In conclusion, our study demonstrates the potential of PPARβ/δ agonist as a therapeutic target for the treatment of osteoporosis and immune homeostasis disorder in diabetic patients.Miao ChenMiao ChenWeimin LinRui YeRui YeJianru YiJianru YiZhihe ZhaoZhihe ZhaoFrontiers Media S.A.articlePPARβ/δdiabetes mellitusdiabetic osteoporosismacrophage polarizationinflammationBiology (General)QH301-705.5ENFrontiers in Cell and Developmental Biology, Vol 9 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	PPARβ/δ diabetes mellitus diabetic osteoporosis macrophage polarization inflammation Biology (General) QH301-705.5
spellingShingle	PPARβ/δ diabetes mellitus diabetic osteoporosis macrophage polarization inflammation Biology (General) QH301-705.5 Miao Chen Miao Chen Weimin Lin Rui Ye Rui Ye Jianru Yi Jianru Yi Zhihe Zhao Zhihe Zhao PPARβ/δ Agonist Alleviates Diabetic Osteoporosis via Regulating M1/M2 Macrophage Polarization
description	Diabetic osteoporosis is a common complication in diabetic patients, leading to increased fracture risk and impaired bone healing. As a member of the peroxisome proliferator-activated receptor (PPAR) family, PPARβ/δ agonist is suggested as a therapeutic target for the treatment of metabolic syndrome, and has been reported to positively regulate bone turnover by improving osteogenesis. However, its regulatory role in diabetic osteoporosis has not been reported yet. Here, we explored the therapeutic effects and potential mechanisms of PPARβ/δ agonist to the osteoporotic phenotypes of diabetic mice. Our results indicated that the osteoporotic phenotypes could be significantly ameliorated in diabetic mice by the administration of PPARβ/δ agonists. In vitro experiments suggested that PPARβ/δ agonist treatment could alleviate the abnormal increase of osteoclast activity in diabetic mice by rectifying high glucose-mediated macrophage dysfunction instead of directly inhibiting osteoclast differentiation. Mechanistically, Angptl4 may act as a downstream target of PPARβ/δ to regulate macrophage polarization. In conclusion, our study demonstrates the potential of PPARβ/δ agonist as a therapeutic target for the treatment of osteoporosis and immune homeostasis disorder in diabetic patients.
format	article
author	Miao Chen Miao Chen Weimin Lin Rui Ye Rui Ye Jianru Yi Jianru Yi Zhihe Zhao Zhihe Zhao
author_facet	Miao Chen Miao Chen Weimin Lin Rui Ye Rui Ye Jianru Yi Jianru Yi Zhihe Zhao Zhihe Zhao
author_sort	Miao Chen
title	PPARβ/δ Agonist Alleviates Diabetic Osteoporosis via Regulating M1/M2 Macrophage Polarization
title_short	PPARβ/δ Agonist Alleviates Diabetic Osteoporosis via Regulating M1/M2 Macrophage Polarization
title_full	PPARβ/δ Agonist Alleviates Diabetic Osteoporosis via Regulating M1/M2 Macrophage Polarization
title_fullStr	PPARβ/δ Agonist Alleviates Diabetic Osteoporosis via Regulating M1/M2 Macrophage Polarization
title_full_unstemmed	PPARβ/δ Agonist Alleviates Diabetic Osteoporosis via Regulating M1/M2 Macrophage Polarization
title_sort	pparβ/δ agonist alleviates diabetic osteoporosis via regulating m1/m2 macrophage polarization
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/785659e95fb1427e88550f87400afd8f
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PPARβ/δ Agonist Alleviates Diabetic Osteoporosis via Regulating M1/M2 Macrophage Polarization

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