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Interaction between diabetes and osteoporosis: imbalance between inflammation and bone remodeling.

作者信息

Zhang Xiao, Xu Dong, Zhang Rui, Wang Hui, Yang Gangyi

机构信息

Department of Endocrinology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, 400037, China.

Department of Endocrinology, Xinqiao Hospital, Army Medical University, Chongqing, 400010, China.

出版信息

Osteoporos Int. 2025 Sep 8. doi: 10.1007/s00198-025-07636-5.


DOI:10.1007/s00198-025-07636-5
PMID:40921862
Abstract

Diabetes and osteoporosis are common chronic diseases worldwide, and there is a complex pathological relationship between the two. Due to hyperglycemia, insulin resistance, and accumulation of advanced glycation end products (AGEs), diabetic patients often show a higher risk of fractures. At the same time, chronic low-grade inflammation and oxidative stress caused by diabetes also play an important role in the occurrence of osteoporosis, disrupting the balance of bone remodeling. This review deeply explores the effects of chronic inflammation caused by diabetes on the function of osteoblasts and osteoclasts, analyzes the mechanism of increased bone resorption and decreased bone formation during bone remodeling, and summarizes potential therapeutic intervention strategies, such as anti-inflammatory therapy, bone remodeling promoters, and the application prospects of new targeted drugs.

摘要

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本文引用的文献

[1]
Metformin adherence is associated with lower risk of osteoporotic fracture among patients with advanced type 2 diabetes.

Diabetes Res Clin Pract. 2025-7

[2]
FTZ alleviates lipid deposition in diabetic kidney disease by AMPK/ACC/SREBP signaling pathway.

Acta Diabetol. 2025-4-1

[3]
Risk of bone fracture by using dipeptidyl peptidase-4 inhibitors, glucagon-like peptide-1 receptor agonists, or sodium-glucose cotransporter-2 inhibitors in patients with type 2 diabetes mellitus: a network meta-analysis of population-based cohort studies.

Front Endocrinol (Lausanne). 2024

[4]
Investigating mechanical and inflammatory pathological mechanisms in osteoarthritis using MSC-derived osteocyte-like cells in 3D.

Front Endocrinol (Lausanne). 2024

[5]
The multiple actions of dipeptidyl peptidase 4 (DPP-4) and its pharmacological inhibition on bone metabolism: a review.

Diabetol Metab Syndr. 2024-7-25

[6]
Association of sodium-glucose cotransporter 2 inhibitor use with risk of osteoporotic fracture among older women: A nationwide, population-based cohort study.

Diabetes Res Clin Pract. 2024-7

[7]
RUFY4 deletion prevents pathological bone loss by blocking endo-lysosomal trafficking of osteoclasts.

Bone Res. 2024-5-15

[8]
A clinical-stage Nrf2 activator suppresses osteoclast differentiation via the iron-ornithine axis.

Cell Metab. 2024-8-6

[9]
Metformin treatment reduces the incidence of osteoporosis: a two-sample Mendelian randomized study.

Osteoporos Int. 2024-6

[10]
High-Performance Hydrogel-Encapsulated Engineered Exosomes for Supporting Endoplasmic Reticulum Homeostasis and Boosting Diabetic Bone Regeneration.

Adv Sci (Weinh). 2024-5

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