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Osteoking Ameliorates Type 2 Diabetes Osteoporosis by Enhancing Osteoblast Differentiation via PI3K/AKT/GSK‐3β Pathway Activation

Rong Li,Jiangli Lu,Peijin Wang,Yulan Zhao,Yi Yang,Jianlin Jiao,Zhongyi Qian,Limei Wang,Hong Zheng

Published 2025 in Cell Biochemistry and Function

ABSTRACT

Osteoking (OK) exerts bone formation‐promoting effects on menopausal osteoporosis and osteoporotic fractures. However, it remains to be determined whether OK ameliorates type 2 diabetic osteoporosis (T2DOP) via PI3K/AKT/GSK‐3β pathway activation. Thus, the T2DOP animal model was established in db/db mice in this study. Microcomputed tomography (micro‐CT) analysis revealed that OK significantly increased bone strength, improved bone metabolism, and promoted bone formation. GS and p‐GSK‐3β expression levels were increased in OK group as compared with db/db group by western blot analysis. IL‐6, IL‐17A, IFN‐γ, TNF‐α, and IL‐1β were lower levels in the OK group compared to the db/db group, nevertheless, the IL‐10 level was significantly higher. Furthermore, an in vitro cells model was constructed by stimulating with high glucose (HG, 30 mM). ALP protein was significantly elevated in the OK treatment group. Administration of OK at 0.288 mg/mL significantly increased p‐AKT/AKT expression, while, combined with LY294002, an inhibitor of PI3K, OK significantly reduced the expression levels of p‐PI3K/PI3K, p‐AKT/AKT, and p‐GSK‐3β/GSK‐3β. In conclusion, this study reveals OK exhibits efficacy against T2DOP in db/db mice by promoting osteogenesis of preosteoblast MC3T3‐E1 cells through PI3K/AKT/GSK‐3β pathway regulation.

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