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Biochemical and biophysical research communications v.494 no.3/4, 2017년, pp.626 - 633   SCI SCIE
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1α,25-Dihydroxyvitamin D3 increases implant osseointegration in diabetic mice partly through FoxO1 inactivation in osteoblasts

Xiong, Yi (State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China ); Zhang, Yixin (State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China ); Guo, Yanjun (State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China ); Yuan, Ying (State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China ); Guo, Qiang (State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China ); Gong, Ping (State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China ); Wu, Yingying (State Key );
  • 초록  

    Abstract Oral implant osseointegration is delayed by hyperglycemia-generated oxidative stress (OS). Forkhead transcription factor 1 (FoxO1) is known to be viewed as a sensor to OS since reactive oxide species like H 2 O 2 regulates its activity. We previously demonstrated that 1,25(OH) 2 D 3 favored glucose homeostasis and implant osseointegration in diabetic rats. In this study, we investigated the role of FoxO1 OB in the regulation process of 1,25(OH) 2 D 3 on glycometabolism and bone metabolism. We show herein that, with the treatment of 1,25(OH) 2 D 3 , mice lacking FoxO1 in osteoblasts (FoxO1 OB −/- ) exhibited decreased serum glucose that was gradually elevated in untreated diabetic mice. An optimal increase of bone mass and bone-implant contact (BIC) was observed in 1,25(OH) 2 D 3 treated FoxO1 OB −/- mice after 2-month healing. Surprisingly, FoxO1 OB −/- mice without 1,25(OH) 2 D 3 treatment also showed an improvement on bone formation and BIC. Same effect could be found in the expression of bone-related markers Runx2, Osterix and BSP, which elevated in 1,25(OH) 2 D 3 treated FoxO1 OB −/- mice as compared to untreated WT mice. In addition, in vitro study showed that high glucose induced FoxO1 nuclear localization while the effect was ameliorated by 1,25(OH) 2 D 3 treatment. These results suggest that FoxO1 OB might be involved in the regulation of 1,25(OH) 2 D 3 on glucose homeostasis and bone formation, and that FoxO1 OB might act as a key modulator of the capacity of the skeleton regulating metabolic homeostasis. Our study also provides a new idea that a combination of systemic 1,25(OH) 2 D 3 and local FoxO1 inhibitor may be a new approach to enhance implant osseointegration. Highlights FoxO1 ablation in osteoblasts favors glucose homeostasis in diabetic mice. 1,25(OH) 2 D 3 regulates glucose and bone metabolism partly through inactivation of FoxO1. FoxO1 inhibitor may be a novel approach to enhance implant osseointegration.


  • 주제어

    1α,25-Dihydroxyvitamin D3 .   Forkhead transcription factor 1 .   Diabetes mellitus .   Glucose homeostasis .   Dental implant .   Osseointegration.  

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