ArticleHeliyon2023
AdipoRon accelerates bone repair of calvarial defect in diet-induced obesity mice.
Article in Heliyon, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 4 citations in OpenAlex.
- Obesity prolongs the pro-inflammatory response and attenuates bone healing on titanium implants.Acta biomaterialia · 2025Article
- Differential Effects of High Fat Diets on Resilience to HAntioxidants (Basel, Switzerland) · 2023Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: To investigate the role of AdipoRon in bone wound healing of calvaria critical-sized defects (CSD) in diet-induced obesity (DIO) mice. Materials and methods: After establishing the calvaria CSD in normal-chow (NC), DIO and Adiponectin knockout (APNKO) mice, AdipoRon or vehicle was orally gavaged for 3 weeks. The bone defects were analyzed by micro-CT and H&E staining. The expression of osteogenesis-related factor in the defect area, and the chemotactic gradient of SDF-1 between bone marrow and bone defect area were further analyzed. Results: AdipoRon downregulated body weight and alleviated fasting blood glucose level of DIO mice after treatment with AdipoRon in 14 and 21 days. Newly formed bone was significantly increased in the defect area of DIO and APNKO mice after treatment with AdipoRon compared with vehicle treatment. No significant difference was shown in NC mice. Furthermore, compared with NC mice, a significant decrease of BV/TV%, Tb.N value and formed bone percentage were shown in DIO and APNKO mice. The treatment with AdipoRon could reverse of decreased value and increase the newly formed bone in those mice. AdipoRon promoted col-1α expression in wound sites in DIO and APNKO mice. AdipoRon nearly quadrupled the chemotactic gradient of SDF-1 by decreasing SDF-1 expression in bone marrow and increasing it in the bone defect area in APNKO and DIO treated mice. Conclusion: AdipoRon alleviates the obesity status in DIO mice with calvarial defect and increase new bone formation in calvarial defects in DIO and APNKO mice by modulating chemotactic gradient of SDF-1.
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