25dkou223 10.3205/25dkou223 urn:nbn:de:0183-25dkou2236 Meeting Abstract Zhou Zhou Pengcheng P

Department of Trauma and Reconstructive Surgery, BG Trauma Center Tübingen, Siegfried Weller Institute for Trauma Research, Eberhard Karls University Tübingen, Tübingen, Deutschland

author Hammour Hammour Mohammad Majd MM

Department of Trauma and Reconstructive Surgery, BG Trauma Center Tübingen, Siegfried Weller Institute for Trauma Research, Eberhard Karls University Tübingen, Tübingen, Deutschland

author Linnemann Linnemann Caren C

Department of Trauma and Reconstructive Surgery, BG Trauma Center Tübingen, Siegfried Weller Institute for Trauma Research, Eberhard Karls University Tübingen, Tübingen, Deutschland

author Hobloss Hobloss Zaynab Z

Department of Systems Toxicology, Leibniz Institute for Work Physiology and Human Factors (IfADo) at TU Dortmund, Dortmund, Deutschland

author Ghallab Ghallab Ahmed A

Department of Systems Toxicology, Leibniz Institute for Work Physiology and Human Factors (IfADo) at TU Dortmund, Dortmund, Deutschland

author Hengstler Hengstler Jan G. JG

Department of Systems Toxicology, Leibniz Institute for Work Physiology and Human Factors (IfADo) at TU Dortmund, Dortmund, Deutschland

author Histing Histing Tina T

Department of Trauma and Reconstructive Surgery, BG Trauma Center Tübingen, Eberhard Karls University Tübingen, Tübingen, Deutschland

author Nüssler Nüssler Andreas A

Department of Trauma and Reconstructive Surgery, BG Trauma Center Tübingen, Siegfried Weller Institute for Trauma Research, Eberhard Karls University Tübingen, Tübingen, Deutschland

author Maisenbacher Maisenbacher Tanja C. TC

Department of Trauma and Reconstructive Surgery, BG Trauma Center Tübingen, Siegfried Weller Institute for Trauma Research, Eberhard Karls University Tübingen, Tübingen, Deutschland Department of Trauma and Reconstructive Surgery, BG Trauma Center Tübingen, Eberhard Karls University Tübingen, Tübingen, Deutschland

author German Medical Science GMS Publishing House

Düsseldorf

610 20251031 engl This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). M0634 223 Deutsche Gesellschaft für Orthopädie und Unfallchirurgie Deutsche Gesellschaft für Orthopädie und Orthopädische Chirurgie Deutsche Gesellschaft für Unfallchirurgie Berufsverband für Orthopädie und Unfallchirurgie Deutscher Kongress für Orthopädie und Unfallchirurgie (DKOU 2025) Grundlagenforschung | Cell & Bone 1 Berlin 20251028 20251031 AB31-4406 TextObjectives and questions: Obesity has emerged as a global health crisis, with growing evidence linking it to metabolic disturbances, and impaired bone homeostasis. However, the mechanisms underlying vitamin D deficiency in obesity and its impact on bone quality remain unclear. This study aims to explore the interaction between obesity-related vitamin D deficiency and bone metabolism alterations using a high-fat diet-induced obesity mouse model to identify potential therapeutic targets for improving bone health in obese individuals.Material and methods: 24 male C57Bl6/N mice were fed either a standard diet (SD) or a Western diet (WD; 40 kcal% carbohydrate, 40 kcal% fat, 20 kcal% protein) ad libitum for 48 weeks. Body weight was recorded weekly, while blood glucose levels were measured and liver and bones were collected at week 48. Liver RNA-seq was used to analyze vitamin D metabolism associated genes, while bone microarchitecture and biomechanical properties were assessed using micro-CT and three-point bending test. Histology and RT-PCR were performed to examine markers for vascular structures, Vitamin D receptor, and inflammation in the bone. Mann-Whitney-U Test tested statistical significance; significance was assumed to be p<0.05. Results: The WD group showed a significantly higher weight, and blood glucose levels exhibited an upward trend. Liver RNA-seq revealed a significant reduction in CYP2R1, CYP27A1, and DHCR7, key enzymes in vitamin D metabolism, in the WD group. Micro-CT analysis showed significantly lower bone density in WD group (p = 0.0003). Biomechanical testing suggested a trend towards increased bone stiffness in the WD group (p = 0.0610).RT-PCR analysis demonstrated decreased vitamin D receptor and elevated osteoclast markers in WD bones. However, no differences were observed in osteoblast markers. Expression of angiogenic factors CD31 and VEGF showed a decreased trend in WD bones, while inflammatory markers showed no significant differences. Histological analysis revealed that perilipin was significantly increased in the WD bones and vascular staining indicated a lower number of vascular structures in WD bones.Discussion and conclusions: Our findings reveal that obesity induced by WD significantly reduces the activity of enzymes involved in vitamin D metabolism in the liver. Furthermore, Vitamin D deficiency primarily leads to bone loss by promoting osteoclast activity and bone resorption. These findings strongly suggest that restoring normal vitamin D metabolism or vitamin D supplementation could be a promising treatment of bone loss in obese patients, providing critical evidence for the clinical management of osteoporosis in obesity. 0 0 0 0