Metformin regulates bone marrow stromal cells to accelerate bone healing in diabetic mice
Abstract
Abstract Diabetes mellitus is a group of chronic diseases characterized by high blood glucose levels. Diabetic patients have a higher risk of sustaining osteoporotic fractures than non-diabetic people. The fracture healing is usually impaired in diabetics and our understanding of the detrimental effects of hyperglycemia on fracture healing is still inadequate. Metformin is the first-line medicine for type-2 diabetes (T2D). However, its effects on bone in T2D patients remain to be studied. To assess the impacts of metformin on fracture healing, we compared the healing process of closed wound fixed fracture, non-fixed radial fracture, and femoral drill-hole injury models in T2D mice with and without metformin treatment. Our results demonstrated that metformin rescued the delayed bone healing and remolding in T2D mice in all the three injury models. The proliferation, osteogenesis, chondrogenesis of the bone marrow stromal cells (BMSCs) derived from WT and T2D mice treated with or without metformin were compared in vitro and in vivo by assessing the subcutaneous ossicle formation of the BMSC implants in recipient T2D mice. In vivo treatment with metformin to T2D mice could effectively rescue the impaired differentiation potential and detrimental lineage commitment of BMSCs, caused by the hyperglycemic conditions. Moreover, the Safranin O staining of cartilage formation in the endochondral ossification under hyperglycemic condition significantly increased at day 14 post-fracture…
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Evidence Hub reads this as a preprint, done in animal, not in people. Its evidence level is 5 of 5 (Very low · case / narrative / animal / in vitro / in silico). Case reports, narrative reviews, and animal, cell or computer-model studies give the weakest evidence for human health.
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