Metformin Rescues the Impaired Osteogenesis Differentiation Ability of Rat Adipose-Derived Stem Cells in High Glucose by Activating Autophagy.

Early human evidence such as case series or small samples is exploring possible benefits.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

The incidence and morbidity of diabetes osteoporosis (DOP) are increasing with each passing year. Patients with DOP have a higher risk of bone fracture and poor healing of bone defects, which make a poor quality of their life. Bone tissue engineering based on autologous adipose-derived stem cells (ASCs) transplantation develops as an effective technique to achieve tissue regeneration for patients with bone defects. With the purpose of promoting auto-ASCs transplantation, this research project explored the effect of metformin on the osteogenic differentiation of ASCs under a high-glucose culture environment. In this study, we found that 40 mM high glucose inhibited the physiological function of ASCs, including cell proliferation, migration, and osteogenic differentiation. Indicators of osteogenic differentiation were all downregulated by 40 mM high glucose, including alkaline phosphatase activity, runt-related transcription factor 2, and osteopontin gene expression, and Wnt signaling pathway. At the same time, the cell autophagy makers BECLIN1 and microtubule-associated protein 1 light chain 3 (LC3 I/II) were decreased. While 0.1 mM metformin upregulated the expression of BECLIN1 and LC3 I/II gene and inhibited the expression of mammalian target of rapamycin (mTOR) and GSK3β, it contributed to reverse the osteogenesis inhibition of ASCs caused by high glucose. When 3-methyladeni

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

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