| Objective To investigate the osteogenic differentiation ability of adipose-derived stem cells (ADSCs) in type 2 diabetic osteoporosis rats in vitro. Methods Sixty SD rats were divided into three groups, including control group, osteoporosis group (OP group), and type 2 diabetic osteoporosis group (DOP group), with twenty rats in each group. After feeding with high-fat and high-sugar diet, the rats in DOP group were injected with STZ into the lower left abdomen to establish the type 2 diabetic model. Ovariectomy was then performed to establish the type 2 diabetic osteoporosis model. Periovarian fat was removed only in rats of the control group. Ten rats were randomly selected from the control group and ten rats from DOP group and OP group, respectively, were randomly selected from the successfully modeled rats. ADSCs were isolated from the inguinal adipose tissue of the rats, and cultured and passaged. The 3rd generation cells were stained for osteoblasts and quantitatively analyzed. The expression of osteogenic genes RUNX2, OCN, OPN, and ALP was detected using PCR. Results BMD in DOP group was significantly lower than that in both control and OP group (P<0.05). There was no significant difference in morphology and proliferation of ADSCs among the three groups. Microscopic observation showed that the number of calcified nodules in DOP group and OP group was less than that in control group. The number of calcified nodules was lest in DOP group. The large calcified nodules were absent and the staining was light. Quantitative analysis of osteogenesis showed that the OD value of ADSCs in DOP group was lower than that in control group and OP group. The expression of osteogenic genes RUNX2, OCN, OPN, and ALP in DOP group and OP group was lower than that in control group (P<0.05). The expression of RUNX2 and ALP in DOP group was lower than in OP group (P<0.05), while the expression of OCN and OPN was not significantly different between the two groups (P>0.05). Conclusion The osteogenic differentiation ability of ADSCs in DOP rats is weaker than that in OP rats, which may be related to the decrease of ALP and RUNX2 expression in ADSCs under hyperglycemia. |