Hyperglycemia enhances
bone resorption and impairment. Controlling
blood glucose via
metformin benefits bonecells.
Hyperglycemia enhances basal
phosphorylation of
p38 mitogen-activated protein kinase (MAPK), whichaggravates
bone resorption. Therefore, the aim of this study was to assess the osteoprotective effects of
metformin andp38 MAPK inhibitor in non-obese T2DM
rats. In this study, non-obese T2DM (Goto-kakizaki, GK)
rats were dividedinto four groups, including DM group,
metformin treatment, SB203580
treatment, and
metformin combined withSB203580.
Wistar rats were used as
control group.
Femur,
tibia, and iliac
rat bones were collected to determine boneporosity via
synchrotron radiation microtomography. Primary
osteoblasts were isolated from
calvaria to investigatecell proliferation and
osteoblast function, including
alkaline phosphatase (ALP) expression and
calcium deposition.The results showed that diabetes increase
bone porosity.
Treatment with
metformin significantly reduced
porosity intrabecular and
cortical bone of the
femur,
tibia, and iliac, while SB203580 significantly reduced
porosity in corticalbone. A combination group showed significantly reduced
bone porosity only in
trabecular bone of the
femur. Isolatedosteoblasts showed lower
growth rates.
Treatment with
metformin significantly increased
cell proliferation, ALPexpression, and
calcium deposition. In summary,
metformin treatment improved
bone quality by reducing boneporosity, increasing
cell proliferation, and improving
osteoblast characteristics.