Obesity, diabetes, and high fracture risk is linked, but the mechanism is unclear. However, impaired acute adipose tissue inflammation may be a common denominator for these conditions. Impaired adipose tissue inflammation leads to low adipogenesis, insufficient adipose expansion, and signs of diabetes.
The aim of this study was to investigate if the low adipogenesis induced by impaired adipose tissue inflammation is coupled to increased osteoblastogenesis, and if this results in high BMD and fracture risk, as seen in patients with type 2 diabetes.
High fat diet (HFD) was fed for 11 weeks to female and male RID transgenic (tg) mice, which have an impaired adipose tissue inflammation, and wildtypes. Body composition, including BMD, was determined throughout the study by dual energy X-ray absorptiometry. At termination, femur was collected for analysis by peripheral quantitative computed tomography. This study was approved by the ethical committee for animal experiments in Gothenburg.
Male RID tg mice had higher total BMD at 4 (+5.0%, P=0.002), 8 (+5.4%, P<0.001), and 11 (+3.6%, P=0.006) weeks of HFD, as well as higher lumbar BMD at 4 (+10.6%, P=0.002), 8 (+16.8%, P<0.001), and 11 (+7.5%, P=0.02) weeks of HFD, compared with wildtypes. Male RID tg mice also had higher femoral trabecular BMD (+9.1%, P=0.02) and cortical content (+9.7%, P=0.02) than wildtypes. For female mice, the bone phenotype was not apparent until 11 weeks of HFD, when female RID tg mice had higher lumbar (+16.5%, P<0.001), but not total, BMD than wildtypes. Female RID tg mice also had higher femoral trabecular BMD (+10.8%, P=0.01) and cortical content (+8.2%, P=0.005) than wildtypes.
In conclusion, male and female mice with an impaired adipose tissue inflammation had higher BMD than wildtypes. However, the effect was delayed in females. The fracture risk and osteoblastogenesis remains to be investigated.
14 May 2016 - 17 May 2016