Bone Abstracts

Introduction: Type 2 diabetes mellitus (T2DM) is a risk factor for the development of fractures. Several studies have shown an inverse relationship between osteoblastogenesis and adipogenesis through a competition model between these processes.

PPARγ acts as regulator of adipogenesis and its increased expression is associated to decreased osteoblastogenesis. The treatment of insulin resistance with glitazones, one of the ligands of PPARγ, reduces bone mineral density increasing risk of fractures. Thus, T2DM patients may have higher levels of PPARγ inhibiting bone mineralization and increasing adipogenesis and bone fragility.

Objectives: To examine serum levels of PPARγ in T2DM patients without treatment with glitazones, checking endogenous serum PPARγ expression in patients with osteoporosis and vertebral fractures (VF).

Methods: Cross-sectional study including 75 patients with T2DM with presence/absence of osteoporosis and morphometric VF. Anthropometric and biochemical parameters, calciotropic hormones, bone turnover markers (MRO) and bone mineral density (BMD) were evaluated. PPARγ levels were determined by ELISA techniques (Cusabio).

Results: No significant differences of serum PPARγ concentrations were observed according to the presence/absence of osteoporosis (P=0.208). Neither, correlation between PPARγ levels, MRO nor BMD values was observed (P>0.05). However, circulating levels of PPARγ were significantly higher in the T2DM group with VF compared to patients without VF (P=0.001). In a logistic regression model including age, sex, sedentary lifestyle, family history of fracture, vitamin D levels and HbA1c as independent variables, only PPARγ levels were independently associated with the presence of morphometric VF (OR 1.002 (95% CI 1000–1004); P=0.018) indicating an increase of 2% in fracture risk per pg/ml of increased PPARγ.

Conclusions: Serum levels of PPARγ are increased in T2DM patients with fractures suggesting that this receptor might be involved in the regulation of mineral metabolism and bone fragility in T2DM.