Effects of Fructose-induced Metabolic Syndrome (MS) and long-term Metformin (MET) treatment on bone microarchitecture and biomechanics

WANIONOK N; AGUIRRE I; MOLINUEVO MS; FERNANDEZ JM; CORTIZO AM; CASTILLO EJ; JIRON JM; SEDLINSKY C; SCHURMAN L; MCCARTHY A

Congreso; XXXVI Reunión Anual AAOMM; 2019

MS in rats decreases the osteogenic potential of bone marrow stromal cells (BMSC), and this can be prevented by oral MET. However, long-term MET treatment of rats without MS may affect BMSC increasing their RANKL/OPG ratio. Here we evaluate long-term effects of MS and/or MET on bone microarchitecture and biomechanics.46 young male Wistar rats were allocated (n=8-10) to: B (Baseline); C (Control, drinking water); F (20% Fructose in drinking water); M (100 mg/kg/day MET in drinking water); and FM (Fructose+MET in drinking water). Except B, all treatments were continued for 3 months. Double fluorochrome labelling and blood sampling was performed before sacrifice. We dissected: tibiae and 2nd lumbar vertebrae for static and dynamic histomorphometry and pQCT; femora for mechanical tests.Group F (vs C) increased glycemia and triglyceridemia, which was prevented by MET (group FM). No significant differences were found between groups F and C for any bone parameter evaluated. All MET-treated animals (groups M and FM) showed alterations in the tibiae versus group C: significant decreases in trabecular BV/TV, Tb area, Tb.Th, total and trabecular BMC, and trabecular BMD; and a significant increase in Tb.Sp and trabecular eroded surface. No differences between groups were found for dynamic histomorphometry or biomechanics.Thus, Fructose-induced MS does not induce long-term bone alterations. Long-term MET treatment (in the presence or absence of MS) alters appendicular trabecular bone microarchitecture (possibly due to an increase in trabecular resorption) but not biomechanical properties.