Felice Juan Ignacio, Schurman León, McCarthy Antonio Desmond, Sedlinsky Claudia, Aguirre José Ignacio, Cortizo Ana María
Laboratorio de Investigaciones en Osteopatías y Metabolismo Mineral (LIOMM), Facultad de Ciencias Exactas, Universidad Nacional de La Plata, Argentina.
Department of Physiological Sciences, University of Florida, Gainesville, FL, USA.
Diabetes Res Clin Pract. 2017 Apr;126:202-213. doi: 10.1016/j.diabres.2017.02.011. Epub 2017 Feb 14.
Deleterious effects of metabolic syndrome (MS) on bone are still controversial. In this study we evaluated the effects of a fructose-induced MS, and/or an oral treatment with metformin on the osteogenic potential of bone marrow mesenchymal stromal cells (MSC), as well as on bone formation and architecture.
32 male 8week-old Wistar rats were assigned to four groups: control (C), control plus oral metformin (CM), rats receiving 10% fructose in drinking water (FRD), and FRD plus metformin (FRDM). Samples were collected to measure blood parameters, and to perform pQCT analysis and static and dynamic histomorphometry. MSC were isolated to determine their osteogenic potential.
Metformin improved blood parameters in FRDM rats. pQCT and static and dynamic histomorphometry showed no significant differences in trabecular and cortical bone parameters among groups. FRD reduced TRAP expression and osteocyte density in trabecular bone and metformin only normalized osteocyte density. FRD decreased the osteogenic potential of MSC and metformin administration could revert some of these parameters.
FRD-induced MS shows reduction in MSC osteogenic potential, in osteocyte density and in TRAP activity. Oral metformin treatment was able to prevent trabecular osteocyte loss and the reduction in extracellular mineralization induced by FRD-induced MS.
代谢综合征（MS）对骨骼的有害影响仍存在争议。在本研究中，我们评估了果糖诱导的MS和/或口服二甲双胍对骨髓间充质基质细胞（MSC）成骨潜能以及骨形成和骨结构的影响。
将32只8周龄雄性Wistar大鼠分为四组：对照组（C）、对照组加口服二甲双胍组（CM）、饮用含10%果糖水的大鼠组（FRD）以及FRD加二甲双胍组（FRDM）。采集样本以测量血液参数，并进行外周定量计算机断层扫描（pQCT）分析以及静态和动态组织形态计量学分析。分离MSC以确定其成骨潜能。
二甲双胍改善了FRDM大鼠的血液参数。pQCT以及静态和动态组织形态计量学分析显示，各组间小梁骨和皮质骨参数无显著差异。FRD降低了小梁骨中抗酒石酸酸性磷酸酶（TRAP）表达和骨细胞密度，而二甲双胍仅使骨细胞密度恢复正常。FRD降低了MSC的成骨潜能，给予二甲双胍可使其中一些参数恢复。
FRD诱导的MS表现为MSC成骨潜能、骨细胞密度和TRAP活性降低。口服二甲双胍治疗能够预防小梁骨细胞丢失以及FRD诱导的MS所导致的细胞外矿化减少。
