Background and Aim: Since the 1980s high fructose corn syrup (HFCS-55) has gradually replaced sucrose as the predominant caloric sweetener used in the USA. Studies have shown a correlation between caloric sweetener consumption in adolescents with a reduction in bone density and an increased risk of bone fractures. In order to maintain bone strength and mineral homeostasis bone must undergo continuous resorption of old bone by osteoclasts (OCls) and formation of new bone by osteoblasts (OBs). The aim of this study was to investigate whether there is a direct effect of HFCS-55 on OBs and OCls in vitro.

Method: Kusa 4b10, a mouse marrow stromal cell line, and mouse bone marrow stromal cells (BMSC) were cultured and induced to differentiate into OBs and OCls respectively. Cells were treated with 5.5 mM solutions of glucose, fructose, sucrose, HFCS or a 1:1 ratio of glucose and fructose. Following treatment for 14-21 days (OBs), cell number, mineralisation and collagen Type I (Coll-I) expression were measured. Following treatment for 6 days (OCls), cell number and Cathepsin K gene expression were analysed. Protein expression of fructose transporter GLUT5 was determined by immunocytochemistry for both cell lines.

Results: GLUT5 was localised in both OBs and OCls. No treatment altered parameters measured above with the exception of a significant increase in Cathepsin K expression with fructose treatment. 

Conclusion: This is the first study identifying GLUT5 in Kusa 4b10 OBs and BMSC OCls suggesting fructose may be an energy source and/or provide a role in cell function. HFCS did not directly affect OBs or OCls although fructose increased expression of Cathepsin K. This research suggests there may be an association between fructose consumption and bone loss, however further study is required.