Building an in vitro model of sarcopenic obesity

Background: Sarcopenic obesity (SO) is a clinical condition characterized by coexistence of obesity and sarcopenia. The crosstalk that occurs between muscle tissue and adipose tissue is a complex and dynamic interaction with a crucial role in the development and progression of SO. Adipose tissue has been shown to release fatty acids affecting muscle lipid metabolism. Deeper knowledge of these interactions is crucial for understanding the etiopathogenesis of SO and for identifying new therapeutic targets. Thus, the present study aimed to develop a cell model useful for studying the perturbed crosstalk between muscle and adipose tissue cells in SO. Methods: To replicate the cellular stress conditions induced by excess fat, C2C12 (myoblast) and 3T3L-1 (adipocyte) cell lines were exposed to increasing concentrations of palmitate (200–400 μM) for six days. Results: The exposure of muscle cells to palmitic acid increased the release of the pro-inflammatory cytokines interleukin-6 and tumor necrosis factor-alpha. Furthermore, impairment of the cells’ differentiation capacity was observed with a reduction in the expression of the transcript for the slow myosin heavy chain I and an increase in the expression of fast myosin heavy chain IIa and IIb, the latter being late differentiation markers. The treatment of adipose cells with palmitate induced an increase in the amount of lipid droplets. Conclusion: These results demonstrate that chronic in vitro exposure to palmitic acid induces, in muscle and adipose tissue cells, effects that partially overlap the disturbances in the homeostasis of these tissues typically observed in SO.