Diabetes induces differences in the F-actin spatial organization of striated muscles

Studies have shown the cytoskeleton disorganization produced by diabetes and quantified F-actin fluorescence in the striated muscles of diabetic animals. However, at present, there are no studies that have quantified F-actin spatial organization (F-actin-SO). Through our research, we analyzed the effect of diabetes on F-actin-SO in the cardiac and skeletal muscles of a mouse model. The muscle samples were labeled with phalloidin-rhodamine and analyzed with confocal microscopy. The analysis was done in two dimensions using four approaches: quantitation of (a) phalloidin-occupied areas; (b) number of F-actin-unoccupied areas per muscular fiber; (c) F-actin filament discontinuity; and (d) costamere periodicity. Our results showed that both the cardiac and skeletal muscles of the control mice had more phalloidin-occupied areas than the diabetic mice. The skeletal muscles had a significantly higher number of F-actin-unoccupied areas per muscular fiber and more F-actin discontinuities. Additionally, using western blot analyses, we showed that those differences were not due to α-actin protein expression. Finally, we considered the importance of these findings in dysfunctional contraction, disassembly in cell-cell communication, conduction of muscle impulse, and changes in cell nanomechanics. Our results quantitatively demonstrated that diabetes severely affects F-actin-SO in striated muscles.