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. Author manuscript; available in PMC: 2014 Dec 1.
Published in final edited form as: Free Radic Biol Med. 2013 Jun 29;65:10.1016/j.freeradbiomed.2013.06.042. doi: 10.1016/j.freeradbiomed.2013.06.042

Fig. 5.

Fig. 5

Role of NOS uncoupling on insulin resistance-induced Ca2+ leak. Cardiomyocytes from control or sucrose-fed mice with or without folic acid treatment were assessed for intracellular Ca2+ levels for 80 seconds in the presence of a 0Na+-0Ca2+ buffer. A: Representative traces from control and insulin resistant murine cardiomyocytes with and without the RYR inhibitor tetracaine (1 mM); B: Diastolic Ca2+ leak as calculated by the difference in AUC between 0Na+-0Ca2+ and 0Na+-0Ca2++tetracaine; C: Number of spontaneous contraction. Mean ± SEM, n = 18 – 30 cells from 3 mice per group, *p < 0.05 vs. Control, #p < 0.05 vs. Sucrose group.