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. Author manuscript; available in PMC: 2013 Mar 1.
Published in final edited form as: Hypertension. 2012 Jan 23;59(3):680–693. doi: 10.1161/HYPERTENSIONAHA.111.181867

Fig. 8.

Fig. 8

Influence of IGF-1 on palmitate-induced responses of glucose uptake, aconitase activity, cell survival and cardiomyocyte contractile properties. Cardiomyocytes from control FVB mice maintained in DEME medium at 37°C were exposed to palmitate (100 µM) in the absence or presence of IGF-1 (10 nM), the mitochondrial uncoupler FCCP (1 µM), or the GSK3β inhibitor SB216763 (10 µM) for 6 hrs prior to assessment of mechanical and biochemical properties A: Insulin (10 nM)-stimulated cardiomyocyte glucose uptake; B: Myocardial aconitase activity; C: Cardiomyocyte survival rate; D: Peak shortening (% of cell length); E: Maximal velocity of shortening and relengthening (± dL/dt); and F: Time-to-90% relengthening (TR90); Mean ± SEM, n = 5 isolations or 60 cells, *p < 0.05 vs. Control group, #p < 0.05 vs. Palmitate group.