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. 2007 Dec 12;104(51):20517–20522. doi: 10.1073/pnas.0610290104

Fig. 5.

Fig. 5.

FoxO attenuates insulin responses in cardiomyocytes. Cardiomyocytes were infected with adenovirus as indicated, and whole-cell lysates were harvested at 24 h after infection. (A and B) Western blots and densitometric analyses showing insulin (Ins, 10 nM) -induced phosphorylation of Akt and GSK-3 in cells expressing GFP or caFoxO1-GFP. Con, vehicle treated control. **, P < 0.01. (C) Time course studies showing IGF-1 (10 nM) -induced phosphorylation of Akt and GSK3 in cells expressing GFP or caFoxO1-GFP. (D) Western blots of insulin-induced Glut4 membrane translocation in cells expressing GFP or caFoxO1-GFP. (E) FoxO inhibits insulin-stimulated glucose uptake. (Upper) Glucose uptake measured 3 and 26 h after cells were infected with GFP or caFoxO1 and subsequently treated with insulin (10 nM, 10min). (Lower) Phosphorylated Akt levels at corresponding time points (experiments repeated twice with triplicate samples). ***, P < 0.001 (*, P < 0.01) vs. GFP without INS; §§, P < 0.01 vs. caFoxO1 without insulin. (F) Western blots showing levels of Akt phosphorylation and protein abundance in adult mouse cardiac myocytes isolated from FoxO3 knockout or wild-type littermates and treated with insulin (INS) (10 nM, 10 min). (G) Proposed working model. IR, insulin receptor.