Enhanced AMPK activity is attributable to the better glucose homeostasis in DARP-/- mice.

<p>(A) Glucose tolerance was analyzed in WT or DARP-/- mice treated with AICAR at the age of 24 weeks old (n = 6 for WT mice, n = 7 for DARP-/- mice). Administration of AICAR abolished the better glucose tolerance in DARP-/- mice. (B) Phosphorylation of AMPK and ACC in skeletal muscle of WT or DARP-/- mice treated with AICAR was assessed by immunoblotting. #Not significant (n = 7 each). (C) LKB1 expression in skeletal muscle was assessed by immunoblotting. Protein expression of LKB1 increased in skeletal muscle of DARP-/- mice comparing to that in WT mice. *P<0.05 (n = 4 each). (D) LKB1 expression in C2C12 myotubes transfected with either negative (scramble) or DARP siRNA (DARP-KD) was assessed by immunoblotting. Protein expression of LKB1 increased in DARP-KD myotubes comparing to that in scramble control cells. **P<0.01 (n = 3 each). (E) Quantitative analysis for LKB1 mRNA expression in skeletal muscle of WT or DARP-/- mice (n = 6 for WT and n = 5 for DARP-/-). LKB1 expression in skeletal muscle was not significantly different between WT and DARP-/- mice. (F) Quantitative analysis for LKB1 mRNA expression in C2C12 myotubes transfected with either negative (scramble) or DARP siRNA (DARP-KD). LKB1 expression in myotubes was not significantly different between scramble and DARP-KD cells (n = 4 each).