Fig 3.

AMPK β2 mutant animals have normal glucose and lipid profiles but impaired AICAR-stimulated glucose uptake. Shown are basal glucose levels (A) and glucose tolerance tests (B) in WT and β2 mutant mice (n = 6 to 10 for each group). (C) Immunoblot analysis of total Glut4 in WT and β2 mutant skeletal muscle. (D and E) AICAR-stimulated 2-[³H]deoxyglucose uptake by epitrochlearis and extensor digitorum longus (EDL) muscles isolated from WT and β2 mutant animals (n = 6 to 10 for each group). *, P = 0.0001; **, P = 0.003. (F) Immunoblot using pAMPK, pACC, pRaptor, pULK, and pS6 antibodies shows AICAR-stimulated levels of active AMPK and phosphorylation of AMPK downstream targets in gastrocnemius muscle of WT and β2 mutant animals. Total AMPK, ACC, and S6 are also shown. β-Actin was used as a loading control. (G) Densitometry of pAMPK and pACC levels in control and AICAR-stimulated WT and β2 mutant gastrocnemius muscle. #, P ≤ 0.005. (H to J) Levels of serum cholesterol, triglyceride, and free fatty acid (FFA) in β2 mutant animals (n = 6 to 10 for each group).