AMPK Activity Regulates Switch between PGC-1α-Dependent and -Independent Mechanisms of Mitochondrial Regulation by SIRT1 (A) Immunoblot for p-AMPK (Thr172) and AMPK in SIRT1 flox/flox Cre-ERT2 primary myoblasts treated with vehicle (0 hr) or OHT to induce SIRT1 excision. (B) Immunoblot for p-ACC (Ser79) and ACC in SIRT1 flox/flox Cre-ERT2 primary myoblasts treated with vehicle or OHT for 48 hr (SIRT1 iKO) and infected with AMPK-DN adenovirus. (C) Expression of nuclear- and mitochondrially encoded genes as in SIRT1 flox/flox Cre-ERT2 primary myoblasts treated with vehicle or OHT (SIRT1 iKO) and infected with empty or AMPK-DN adenovirus for the same period of time (n = 4, ∗p < 0.05 versus vehicle; #p < 0.05 versus SIRT1 iKO). (D) Immunoblot for p-AMPK (Thr172) and AMPK in SIRT1 flox/flox Cre-ERT2 primary myoblasts treated with vehicle or OHT for 24 or 48 hr, after which cells were infected with control or TFAM adenovirus. (E) Immunoblot for p-AMPK (Thr172) and AMPK in gastrocnemius of WT and SIRT1 iKO mice under fed and fasted conditions. (F) Representative immunoblot for p-AMPK (Thr172) and AMPK in gastrocnemius of 6- and 22-month-old mice. Nuclear- and mitochondrially encoded genes were ND1, Cytb, COX1, ATP6, and NDUFS8, SDHb, Uqcrc1, COX5b, and ATP5a1, respectively. Values are expressed as mean ± SEM.