AMPK is activated by phosphorylation of upstream kinases. The main upstream AMPK kinases are the tumor suppressor liver kinase B1 (LKB1) and Ca2+/calmodulin-dependent protein kinase kinase α and β (CaMKKα and CaMKKβ), which phosphorylate AMPK at Thr172 (14,15). AMPK phosphorylation levels are also regulated by protein phosphatase-2Cα (PP2Cα) (14,15). Our data show that CaMKKβ (but not CaMKKα) protein levels were reduced and PP2Cα increased in the hypothalamus of nicotine-treated rats (Fig. 2E), whereas no changes were detected in the phosphorylation levels of LKB1 (pLKB1; Fig. 2E).
