AMPK-associated signaling to bridge the gap between fuel metabolism and hepatocyte viability

Figure 4 Dual regulation of fuel metabolism and cell viability by adenosine monophosphate-activated protein kinase. The adenosine monophosphate-activated protein kinase (AMPK)-S6 kinase-1 (S6K1) pathway regulates metabolic signaling flow. In addition, AMPK controls the redox-state and mitochondrial function, therefore its activation protects cells from apoptosis. AMPK is the key molecule to bridge the gap between fuel metabolism and hepatocyte viability. IR: Insulin receptor; IRS1: Insulin receptor substrate-1; PI3K: Phosphoinositide-3 kinase; TSC1: Tuberous sclerosis complex 1; ROS: Reactive oxygen species; mTOR: Mammalian target of rapamycin; LXRα: Liver X receptor-α; GSK3β: Glycogen synthase kinase 3β; SREBP-1c: Sterol regulatory element, binding protein-1c; VDAC: Voltage-activated anion channel; ANT: Adenine nucleotide translocator.