Evaluation of AMPK activity in mice by measuring activator-induced glucose uptake

Jiang, Peng; Li, Zhi; Ren, Lejiao; Hu, Xinli; Xiao, Rui‐Ping

doi:10.1016/j.xpro.2021.100496

Cited by 1 publication

(1 citation statement)

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“…Mice between 10 and 12 weeks of age were used for the experiment. MK8722 was prepared in a solution containing 10% DMSO, 40% PEG300, 5% Tween 80, and 45% saline following the protocol reported previously 58 . Torin1 was prepared in a solution containing 20% N -methyl-2-pyrrolidone, 40% PEG400, and 40% water following the protocol reported previously 59 .…”

Section: Methodsmentioning

confidence: 99%

Redefining the role of AMPK in autophagy and the energy stress response

2023

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Autophagy maintains cellular homeostasis during low energy states. According to the current understanding, glucose-depleted cells induce autophagy through AMPK, the primary energy-sensing kinase, to acquire energy for survival. However, contrary to the prevailing concept, our study demonstrates that AMPK inhibits ULK1, the kinase responsible for autophagy initiation, thereby suppressing autophagy. We found that glucose starvation suppresses amino acid starvation-induced stimulation of ULK1-Atg14-Vps34 signaling via AMPK activation. During an energy crisis caused by mitochondrial dysfunction, the LKB1-AMPK axis inhibits ULK1 activation and autophagy induction, even under amino acid starvation. Despite its inhibitory effect, AMPK protects the ULK1-associated autophagy machinery from caspase-mediated degradation during energy deficiency, preserving the cellular ability to initiate autophagy and restore homeostasis once the stress subsides. Our findings reveal that dual functions of AMPK, restraining abrupt induction of autophagy upon energy shortage while preserving essential autophagy components, are crucial to maintain cellular homeostasis and survival during energy stress.

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Section: Methodsmentioning

confidence: 99%