Adenosine monophosphate-activated protein kinase is elevated in human cachectic muscle and prevents cancer-induced metabolic dysfunction in mice.
Steffen H RaunMona S AliXiuqing HanCarlos Henríquez-OlguínT C Phung PhamRoberto Meneses-ValdésJonas R KnudsenAnna C H WillemsenSteen LarsenThomas E JensenRamon LangenLykke SylowPublished in: Journal of cachexia, sarcopenia and muscle (2023)
Protein contents of AMPK subunits were upregulated in skeletal muscle of patients with NSCLC. AMPK activation seemed protectively inferred by AMPK-deficient mice developing metabolic dysfunction in response to cancer, including AMPK-dependent regulation of multiple proteins crucial for glucose metabolism. These observations highlight the potential for targeting AMPK to counter cancer-associated metabolic dysfunction and possibly cachexia.
Keyphrases
- skeletal muscle
- protein kinase
- papillary thyroid
- insulin resistance
- oxidative stress
- endothelial cells
- squamous cell
- small cell lung cancer
- type diabetes
- squamous cell carcinoma
- mouse model
- small molecule
- high fat diet induced
- protein protein
- risk assessment
- metabolic syndrome
- climate change
- amino acid
- human health
- advanced non small cell lung cancer
- childhood cancer