Ground-breaking discoveries have established 5' AMP-activated protein kinase (AMPK) as a key cellular sensor of metabolic stress. Multiple findings support the notion that AMPK is a crucial regulator of cell catabolism. However, recent studies have revealed that AMPK’s role in cell homeostasis might not be as unidirectional as originally thought.
This talk explores emerging evidence for AMPK as a promoter of cell survival and an enhancer of anabolic capacity in skeletal muscle during catabolic crises. AMPK plays three fundamental roles in metabolic tissues, namely the provision of cellular energy status, modulation of insulin sensitivity, and regulation of protein turnover. AMPK supports energy provision via the generation of ATP through increased nutrient uptake and oxidation, and upregulation of mitochondrial capacity. Nutrient uptake is further augmented by AMPK via its insulin-sensitizing effects, which allow tissues to maintain energy provision when internal energy stores are low. Lastly, AMPK serves as a crucial regulator of protein turnover by providing essential signals to finely adjust anabolic processes, including protein synthesis.
In this talk, I will focus on AMPK’ role in muscle preservation in cancer cachexia, focusing on AMPK’s insulin sensitivity enhancing effect. I will put forward the argument that call for a shift in the current dogma of AMPK as a mere regulator of cell catabolism, concluding that AMPK plays an unexpected role in tissue preservation, aided by its imperative role in insulin sensitivity.