Steffen Henning Raun

This study identifies MCT6 as an intestinal exporter of Lac-Phe, showing its role in metformin-induced weight loss and systemic metabolite regulation.

This study shows that Rac1 deficiency in muscle reduces mitochondrial function and fatty acid metabolism, leading to muscle wasting and highlights potential therapeutic targets for age-related muscle decline.

The paper identifies an IL-6-associated SAA axis linked to muscle wasting and poor survival in cancer cachexia through plasma proteomics and functional studies.

This study shows that reduced food intake in cancer cachexia increases skeletal muscle insulin responsiveness through AKT signaling, independent of tumor presence.

The paper identifies proteomic and phosphoproteomic changes in skeletal muscle of lung cancer patients with cachexia, linking them to muscle wasting and signaling pathways.

The paper investigates muscle remodeling in NSCLC patients, identifying changes in fibro-adipogenic progenitors, mitochondrial function, and immune cells that contribute to muscle wasting.

This study shows that blocking ActRIIA/IIB increases muscle mass and strength in mice but causes glucose intolerance and reduced voluntary activity.

This study shows that housing temperature affects molecular and systemic responses to cancer in mice, influencing metabolic adaptations and cytokine levels.

This study identifies PanK4 as a regulator of skeletal muscle energy metabolism, showing its role in acetyl-CoA regulation and metabolic flexibility.

This study identifies SLIRP as a mitochondrial mRNA stabilizing protein that regulates mitochondrial structure and respiration in skeletal muscle, with exercise improving mitochondrial function through increased mitoribosome capacity.

This study identifies a secondary BHB metabolic pathway mediated by CNDP2, leading to BHB-amino acid metabolites that regulate energy balance in mice and humans.

This study identifies Rac1 as a key regulator of exercise training adaptations by showing its role in protein synthesis, glycogen resynthesis, and running capacity in mice and human muscle.

This study shows that AMPK is upregulated in human cachectic muscle and that AMPK deficiency in mice worsens cancer-induced metabolic dysfunction and cachexia.