Cancer cachexia is a metabolic disease characterized by a negative energy balance associated with systemic weight loss and poor quality of life. In particular, skeletal muscle, which represents almost 50% of the total body mass, is strongly affected, and metabolic alterations therein (e.g., insulin resistance and mitochondrial dysfunction) can eventually support tumor growth by facilitating nutrient scavenging by the growing mass. Interestingly, metabolic interventions on wasting muscle have been proven to be protective, advocating for the importance of metabolic regulation in the wasting muscle. Here, we will briefly define the current knowledge of metabolic regulation in cachexia and provide a protocol to grow and differentiate in vitro myotubes for the assessment of mitochondrial metabolism during cachexia.

Assessing metabolic dysregulation in muscle during cachexia

Hsu M. Y.;Porporato P. E.;Wyart E.
2019

Abstract

Cancer cachexia is a metabolic disease characterized by a negative energy balance associated with systemic weight loss and poor quality of life. In particular, skeletal muscle, which represents almost 50% of the total body mass, is strongly affected, and metabolic alterations therein (e.g., insulin resistance and mitochondrial dysfunction) can eventually support tumor growth by facilitating nutrient scavenging by the growing mass. Interestingly, metabolic interventions on wasting muscle have been proven to be protective, advocating for the importance of metabolic regulation in the wasting muscle. Here, we will briefly define the current knowledge of metabolic regulation in cachexia and provide a protocol to grow and differentiate in vitro myotubes for the assessment of mitochondrial metabolism during cachexia.
Methods in Molecular Biology
Humana Press Inc.
1928
337
352
978-1-4939-9026-9
978-1-4939-9027-6
http://www.springer.com/series/7651
Cachexia; Energy metabolism; Muscle wasting; Myotube differentiation; Oxygen consumption; Cachexia; Humans; Mitochondria; Muscle Fibers, Skeletal; Muscle, Skeletal; Muscular Atrophy; Neoplasms; Oxygen; Energy Metabolism
Hsu M.Y.; Porporato P.E.; Wyart E.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2318/1732736
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