Table 1.

Cachexia’s phenotypes and respective molecular pathways and components.

Cachexia Phenotypes	Molecular Pathways and Components
Inflammation	Increased levels of tumor necrosis factor alpha (TNF-α), interleukin (IL)-6, IL-1, interferon gamma (IFN-γ), and IL-8
Skeletal and cardiac muscle wasting	Up-regulation of the ubiquitin-mediated proteasome degradation system (UPS)
	Autophagy
	Calcium-activated protease calpains
	Low circulating levels of insulin-like growth factor 1 (IGF-1)
	Insulin resistance
	Myostatin
	Proteolysis-inducing factor (PIF)
	Impaired mitochondrial metabolism
Adipose tissue depletion	Lipolysis
	Inhibition of lipogenesis
	Browning
Hepatic metabolic changes	Acute-phase response
Altered energy balance	Tumor metabolism and inflammation might increase resting energy expenditure and simultaneously decrease energy intake (anorexia), shifting the scale towards negative energy balance
Central neuroinflammation	Inflammatory cytokines bind to receptors on hypothalamic neuronal populations, triggering an acute illness response, leading to anorexia, weight loss, skeletal muscle-protein catabolism, and lipolysis. Neuropeptide Y (NPY), melanocortins, and serotonin involved.
Gastrointestinal tract malfunction	Impaired barrier function and malabsorption