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Abstract
Cachexia, characterized by muscle loss, reduced food intake, and decreased activity, is a common complication of chronic diseases such as cancer, renal failure, heart failure, and chronic infection. Despite diverse underlying pathologies, cachexia is consistently associated with systemic inflammation, and experimental cytokine infusion reproduces its features. However, mechanisms driving cachexia remain unclear, and treatment options are limited. This thesis aimed to identify the anatomical sites where inflammatory cytokines act to produce behavioral and metabolic changes underlying cachexia, providing insight into its pathophysiology and potential therapeutic targets.