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Cachexia is a common pathological syndrome associated with cancer and other chronic illnesses, that encompasses both the loss of appetite (anorexia) and the inability to conserve energy. Nevertheless, recent studies of metabolic dysregulation syndromes have revealed important contributions of hypothalamic systems functioning independently of leptin, as illustrated by two recent studies of tumor-induced anorexia and cachexia, including the accompanying paper by Wisse et al. To summarize this concept, during periods of nutrient abundance, leptin secretion is increased, leading to decreased appetite and increased caloric disposal, whereas caloric deficit leads to decreased leptin secretion, increased appetite, and a shift to a neuroendocrine profile that facilitates metabolic adaptation ( 3).
Overall, a picture of normal energy homeostasis has emerged wherein leptin acts on the central nervous system to help orchestrate the regulation of food intake and caloric disposition, and conversely, the neuroendocrine and metabolic adaptation to inadequate nutrient availability ( 2). Understanding of the regulation of appetite and satiety has been revolutionized by the discovery of leptin ( 1), a white adipose tissue-derived cytokine that is secreted into the bloodstream.