title: Tumor necrosis factor-alpha regulates secretion of the adipocyte-derived cytokine, leptin.
abstract: The seminal observation that secretion of the adipocyte-derived hormone leptin was induced by inflammatory challenge has been expanded upon to demonstrate the importance of the pro-inflammatory cytokines, especially tumor necrosis factor (TNF)-alpha, in inflammatory hyperleptinemia. Initially, it was thought that cytokine-induced hyperleptinemia might somehow be involved in the anorexia and cachexia that often accompany chronic infectious, neoplastic, and autoimmune disease. While the role of leptin in disease-associated anorexia and cachexia appears tenuous in light of recent findings, there is evidence that the hyperleptinemia induced by cytokines is an integral part of the acute phase response and necessary for comprehensive immunocompetence. This hints at the existence of an integrated communication network, wherein the energy status of the animal impacts its ability to fight pathogens.
authors.affiliation: Laboratory of Integrative Biology, Department of Animal Sciences, University of Illinois, Urbana-Champaign, Illinois 61801, USA.
authors.forename: B N
authors.initials: BN
authors.lastname: Finck
authors.forename: R W
authors.initials: RW
authors.lastname: Johnson
mesh_terms: D000818:Animals; D002100:Cachexia / Q000209:etiology; D006801:Humans; D007107:Immune System / Q000502:physiology; D007249:Inflammation / Q000209:etiology; D020738:Leptin / Q000378:metabolism*; D054411:Receptors, Leptin; D018124:Receptors, Tumor Necrosis Factor / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology*
chemical_list: C515448:LEPR protein, human; D020738:Leptin; D054411:Receptors, Leptin; D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha