title: Increased uncoupling protein-2 gene expression in brain of lipopolysaccharide-injected mice: role of tumour necrosis factor-alpha?
abstract: In order to understand the role of brain localized uncoupling proteins, we have examined the UCP2 and BMCP-1 gene expression in mice brain in two different catabolic states: administration of lipopolysaccharide (LPS) (2.5 mg/kg, i.p.) and tumour burden. Administration of LPS resulted in an increased UCP2 gene expression both in brain (208%) and cerebellum (77%). An increase in UCP2 gene expression was also observed after LPS treatment in double knockout mice for tumour necrosis factor-alpha (TNF) receptors 1 and 2 (75% in brain and 33% in cerebellum). Tumour growth also resulted in increased brain UCP2 gene expression (80%) in mice bearing the Lewis lung carcinoma as compared with the non-tumour-bearing controls. No changes were observed in BMCP-1 mRNA levels of either LPS-injected or tumour-bearing mice. From the results presented it may be suggested that: (a) the brain may contribute significantly to the increase in energy expenditure associated with hypermetabolic states such as fever and tumour burden, and (b) the regulation of UCP2 gene expression in brain does not seem to be influenced by TNF; therefore the action of other cytokines cannot be discarded.
authors.affiliation: Departament de Bioquímica i Biologia Molecular, Unitat B, Facultat de Biologia, Universitat de Barcelona, Diagonal 645, 08028-, Barcelona, Spain.
authors.forename: S
authors.initials: S
authors.lastname: Busquets
authors.forename: B
authors.initials: B
authors.lastname: Alvarez
authors.forename: M
authors.initials: M
authors.lastname: Van Royen
authors.forename: M T
authors.initials: MT
authors.lastname: Figueras
authors.forename: F J
authors.initials: FJ
authors.lastname: López-Soriano
authors.forename: J M
authors.initials: JM
authors.lastname: Argilés
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000235:genetics; D001921:Brain / Q000378:metabolism*; D002352:Carrier Proteins / Q000235:genetics; D004734:Energy Metabolism; D005260:Female; D015870:Gene Expression / Q000187:drug effects; D007473:Ion Channels; D008070:Lipopolysaccharides / Q000633:toxicity; D008175:Lung Neoplasms / Q000235:genetics / Q000378:metabolism; D008297:Male; D026901:Membrane Transport Proteins; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D024101:Mitochondrial Proteins; D000071245:Mitochondrial Uncoupling Proteins; D009419:Nerve Tissue Proteins / Q000235:genetics; D011506:Proteins / Q000235:genetics*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D018124:Receptors, Tumor Necrosis Factor / Q000235:genetics; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*; D000071246:Uncoupling Protein 2
chemical_list: D015703:Antigens, CD; D002352:Carrier Proteins; D007473:Ion Channels; D008070:Lipopolysaccharides; D026901:Membrane Transport Proteins; D024101:Mitochondrial Proteins; D000071245:Mitochondrial Uncoupling Proteins; D009419:Nerve Tissue Proteins; D011506:Proteins; D012333:RNA, Messenger; D018124:Receptors, Tumor Necrosis Factor; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; C492124:Slc25a14 protein, mouse; D014409:Tumor Necrosis Factor-alpha; C000604390:Ucp2 protein, mouse; D000071246:Uncoupling Protein 2