Leptin is an endogenous protective protein against the toxicity exerted by tumor necrosis factor.
J Exp Med
; 189(1): 207-12, 1999 Jan 04.
Article
en En
| MEDLINE
| ID: mdl-9874578
ABSTRACT
Tumor necrosis factor (TNF) is a central mediator of a number of important pathologies such as the systemic inflammatory response syndrome. Administration of high TNF doses induces acute anorexia, metabolic derangement, inflammation, and eventually shock and death. The in vivo effects of TNF are largely mediated by a complex network of TNF-induced cytokines and hormones acting together or antagonistically. Since TNF also induces leptin, a hormone secreted by adipocytes that modulates food intake and metabolism, we questioned the role of leptin in TNF-induced pathology. To address this question, we tested mouse strains that were defective either in leptin gene (ob/ob) or in functional leptin receptor gene (db/db), and made use of a receptor antagonist of leptin. Ob/ob and db/db mice, as well as normal mice treated with antagonist, exhibited increased sensitivity to the lethal effect of TNF. Exogenous leptin afforded protection to TNF in ob/ob mice, but failed to enhance the protective effect of endogenous leptin in normal mice. We conclude that leptin is involved in the protective mechanisms that allow an organism to cope with the potentially autoaggressive effects of its immune system.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Proteínas
/
Proteínas Portadoras
/
Factor de Necrosis Tumoral alfa
/
Receptores de Superficie Celular
Límite:
Animals
Idioma:
En
Revista:
J Exp Med
Año:
1999
Tipo del documento:
Article
País de afiliación:
Bélgica