| First Author | Faggioni R | Year | 1999 |
| Journal | Am J Physiol | Volume | 276 |
| Issue | 1 Pt 2 | Pages | R136-42 |
| PubMed ID | 9887187 | Mgi Jnum | J:52477 |
| Mgi Id | MGI:1329538 | Doi | 10.1152/ajpregu.1999.276.1.R136 |
| Citation | Faggioni R, et al. (1999) Leptin deficiency enhances sensitivity to endotoxin-induced lethality. Am J Physiol 276(1 Pt 2):R136-42 |
| abstractText | Leptin is induced by lipopolysacchande (LPS) and cytokines. We investigated the role of leptin in LPS- induced toxicity using leptin-deficient (ob/ob) and leptin receptor-deficient (db/db) mice. Sensitivity to LPS- induced mortality is significantly greater in ob/ob mice compared with their own lean littermates but not in db/db mice. LPS reduced serum glucose in both ob/ob and db/db mice but induced corticosterone only in db/db mice. Despite the very high basal levels of serum leptin in db/db mice, a twofold increase in serum leptin levels was observed after LPS in both db/db mice and their lean littermates. No differences were detected in LPS-induced serum levels of interleukin (IL)-1 beta, tumor necrosis factor, macrophage inflammatory protein-1 alpha, and interferon-gamma in ob/ob mice compared with their own littermates. In contrast, a blunted induction of IL-10 and IL-1 receptor antagonist (IL-1Ra) was observed in ob/ob mice compared with their littermates. In vitro, leptin induced IL-1Ra production and upregulated the IL-1Ra induction by LPS in macrophages. Moreover, treatment with leptin reversed the increased sensitivity to LPS-induced lethality found in ob/ob mice. These results suggest that leptin participates in the host response to inflammation by modulating the host immune and cytokine responses after LPS. |
