LPS-induced anorexia in leptin-deficient (ob/ob) and leptin receptor-deficient (db/db) mice

Am J Physiol. 1997 Jul;273(1 Pt 2):R181-6. doi: 10.1152/ajpregu.1997.273.1.R181.


Administration of endotoxin (lipopolysaccharide, LPS) induces profound anorexia. Injection of leptin decreases food intake in mice. Recently, we reported that LPS and cytokines increase leptin levels in hamsters. To further investigate the role of leptin in the LPS-induced anorexia, we administered LPS to leptin receptor-deficient (db/db) and leptin-deficient (ob/ob) mice. We found that LPS caused anorexia in both db/db and ob/ob mice. As might be predicted if leptin had a role in anorexia, the db/db mice were somewhat resistant to LPS-induced anorexia. However the ob/ob mice were more sensitive to LPS-induced anorexia. No differences between db/db and ob/ob mice and their respective littermate were observed in circulating tumor necrosis factor levels after LPS. These data suggest that leptin per se is not essential for LPS-induced anorexia.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Analysis of Variance
  • Animals
  • Anorexia / chemically induced*
  • Anorexia / genetics
  • Anorexia / physiopathology
  • Carrier Proteins / genetics
  • Carrier Proteins / physiology*
  • Cricetinae
  • Dose-Response Relationship, Drug
  • Feeding Behavior / drug effects*
  • Female
  • Genotype
  • Leptin
  • Lipopolysaccharides / toxicity*
  • Mice
  • Mice, Inbred C57BL
  • Mice, Mutant Strains
  • Mice, Obese
  • Proteins / genetics
  • Proteins / physiology*
  • Receptors, Cell Surface*
  • Receptors, Leptin
  • Species Specificity
  • Time Factors
  • Tumor Necrosis Factor-alpha / analysis


  • Carrier Proteins
  • Leptin
  • Lipopolysaccharides
  • Proteins
  • Receptors, Cell Surface
  • Receptors, Leptin
  • Tumor Necrosis Factor-alpha
  • leptin receptor, mouse