Leptin regulates proinflammatory immune responses

S. Loffreda, S. Q. Yang, H. Z. Lin, C. L. Karp, M. L. Brengman, D. J. Wang, A. S. Klein, G. B. Bulkley, C. Bao, P. W. Noble, M. D. Lane, A. M. Diehl

Research output: Contribution to journalArticlepeer-review

1043 Scopus citations


Obesity is associated with an increased incidence of infection, diabetes, and cardiovascular disease, which together account for most obesity-related morbidity and mortality. Decreased expression of leptin or of functional leptin receptors results in hyperphagia, decreased energy expenditure, and obesity. It is unclear, however, whether defective leptin- dependent signal transduction directly promotes any of the conditions that frequently complicate obesity. Abnormalities in tumor necrosis factor α expression have been noted in each of the above comorbid conditions, so leptin deficiency could promote these complications if leptin had immunoregulatory activity. Studies of rodents with genetic abnormalities in leptin or leptin receptors revealed obesity-related deficits in macrophage phagocytosis and the expression of proinflammatory cytokines both in vivo and in vitro. Exogenous leptin up-regulated both phagocytosis and the production of proinflammatory cytokines. These results identify an important and novel function for leptin: up-regulation of inflammatory immune responses, which may provide a common pathogenetic mechanism that contributes to several of the major complications of obesity.

Original languageEnglish (US)
Pages (from-to)57-65
Number of pages9
JournalFASEB Journal
Issue number1
StatePublished - 1998


  • Cytokine
  • Lipopolysaccharide
  • Macrophage
  • Obesity
  • Phagocytic function
  • TNF

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics


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