Leptin accelerates autoimmune diabetes in female NOD mice

Giuseppe Matarese, Veronica Sanna, Robert I. Lechler, Nora Sarvetnick, Silvia Fontana, Seraflno Zappacosta, Antonio La Cava

Research output: Contribution to journalArticlepeer-review

150 Scopus citations


We have recently shown that leptin, the product of the obese gene, can directly influence T-cell function. In the work presented here, we explored the role of leptin in the development of spontaneous autoimmunity in the nonobese diabetic (NOD) mouse, an animal model for the study of human insulin-dependent diabetes mellitus (type 1 diabetes). We found that expression of serum leptin increased soon before the onset of hyperglycemia and diabetes in susceptible females. A pathogenetic role of leptin was assessed by administering recombinant leptin to young female and male NOD mice. Intraperitoneal injections of leptin accelerated autoimmune destruction of insulin-producing β-cells and significantly increased interferon-γ production in peripheral T-cells. These findings indicate that leptin can favor proinflammatory cell responses and directly influence development of autoimmune disease mediated by Th1 responses.

Original languageEnglish (US)
Pages (from-to)1356-1361
Number of pages6
Issue number5
StatePublished - 2002
Externally publishedYes

ASJC Scopus subject areas

  • Internal Medicine
  • Endocrinology, Diabetes and Metabolism


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