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Diabetes 51:1356-1361, 2002
© 2002 by the American Diabetes Association, Inc.

Leptin Accelerates Autoimmune Diabetes in Female NOD Mice

Giuseppe Matarese1, Veronica Sanna2, Robert I. Lechler3, Nora Sarvetnick4, Silvia Fontana2, Serafino Zappacosta1, and Antonio La Cava4

1 Cattedra di Immunologia, Dipartimento di Biologia e Patologia Cellulare e Molecolare, Università di Napoli "Federico II," Napoli, Italy
2 Centro di Endocrinologia e Oncologia Sperimentale del CNR, Napoli, Italy
3 Department of Immunology, Imperial College School of Medicine, Hammersmith Hospital, London, U.K.
4 Department of Immunology, the Scripps Research Institute, La Jolla, California

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 ß-cells and significantly increased interferon-{gamma} 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.


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