The hormone leptin, primarily produced in fat cells, helps regulate food intake, metabolism and reproduction. It has also been shown to promote and sustain the bodys immune response by binding to T lymphocytes - the frontline cells that protect against infection.
The disease experimental autoimmune encephalomyelitis (EAE) in mice is currently used by researchers as a model of human multiple sclerosis (MS). The disease is characterized by the production of autoreactive T lymphocytes that turn against the body and attack cells within the brain and spinal cord, first inducing weight loss and ultimately resulting in paralysis.
In the January 15 issue of the Journal of Clinical Investigation, Giuseppe Matarese and colleagues at IEOS-CNR at Università di Napoli "Federico II", Napoli, Italy report that just prior to developing the clinical symptoms of EAE, mice experience a significant burst of leptin which correlates with a reduction in food intake and weight loss. Furthermore, subjecting mice to acute starvation, which prevents the production of leptin, was found to delay the onset and reduce the severity of disease. In addition, leptin secretion from T lymphocytes was found to further contribute to overall leptin production during EAE.
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