Leptin Modulates Severity of Autoimmune Disease

Researchers studying experimental autoimmune encephalomyelitis (EAE), which is a mouse model for multiple sclerosis, have found that the hormone leptin actively contributes to the pathogenesis of EAE, influencing both its onset and clinical severity. Their findings were published in the January 15, 2003, issue of the Journal of Clinical Investigation.

EAE 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. Since leptin is known to be involved in weight control, investigators from University of Naples (Italy) examined its role in the weight loss seen in EAE.

They found that just before the appearance of clinical symptoms of EAE, the mice experienced a significant burst of leptin, which correlated with a reduction in food intake and weight loss. Moreover, subjecting mice to acute starvation, which prevents the production of leptin, was found to delay the onset and reduce the severity of disease.

The authors concluded that their results showed that leptin actively contributed to the pathogenesis of EAE, influencing both its onset and clinical severity. Since leptin is produced at much higher levels in females than males, this may account for the greater susceptibility of females to autoimmune diseases. Finally, the authors suggested that modulating leptin concentration through dietary approaches and/or the administration of drugs that interfere with the body's own production of leptin, may have potential utility in the treatment of multiple sclerosis and other autoimmune diseases.