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    Fat Hormone Tied to Multiple Sclerosis

    Italian Study: Blocking the Hormone Leptin Curbed Similar Disease in Mice
    WebMD Health News
    Reviewed by Louise Chang, MD

    Jan. 12, 2006 -- Blocking the hormone leptin may help prevent or slow multiple sclerosis (MS).

    The report comes from Italian researchers and appears in The Journal of Clinical Investigation.

    The Italian study didn't include any people. Instead, the scientists studied female mice with an MS-like disease.

    Leptin is a hormone that's mostly made by fatty tissue of the body. Commonly associated with obesity, leptin plays a role in regulating weight and appetite.

    Leptin also affects the immune system and has been associated with MS-like lesions in mice. That's what interested the Italian researchers, who included Giuseppe Matarese, MD, PhD.

    Matarese works in Naples, Italy, at the University of Naples "Federico II" and the Institute of Experimental Endocrinology and Oncology.

    Leptin Sidelined

    Previously, Matarese and colleagues had injected leptin into mice with the MS-like disease. The mice's condition worsened.

    This time, the researchers took the opposite approach. They blocked leptin in a new group of mice with the MS-like disease. For comparison, they left leptin alone in other mice with the same condition.

    Over the next 40 days, the mice that had had leptin blocked fared better than mice in the comparison group. Their disease progressed more slowly.

    That finding is based on two things:

    • Measurements of chemicals made by the mice's immune systems
    • Physical symptoms including paralysis, clumsy movement, and difficulty curling tips of tails

    How They Did It

    The researchers used two strategies to block leptin. Both methods worked.

    One approach used artificial antibodies that attacked leptin. The body's immune system makes antibodies, which target viruses or other threats. Matarese's team injected mice with synthetic antibodies to neutralize leptin.

    The other strategy involved a leptin "chimera." The chimera looked and acted like a leptin receptor. It latched onto leptin and held on tight.

    Unlike a real leptin receptor, the chimera didn't let leptin do its usual job. Leptin was ensnared, locked down, and thwarted by the chimera. For leptin, the chimera was an alluring dead-end road that left the hormone stranded and powerless.

    Blocking leptin might lead to new treatments to stall the start or worsening of the disease, at least in mice, the researchers write.

    However, they aren't recommending either approach for humans just yet. They note a need for further studies to probe leptin's impact on MS.

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