Fat Hormone Tied to Multiple Sclerosis
Italian Study: Blocking the Hormone Leptin Curbed Similar Disease in Mice
WebMD News Archive
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
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
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.
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
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
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
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.