Feed a Cold, Starve MS
Natural Anti-Fat Hormone Seen as Key to Autoimmune Diseases
Jan. 16, 2003 -- Starving saves mice from a kind of multiple sclerosis (MS), a new study shows. The finding adds convincing new evidence linking a fat-fighting hormone to MS and other autoimmune diseases.
In MS, the immune system attacks the body's own nerve linings. As in many other autoimmune diseases, it's one particular arm of the immune system that goes awry: the white blood cells called CD4+ T cells. These cells act as quarterbacks that choose targets and lead the attack. Researchers are trying to find out what sends these quarterbacks into action. The hope is that they can be pulled from the game before they do too much damage.
When the body has had enough food, it makes a hormone called leptin. Leptin abolishes appetite and makes the body lose weight. But those are far from its only effects. Leptin also kicks the immune system into high gear. Giuseppe Matarese, MD, and colleagues at Italy's National Research Council wondered whether this might be what puts the ball in play in MS. They looked at mice with experimental autoimmune encephalomyelitis (EAE) -- a viral disease that closely resembles MS.
"Before getting EAE symptoms, mice have a surge in leptin," Matarese tells WebMD. "There is increased leptin production in the brain. It is made there by [immune cells] that infiltrate the brain during disease."
Just as the body makes leptin when it's had enough food, it stops making leptin when it's starving. So if a leptin surge precedes MS-like disease, what would happen if the mice weren't eating? That's just what the Italian researchers did. They report their findings in the Jan. 15 issue of The Journal of Clinical Investigation.
"If you starve mice for 48 hours before inducing EAE, you can reduce the disease symptoms and reduce [immunity-caused] lesions in the brain," Matarese says.
It's a very important finding, says Stanford University's Lawrence Steinman, MD. Earlier this year, Steinman's lab reported that leptin genes become highly active in the brains of MS patients. This activity is found at the sites of active MS abnormalities.