Attention, chocolate lovers: You may not be able to help yourselves. Swiss and British scientists have linked the widespread love of chocolate to a chemical "signature" that may be programmed into our metabolic systems.
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Blocking Fat Hormone Might Slow MS
THURSDAY, Jan 12 (HealthDay News) -- Mice with an animal form of multiple sclerosis (MS) displayed slowed disease progression when scientists blocked the activity of a hormone called leptin, found primarily in fat cells. The Italian team studied experimental autoimmune encephalomyelitis (EAE) in mice -- a commonly used animal model for researchers investigating MS. "We are the first to report that leptin blockage can alter the EAE symptoms in mice," said Dr. Giuseppe Matarese, of the Universita di Napoli in Napoli, Italy. He is the lead author of the report, published in the February issue of the Journal of Clinical Investigation. MS is an incurable inflammatory disease of the central nervous system marked by muscle weakness, numbness and loss of coordination. Disease severity can range from the relatively benign to cases involving serious disability and death. Many experts consider MS an autoimmune disease, in which the body attacks its own tissues, especially the protective myelin sheath surrounding nerves. About 400,000 people in the United States are diagnosed with MS, according to the National Multiple Sclerosis Society. Leptin is known to play a role in regulating not only food intake and metabolism, but also the body''s immune response. The hormone is expressed in active inflammatory lesions of the central nervous system during both MS and its mouse equivalent, EAE, Matarese said. Leptin also seems to increase the secretion of inflammatory mediators that help damage myelin. However, using anti-leptin antibodies or disabled leptin receptors, Matarese''s team effectively blocked leptin production in mice with EAE. The result: slowed EAE disease progression. Blocking leptin reduced the number of disease relapses for the entire follow-up period of 120 days, the team found, suggesting the effect of leptin blockade is long lasting. The mice''s "clinical score" -- reflecting symptoms -- was also reduced when leptin was blocked, as were levels of inflammation. The new study builds on previous research, Matarese said. "In the past, we also showed that leptin administration to EAE-susceptible mice makes the EAE symptoms and brain inflammatory infiltration worse," he said. Because leptin may play a role in other autoimmune disorders, the Italian researcher said his team will extend their work to include mouse models of type 1 diabetes and rheumatoid arthritis. They also plan to study the effects of leptin blockage in MS patients. However, a spokesman for the National Multiple Sclerosis Society urged caution when interpreting the findings. Dr. John Richert, vice president for research and clinical programs for the society, said other groups have looked at controlling levels of leptin in blood and have not found differences between those with MS and those without, suggesting that leptin blockage may not become effective treatment. Still, he said, the Italian research remains promising. "There is enough information there to indicate it warrants further study, but it''s not a slam-dunk that it is going to be useful for people with MS." More information For more on MS, head to the National Multiple Sclerosis Society.
Last Updated: Jan. 13, 2006 |