( After every meal the body must prevent...)Keeping the immune system from starting a 'food fight'

After every meal, the body must prevent the immune system from launching an all-out fight against food. Now, researchers report the identity of a nutrient "floodgate" that serves to protect against such an inflammatory immune response. Their findings appear in the May 4, 2007 issue of the journal Cell, a publication of Cell Press.

The researchers found that animals lacking a protein enriched in fat cells, called STAMP2, develop acute inflammation in deep pockets of visceral fat. The animals also showed symptoms of metabolic syndrome—including insulin resistance and fatty liver disease—even while eating a regular diet.

In those who regularly consume an overload of nutrients, the flood control protein may become overwhelmed and give out, leading to the chronic, low-grade inflammation characteristic of obesity and other metabolic diseases, the researchers suggest. Treatments designed to reinforce that barrier may therefore provide the "next frontier" of therapies to combat the rising tide of chronic metabolic disease, they said.

"Humans were not meant to deal with little to no exercise and a constant bombardment of nutrients," said Gökhan Hotamisligil of the Harvard School of Public Health of his team’s findings. "If we could find ways to strengthen STAMP2 or prevent its suppression, the body might retain control," effectively unlinking chronic overeating and obesity from other symptoms of metabolic disease. He cautioned, however, that the realization of such a treatment strategy remains uncertain and would require years of continued investigation.

Cells and organisms must strike an appropriate balance between nutrient sufficiency and surplus, the researchers explained. While adequate amounts of nutrients must be obtained to ensure health and survival, chronic overeating can lead to obesity and an array of associated metabolic disorders, including insulin resistance, fatty liver disease, type 2 diabetes, and cardiovascular disease.
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Source:Cell Press

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