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Immune cells in the gut may explain why some people can not lose weight

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by Linda Carroll

Immune cells in the gut may determine whether our metabolisms run hot or cold, a new study suggests.

Experiments done in specially engineered mice found that certain immune cells in the small intestine tend to slow down metabolism and send ingested food to be stored as fat rather than converting it to energy, according to the study published Wednesday in Nature. Mice engineered to lack these immune cells could consume high fat, sugar and salt diets without developing conditions such as obesity, diabetes, hypertension and heart disease, according to researchers.

The hope, experts say, is that these findings will suggest ways to tweak something in the guts of people genetically programmed to have "thrifty" or slow metabolisms. Perhaps by bumping up the levels of certain substances in the gut, metabolisms can be revved up to run hotter, thus allowing people to eat a little more without gaining weight.

"When you eat a meal, your body needs to decide what to do with the energy in the meal," said study co-author Philip Swirski, an associate professor at Harvard Medical School and a Principal Investigator at the Center for Systems Biology at the Massachusetts General Hospital. "The immune cells calibrate that decision and essentially put the brakes on a high metabolism."

Swirski and his colleagues started out by focusing on a protein called the integrin beta7, which directs immune cells to the gut. Mice without the gene for the protein did much more than those with it, but did not gain weight, despite being no more active than the normal mice.

"They just run hot," Swirski said. "They have a higher basal temperature."

The researchers next tried to feed both groups of mice that were high in fat, sugar and sodium, a type of diet known to induce metabolic syndrome – a constellation of symptoms, including high blood pressure, sugar and cholesterol, associated with a higher risk of heart disease.

The mice without beta7 stayed trim and did not develop glucose intolerance, which leads to higher than normal levels of blood sugar and high blood pressure.

In contrast, the normal mice became obese and developed high blood pressure and reduced glucose tolerance.

The researchers looked at the impact of this protein on mice that were vulnerable to developing high cholesterol and hardening of the arteries. Once again, mice that were missing the beta7 protein were healthier, maintaining normal fat levels, despite being fed a high-in-cholesterol diet.

But how was beta7 affecting metabolism?

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