Monday , March 1 2021

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

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Per Linda Carroll

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

Experiments in specially designed mice have found that certain cells in the immune system in the small intestine tend to slow down metabolism and send ingested food to be stored as fat instead of converting it to energy, according to the study published in the journal Nature. Mice designed to lack these immune cells can consume diets high in fat, sugar and salt without developing conditions such as obesity, diabetes, hypertension and heart disease, the researchers report.

The hope, the experts say, is that these findings suggest ways to adjust something in people genetically programmed to have a "frugal" or slow metabolism. Perhaps by increasing the levels of certain substances in the gut, the metabolism can be accelerated to get warmer by 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 of the meal," said study co-author Filip Swirski, associate professor at Harvard Medical School and principal investigator at the Massachusetts Center for Systems Biology. General Hospital. "The immune system cells calibrate that decision and essentially put the brakes on a high metabolism."

Swirski and his colleagues began by focusing on a protein, called integrin beta7, which directs the immune cells to the intestine. Rats without the protein gene ingested far more than those with the gene, but did not gain weight, although they were no more active than normal mice.

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

The researchers tried to feed the two groups of rats that were high in fat, sugar and sodium, the 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.

Mice without beta7 remained in good condition and did not develop glucose intolerance, which leads to higher than normal levels of blood sugar and high blood pressure.

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

The researchers analyzed the impact of this protein in mice vulnerable to the development of high cholesterol and hardening of the arteries. Again, mice that were lacking the beta7 protein were healthier, maintaining normal levels of fat, despite being fed a high-cholesterol diet.

But how was beta7 affecting metabolism?

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