Receive breaking news and special reports. The news and stories that mattered provided the day of the week in the morning.
By Linda Carroll
Immune cells in the gut may determine whether our metabolism is hot or cold, as a new study shows.
Experiments conducted in specially designed mice found that certain immune cells in the small intestine tended to slow down the metabolism and store the ingested food as fat instead of converting it into energy, according to the study published Wednesday in Nature , Mice lacking these immune cells could have diets high in fat, sugar, and salt without conditions such as obesity, diabetes, high blood pressure, and heart disease, the researchers reported.
The hope is that these insights show ways of genetically engineered humans to have "thrifty" or slow metabolic processes. Perhaps metabolism is accelerated by lifting certain ingredients in the intestines to run hotter so that people can eat a little more without gaining weight.
"When you eat a meal, your body has to decide what it should do. Make the energy in the meal," said sophomore Filip Swirski, a senior associate professor at Harvard Medical School and senior investigator at Center for Systems Biology at Massachusetts General Hospital. "The immune cells calibrate this decision, and essentially they slow down a high metabolism."
Swirski and his colleagues initially focused on a protein called integrin beta7, which directs immune cells into the gut. Mice lacking the gene for the protein ate much more than those with the protein but did not gain, although they were no more active than the normal mice.
"They're just running hot," Swirski said. "They have a higher basal body temperature."
Next, the researchers tried to feed both groups of mice rich in fat, sugar and sodium, the type of diet known to trigger a metabolic syndrome ̵
The mice without beta7 remained murky and did not develop glucose intolerance, resulting in increased blood sugar levels and high blood pressure.
In contrast, the normal mice became obese and developed high blood pressure and diminished glucose tolerance.
Next, the researchers investigated the effects of this protein on mice susceptible to the development of high cholesterol and arteriosclerosis. Once again, mice lacking the beta7 protein were healthier and maintained a normal fat content despite high cholesterol feeding.
But how did beta7 affect the metabolism?
To answer this question, Swirski and his colleagues focused on this question certain immune cells known as T cells in the small intestine.
"Here we stumbled upon GLP-1, a metabolism-stimulating protein," said Swirski.
Swirski and his colleagues discovered that the T cells they had studied and had abundant GLP-1 receptors. The mice with more beta7 but not GLP-1 receptors had a faster metabolism. This proved that "the key cells were T cells that express the GLP-1 receptor," Swirski said.
Slow Metabolism Contributed to Survival
Now that the researchers had found the metabolism-slowing cells, Swirski began to wonder why mice – and humans – had a system that slowed down their metabolism.
One possible reason is how humans have evolved to survive food shortages over millions of years. "Having these types of brakes under these conditions would be beneficial for survival," Swirski said. "That would mean that you could keep the food you eat longer because it has been converted to fat if you did not eat regularly."
That has only recently become a problem. "If there is so much overeating, the system goes up in flames," Swirski said.
The new research could be of great importance to humans, said UCLA's gastroenterologist, Dr. Ing. Emeran Mayer, author of "The Mind-Gut Connection: Like the Hidden Conversations in Our Body, Affects Our Mood, Our Possibilities, and Our Overall Health."
Researchers have shown that the immune cells in the gut " Regulate metabolism and contribute to the development of obesity, metabolic syndrome and cardiovascular disease Presence of a high-fat, high-fat diet, "Emeran said in an email.
Why some are not gaining weight
The new research "provocative" was called by Dr. Finkel Finkel, it could help scientists find new ways to help people fight against weight gain. There has long been evidence of an association between the immune system and obesity, said Finkel, director of the Aging Institute of the University of Pittsburgh Medical Center.
"The inflammatory response to obesity drives many of the associated problems.
It is amazing that there are already diabetes medications that mimic GLP-1, according to Finkel.
These new insights into the biology of immune cells and metabolism "are extremely important," said Dr. Michael Blaha , Director of Clinical Research at the Ciccarone Center for the Prevention of Heart Disease in Johns Hopkins Medicine.
It explains why some people tend to be overweight and some are overweight. "And it tells us that the story is a lot more complicated than a simple calculation of "calories in and calories out," he said.
"For a long time we have been dealing with the consequences of obesity – such as blood pressure and high cholesterol – because we could not attack the causes of obesity," Blaha said. "It would be much better if we were to diagnose the causes of obesity