When talking about reasons why someone may have trouble gaining or losing weight, the speed of their metabolism is usually the center of the conversation. Most people believe metabolism speed is something that is solely based on genetics, and while that may be true to some degree, researchers are finding there may be other factors at play.
A Mass General research team led by Filip Swirski,
Intestinal intraepithelial lymphocytes (IEL), are one of the most abundant forms of immune cells in the body. But they are most numerous in the gut, where they help to regulate metabolism and provide the first line of defense against infection.
IEL activity is mediated by a protein called integrin β7, but little was known about the protein’s exact role in the absorption of nutrients.
In their study, the team compared mice that were genetically engineered to lack the gene for integrin β7 with a control group that had a working copy of the gene.
Researchers fed both groups a basic chow diet and found both groups gained weight in a similar fashion. However, the β7-free mice expended more energy and had a higher body temperature, suggesting they had a faster resting metabolism.
To further test their theory, the researchers then provided the mice with a diet high in fat and sugar, which is known to cause high blood pressure, high cholesterol and increased risk of heart disease.
As expected, the control group gained weight and had issues with high cholesterol and blood sugar levels. But even with the high fat and sugar diet, the β7-free mice remained at a normal weight.
Their results suggest that the presence of the integrin β7 gene acts to slow down metabolism. But how?
Swirski and his team found that the IELs, triggered by the presence of the integrin β7 gene, reduce the activity of something called GLP-1, which helps reduce glucose levels in the blood and provides other benefits in metabolism.
The β7-free mice fared better on both the regular diet and the high-fat diet because they had higher amounts of GLP-1 to help process all of the excess sugar and fat they were eating.
But why would our bodies reduce the activity of a
Researchers suspect this function is a product of evolution. Millions of years ago, food was not as abundant as it is today. Slowing down metabolism would help us to conserve energy and increase our chances of survival if food became scarce.
With the abundance of
But Swirski and his colleagues are hopeful that studies such as these can shed light on how modifying immune cell behavior could reduce the risk of heart disease and other cardiovascular diseases in the future.
“Looking forward, we need to better understand IELs function in metabolism. We also need to know whether therapeutic targeting of IELs in humans can be a treatment for obesity, hypercholesterolemia, diabetes, and hypertension.”
-Filip Swirski, PhD
Dr. Swirksi is an investigator in the Center for Systems Biology at Massachusetts General Hospital, an Associate Professor of Radiology at Harvard Medical School and a Patricia and Scott Eston MGH Research Scholar.
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