Connie K. Ho for

A new study by the University of Michigan has found that foods high in fat can influence diabetes and metabolic syndrome. In particular, proteins can activate mindless eating. The researchers saw that the body undergoes molecular changes when a person eats foods that are high in fat content.

The findings are important as doctors will better be able to understand how to treat diabetes and metabolic syndrome. Diabetes is a chronic disease and those who have the illness demonstrate high levels of sugar in the blood. Metabolic syndrome is a group of risk factors that can increase a person’s risk for illnesses such as heart disease, stroke, and type 2 diabetes. Foods that are high in fat can lead to obesity, which is one of the causes related to type 2 diabetes.

In the study, a protein called Bcl10 was discovered to aid free fatty acids in obstructing insulin action and could lead to the increase of blood sugar levels. Insulin plays a role in assisting the control of blood sugar, but insulin resistance may lead to abnormally high levels of blood sugar and signal the possible onset of diabetes.

The researchers discovered that insulin resistance can sometimes be a part of metabolic syndrome. The research, which will be published in the May 31 edition of Cell Reports, showed that lab mice that were lacking in protein Bcl10 were not as likely to develop insulin resistance.

The study fits in with recent research that shows how, as overweight and obesity rates are rising, there is an increase in the number of type 2 diabetes cases and changes to the metabolic syndrome.

“The study also underscores how very short-term changes in diet such as high-fat eating for only a few days, perhaps even less, can induce a state of insulin resistance,” noted senior study author Dr. Peter C. Lucas, an associate professor of pathology at the University of Michigan, in a prepared statement.

In the project, researchers examined how free fatty acids could cause inflammation in the liver and hinder insulin action. The liver is known to be a major target of free fatty acids and the free fatty acids create diacylglycerols via metabolic processes. Following metabolism, inflammation is found in the liver. The difficulty with diacylglycerols is that they can initiate NF-kB signaling, which has been known to be related to cancer as well as metabolic and vascular diseases.

Overall, the scientists believe the study demonstrates that fatty acids need Bcl10 to activate insulin resistance and that it can cause liver inflammation.

“We were surprised to learn that Bcl10, a protein previously known for its critical role in immune cell response to infection, also plays a critical role in the liver’s response to fatty acid,” continued Lucas in the statement. “This is an example of nature co-opting a mechanism fundamental to the immune system and using it in a metabolic organ, in this case, the liver.”

The lab mice that lacked Bcl10 were better able to regulate their blood sugar and the researchers hope to build on this knowledge to produce better treatments for patients.

“These findings reveal a new and important role for Bcl10 and could lead to novel ideas for treating patients with metabolic syndrome and type 2 diabetes,” explained co-senior author Dr. Linda M. McAllister-Lucas, an associate professor of pediatric hematology/oncology at the University of Michigan, in the statement.

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