A study published in the May 31 edition of Cell Reports shows that eating high fat foods has provided new clues about how harmful molecular changes are set in motion.
The findings provide a better understanding of the body’s response to consuming high fat foods and could lead to new treatment options for diabetes and metabolic syndrome. High fat foods are a contributing factor for obesity and increase the risk for developing type 2 diabetes.
The researchers from the University of Michigan discovered that free fatty acids need a key protein called BcI10 in order to debilitate insulin action, which leads to abnormally high elevations of blood sugar. BcI10 are found in high fat foods and are stored in body fat. A laboratory study demonstrated that mice that had been fed a high-fat diet with a BcI10 deficiency were protected from developing insulin resistance.
Whereas insulin helps to control blood sugar, insulin resistance can lead to abnormally high blood sugar levels, the telltale sign of diabetes. The resistance can be caused as part of metabolic syndrome, a variety of conditions that increase the type 2 diabetes and heart disease risk. With millions of overweight and obese Americans, type 2 diabetes and metabolic syndrome are on the increase.
Senior research leader, Peter C. Lucas, M.D., Ph.D., associate professor of pathology at the University of Michigan declares: “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.”
The team decided to examine how free fatty acids cause inflammation and how they debilitate the liver’s insulin action, as scientists believe that the liver represents a key target for the damaging effects of free fatty acids. Free fatty acids undergo metabolism in the liver where they produce diacylglycerols before they cause an inflammatory response. Diacylglycerols activates NF-kB signaling, which has been associated with metabolic and vascular diseases as well as cancer.
They concluded that in order to induce liver inflammation and insulin resistance, fatty acids require BcI10. The study revealed that mice with a BcL10 deficiency displayed a considerable improvement in regulating their blood sugar levels.
“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. 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.”
Linda M. McAllister-Lucas, M.D., Ph.D., associate professor of pediatric hematology/oncology at the University of Michigan, who was the study’s co-senior author concluded: “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.”
Written By Petra Rattue