There are new clues into the health-damaging molecular changes eating high fat foods can have on the liver and insulin resistance, a soon to be released University of Michigan Health System study has found.
A better understanding of the body’s response to indulgent eating could lead to new approaches for treating diabetes and metabolic syndrome, say researchers, noting that high fat foods can contribute to obesity, which in turn increases the risk for developing type 2 diabetes.
The protein called Bcl10 is needed for the free fatty acids, which are found in high fat food and stored in body fat, to impair insulin action and lead to abnormally high blood sugar.
In the laboratory study, researchers found that mice deficient in Bcl10 were protected from developing insulin resistance when fed a high-fat diet. The findings will be published May 31 in Cell Reports.
Researchers say insulin helps control blood sugar, but insulin resistance can lead to the abnormally high blood sugar levels that are the hallmark of diabetes. They say insulin resistance can occur as part of metabolic syndrome, a cluster of conditions that increase the risk for type 2 diabetes and heart disease.
As millions of Americans become overweight and obese, type 2 diabetes and metabolic syndrome are on the rise, according to a press release announcing the study results.
“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,” says senior study author Peter C. Lucas, M.D., Ph.D., associate professor of pathology at the University of Michigan Medical School.
Researchers started by looking at how free fatty acids induce inflammation and impair insulin action in the liver, which is thought to be a major target for the harmful effects of free fatty acids. They concluded that Bcl10 is required for the fatty acids to induce inflammation and insulin resistance. The study found that mice deficient in Bcl10 were significantly better able to regulate their blood sugar.
“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,” Lucas said. “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.
“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,” says co-senior author Linda McAllister-Davis, M.D., Ph.D., associate professor of pediatric hematology/oncology.