New research from the Oklahoma Medical Research Foundation shows that eating a high-fat diet produces a similar effect to starvation in cells.

New research from the Oklahoma Medical Research Foundation shows that eating a high-fat diet produces a similar effect to starvation in cells and could be key in understanding why cells “flip the switch” to burn fat instead of sugar in the early stages of diabetes.

OMRF scientist Mike Kinter, Ph.D., said it started with a simple question: What happens in the heart when people gain weight?

“As people gain weight, it can lead to a series of serious medical issues,” he said. “Two of the big ones are type 2 diabetes and heart disease, which are linked.”

Diabetes is a disease in which the body has trouble producing or using insulin, a hormone that tells our cells to take in sugar as a source of energy. People with type 2 diabetes have fat, liver and muscle cells that develop a resistance to insulin, preventing those cells from using sugar and leaving it to build up in the blood. Over time, high blood sugar can have a toxic effect on cells. An estimated 25.8 million Americans have diabetes, and about 95 percent of those cases are type 2 diabetes.

Obesity is the leading cause of type 2 diabetes. Patients with type 2 diabetes are at a higher risk for heart disease, can develop heart disease earlier and may have a more severe form of the disease.

In order to see how the heart reacts to obesity, Kinter worked with OMRF researchers Luke Szweda, Ph.D., and Paul Rindler, Ph.D., to examine the heart cells of mice that were fed a high-fat diet.

“We found that a high-fat diet produces a response that’s similar to what happens with starvation—in a sense tricking the cells into choosing fat over glucose,” Kinter said. Glucose, a type of sugar, is the only energy source used by brain and fast-twitch muscle cells, so if fat is available, it’s best to use that fat to feed the rest of the cells and preserve the glucose for those important systems.

Having easy access to calories is a relatively new phenomenon, Szweda said. “Our bodies haven’t evolved to deal with our modern problems of too much food and not enough exercise. We store excess calories as fat which can mean that fat is always available to our cells. Since the cells are designed to use fat when it is available, the sugar is left to build up.”

That design was good when people weren’t sure when their next meal was coming, but it’s trouble in today’s food-a-plenty society, Szweda said.

This discovery, which was published in the Journal of Biological Chemistry, gives researchers insight into the “switch” that is flipped in cells to begin burning fat instead of glucose and could lead to a better understanding of the origins of type 2 diabetes.

Rindler said the next step in the research is to prove that, while insulin deficiency is problematic in the long-term and leads to type 2 diabetes, it is initially an appropriate response. If they can pinpoint when it moves from helpful to harmful, it could give researchers clues to how to reverse the disease.