Scientists at the Washington University School of Medicine are gaining national recognition for new breakthrough discoveries in diabetes research.

Diabetes milletus affects an estimated 25.8 million children and adults in the United States, accounting for 8.3% of the population, according to the American Diabetes Association.

Many people afflicted with diabetes must contend with the long-term side effects of the disease, including loss of vision, nerve damage, kidney failure, amputation and increased risk of stroke or heart attack.

These complications are caused by damage to the walls of blood vessels in diabetics. According to University researchers, the depletion of two enzymes, fatty acid synthase (FAS) and nitric oxide synthase (NOS), may be responsible for blood vessel damage in diabetic people.

The depletion of FAS in diabetics is the result of both insulin resistance, found in Type 2 diabetes, and deficiency, characteristic of Type 1 diabetes.

“Regardless of the reason why you get diabetes, it is extremely bad for your blood vessels,” said Clay F. Semenkovich, a professor of internal medicine at the medical school.

In Semenkovich’s lab, researchers studied “FASTie” mice, a strain of genetically engineered mice that could not make FAS in the cells lining blood vessels, or endothelial cells, and compared them with both diabetic and healthy mice.

Both the FASTie mice and the diabetic mice were incapable of producing the necessary lipid, called palmitoylation, which adheres NOS to endothelial cells in the vessel walls. Without this substance, NOS cannot attach to endothelial cell membranes, as in healthy blood cells, which can lead to vascular damage.

The lack of FAS and subsequent loss of palmitylation in the genetically engineered mice also appeared to impede vascular repair, often leading to leaking and infection. These problems, Semenkovich said, are also common in diabetic humans.

“We actually took blood vessel cells and demonstrated that the same processes were taking place using human blood vessel cells, which was pretty exciting,” Semenkovich said.

The researchers hope these discoveries will aid diabetes researchers in finding more effective methods to treat complications caused by blood vessel damage.

Semenkovich added, “We’re trying to develop novels ways to replace this abnormal function by figuring out how to trick the cells into making the right amount of lipid.”