A Colorado State University biochemist is conducting innovative molecular-level research that could revolutionize the understanding and treatment of diabetes.

Scott Summers, assistant professor in the Department of Biochemistry and Molecular Biology at Colorado State, is being funded by grants from the American Diabetes Association, the National Institutes of Health, the American Heart Association and the March of Dimes to conduct groundbreaking research on a cellular metabolite called ceramide. The fatty acid byproduct appears to interfere with normal insulin operation in the body, and Summers believes that excess ceramide may trigger type II diabetes.

"We are studying to determine if we can unequivocally prove that aberrant ceramide production is the cause of type II diabetes in humans," Summers said. "If we find this is true, we can then develop medications or forms of gene therapy to prevent ceramide accumulation and eliminate the need for many diabetics to take insulin."

Type II diabetes results from either a decreased discharge of insulin into the bloodstream or an inability of the released insulin to induce the necessary nutrient storage in body tissues. Summers' research focuses on the latter, where body cells essentially ignore insulin.

Summers hypothesizes that abnormal ceramide accumulations, due to cellular defects in the body, contribute to the development of insulin resistance and lead to the onset of type II diabetes. His research program could lead to novel treatments aimed at lowering ceramide levels, reducing or potentially eliminating the effects of diabetes.

"Our research team is making great progress," Summers said. "We have recently determined that ceramide is undeniably an important factor in the development of insulin resistance in cultured cells, and within the next two years, we should know precisely how ceramide relates to diabetes in rodent models. If a role for ceramide is proven, we will have the knowledge to begin developing appropriate symptom-relieving medications."

In their research lab, Summers and his colleagues are lowering cellular ceramide levels in muscle and fat tissue with the treatment of drugs and also by introducing enzymes to stimulate degradation of the metabolite, assessing if either method reduces insulin resistance. These experiments should indicate whether ceramide or a ceramide derivative cause insulin resistance and lead to the onset of diabetes.

In related research, Summers is studying a newly identified protein, GBPX, to understand its effect on normal insulin functioning and the development of diabetes. He is striving to obtain the complete DNA sequence of the protein which will lead to more complete knowledge of the molecular processes governing insulin action.

Summers' desire to research diabetes began many years ago when his father became afflicted with the disease. Summers started his research in a physiology lab studying diabetic complications as an undergraduate, and he later pursued biochemical studies on the underlying causes of diabetes in graduate and post-doctoral research. At Colorado State, Summers has established a competitive research group dedicated to providing greater insight into the development and treatment of diabetes.

Diabetes affects nearly 16 millions Americans, accounts for about 15 percent of all health care expenditures and totals more than $45 billion in direct medical costs each year in the United States. Type II diabetes is the most common form of the disease, afflicting 90 percent to 95 percent of all diabetics. Although children with the disease typically have type I diabetes, the rate of type II is rapidly rising among young people. Complications of type II diabetes include diseases of the eye, kidney, nervous and cardiovascular systems.

Insulin is a hormone in the body that stimulates the absorption and storage of carbohydrates and other nutrients in muscle and fat tissue. Following a meal, cells in the pancreas secrete insulin into the bloodstream which promotes the absorption and storage of carbohydrates and other nutrients in muscle tissue while simultaneously suppressing glucose production by the liver.