University of Wisconsin researchers have made recent discoveries whose implications will benefit individuals who suffer from diabetes.

By removing the gene Stearoyl-CoA desaturase (SCD-1), researchers have genetically engineered a mouse to resist diabetes.

Such findings are the most recent in an ongoing study. Last year, UW professor of biochemistry and nutritional science James Ntambi and colleagues found that mice missing the SCD-1 gene could keep glucose levels and fatty tissues low, which are often affiliated with the disease.

Ntambi has been researching this subject area for over 15 years since he and his colleagues discovered the SCD-1 gene at Johns Hopkins University Medical School in 1988.

The SCD-1 gene makes the SCD-1 enzyme, which produces fatty acids in the body. Without the gene in the mouse, the mouse does not make the enzyme, so a smaller number of fatty acids are made. The amount of fatty acids in the body is directly related to type-II diabetes, the most common type of diabetes in the United States.

The disease is usually genetically linked and begins after age 40, although the number of children affected by the disease has recently increased due to poor lifestyle.

In type-II diabetes, blood is rich in glucose. This high blood sugar, or hyperglycemia, is a major cause of complications arising from diabetes because of abnormal levels of glucose and insulin.

Ntambi and colleagues have shown that the removal of the SCD-1 gene keeps glucose levels low in the body, so there is not a chance for hyperglycemia.

Researchers have already started to examine what this means for humans.

“Our animal model helps to understand diabetes and obesity in humans. It is used as a target for these conditions, and it models resistance to both,” said Ntambi, adding that the SCD-1 equivalent gene in humans works the same way as in mice.

Everyone is born with the gene, but some may have a mutation that makes them produce different levels of the SCD-1 enzyme. Those with lower levels of the SCD-1 enzyme are often very lean and diabetes-free, and those with high levels are prone to diabetes.

Many drugs today act to inhibit enzymes to diminish their effects, and so researchers are looking at a drug that will inhibit the SCD-1 enzyme so fatty acids will decrease, Ntambi said.

UW assistant professor of pharmacy Maureen Barr agrees that the drugs to target SCD-1 may be a useful treatment of insulin resistance and diabetes.

“This is a valid and testable hypothesis,” Barr said.

Data from human plasma is currently being collected in Europe to help further the knowledge of the SCD-1 gene and enzyme in humans and the mechanisms that lie behind the disease.

“Humans have high levels of fatty acids in the plasma that indicate the activity of the enzyme and the measure of fat parameters in the body,” Ntambi said.

There is still much work to be done, but Ntambi and his fellow researchers are confident that work with the SCD-1 enzyme will eventually lead to the production of a drug to aid those individuals who suffer from diabetes and obesity.