The finding is important because it provides evidence that the same gene in humans could provide clinicians with a powerful tool to determine the likelihood that some individuals will acquire the condition. Moreover, the finding that the gene works through a pathway not generally studied in the context of diabetes, suggests new avenues to explore in the search for new drugs to treat or prevent the disease, says Alan Attie, a UW-Madison professor of biochemistry and the senior author of the study published this week (May 7) in the journal Nature Genetics.
Type 2 diabetes is the most common form of the condition in the United States, with an estimated 16 million Americans afflicted with the disease. It is caused by an inability of the pancreas to produce enough insulin, or by the body's reduced ability to respond to insulin, or both. Insulin is necessary for the body to properly utilize sugar.
Often, the development of type 2 diabetes is caused by obesity. Obese individuals tend to have insulin resistance; that is, it takes more insulin for the body to respond normally. Type 2 diabetes occurs when the pancreas is unable to manufacture enough insulin to compensate for the body's increased demand for the hormone, which it does by growing more insulin-producing beta cells or by ramping up insulin secretion.
The Wisconsin study, comparing two strains of obese mice differing in susceptibility to diabetes, helps explain why this is so.
"Most people who are obese don't have diabetes, but people who are obese are insulin resistant," says Attie. "If there is a fall-off in insulin production, that's when you go from prediabetes to diabetes."