Cystic fibrosis is an inherited disease in which the body produces thick mucus. The disorder interferes with breathing, pancreas function, digestion and other bodily processes. A common complication is cystic fibrosis-related diabetes (CFRD), which shares some characteristics of type 1 diabetes (a disease in which the body mistakenly destroys its insulin-making cells) and type 2 diabetes (a disorder in which the body develops difficulty using insulin).

Although patients with cystic fibrosis now live into their late 30s on average, researchers at the University of Florida report that life expectancy drops by 16 years in females and two years in males when CFRD develops. Patients with CFRD typically still produce some insulin but need regular injections of this glucose-regulating hormone.

Studying mice, the researchers found that CFRD appears to be caused not by destruction of the insulin-making beta cells but rather by malfunction of those pancreatic cells.

"For the longest time, the development of diabetes in cystic fibrosis has been thought to be chronic destruction of pancreas, so eventually you get loss of the insulin-producing beta cells," researcher Dr. Michael Stalvey stated in a press release. "Our study provides some early evidence to suggest there is an inherent difference in beta cell function."

Some of the lab animals had been genetically altered to remove a gene whose absence is implicated in cystic fibrosis. These rodents had more trouble regulating glucose (blood sugar), but those that could still make a protein that prevents cystic fibrosis could maintain normal glucose even when the scientists damaged some of their beta cells with chemotherapy.

"This goes beyond improving our understanding of patients with cystic fibrosis-related diabetes; it also will help us improve our understanding of other forms of diabetes and help us work on strategies for a future cure," Stalvey said in a recent news release.

The study was published in the journal Diabetes.

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