Doctors could be mistreating a rare form of diabetes, which can potentially lead to dangerous health consequences, according to a new study.
The researchers at Washington University School of Medicine in St. Louis, Mo., studied how type 2 diabetes treatments can affect patients with a rare genetic type of the disease that is called the maturity-onset diabetes of the young (MODY-1). Only about three to five percent of all cases involve this type of diabetes.
"People diagnosed with type 2 diabetes are treated with oral medications that make insulin-secreting beta cells very active," said first author Benjamin D. Moore, who was a former postdoctoral fellow at Washington University but is now at Massachusetts General Hospital.
Moore said that these oral medications, when used to treat patients with MODY-1, can actually be damaging the beta cells that are responsible for secreting insulin. The researchers explained that these drugs appear to be causing cellular stress levels to spike up, which can then lead to the destruction of the beta cells. When the beta cells die, patients with MODY-1 will then have to start using insulin injections at a much faster rate.
"But the MODY1 pathway we've uncovered shows that stimulating those cells with those drugs can lead to beta cell death. That means these patients can become dependent on insulin injections much sooner," Moore said.
Moore's research, which he conducted with Jason C. Mills, an associate professor of medicine at Washington University, set out to find out whether or not better treatment plans for patients with MODY-1 can be created. They were able to identify an insulin secretion pathway that contained proteins responsible for regulating insulin-secreting beta cells and enzymes from the stomach, liver, intestines and kidney.
After identifying these proteins, the researchers found that one protein was made up of the same gene that is mutated in patients with MODY-1. The researchers believe that by targeting this pathway, a better form of therapy for patients with MODY-1 could be created.
"It's important to diagnose patients as accurately as possible and to attempt to target the correct pathway," Moore said.
The study was published recently in the The Journal of Biological Chemistry.
