Treating rare genetic form of diabetes with type 2 treatment could be harmful

by Barbara Hewitt on March 21, 2016

Patients with a rare, genetic form of diabetes are often are misdiagnosed as having type 2 diabetes because the two share symptoms but treating it the same could be harmful.

The underlying problems in patients with the genetic form of the disease called maturity onset diabetes of the young (MODY1) are very different from those in and scientists have found that using drugs for type 2 diabetes appears to lead to the destruction of insulin-secreting beta cells that regulate blood sugar.

The new research at Washington University School of Medicine in St. Louis suggests that because treating such patients with therapies designed for type 2 diabetes is potentially harmful treatment guidelines need to change.

Scientists Lab

“People diagnosed with type 2 diabetes are treated with oral medications that make insulin secreting beta cells very active,” said first author Benjamin Moore, PhD, a former postdoctoral fellow at Washington University who is now at Massachusetts General Hospital.

“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,” he explained.

Moore said it’s common for patients with MODY1, who make up 3% to 5% of all patients with diabetes, to transition from oral medications to insulin injections within 10 years of diagnosis as a way to keep their blood sugar in check. The new research suggests, however, that revving up the beta cells with oral medications increases cellular stress levels and eventually kills those cells, thus precipitating the need to switch to insulin.

Instead, patients with MODY1 might benefit from therapies that target a specific pathway that appears to be essential to the function of insulin secreting cells. The researchers noted a relationship between a pair of proteins that regulate cells that secrete insulin and enzymes in the stomach, liver, kidney and intestines. One of those proteins is made by the gene that’s altered in patients who have MODY1 diabetes.

Moore was originally was studying cells in the stomach along with Jason Mills, an associate professor of medicine at Washington University, when he identified the insulin secretion pathway disrupted in the genetic form of diabetes.

Mills and Moore believe the pathway they’ve identified in MODY1 also may be important in disorders that involve cells that secrete other enzymes.

“Nature doesn’t re-invent the wheel. What these different cells secrete is very different, but the machinery is very similar. As with auto plants, although a BMW is very different from a Volkswagen, the factories where those cars are built are not really that different. It appears the same thing may be true for a number of these cells that secrete key enzymes in the gastrointestinal tract,” Mills pointed out.

Mills’ laboratory is continuing to conduct experiments to determine whether the same pathways are active in different types of secretory cells. Meanwhile, they believe doctors treating patients with diabetes need to determine whether they have the MODY1 form of the disorder before moving ahead with treatment.

“It’s important to diagnose patients as accurately as possible and to attempt to target the correct pathway,” Moore added.

The opinions expressed in this article do not necessarily reflect the views of the Community and should not be interpreted as medical advice. Please see your doctor before making any changes to your diabetes management plan.

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