Mayo Clinic investigators discover novel mechanism linked to diabetes risk

Researchers at Mayo Clinic have discovered an unexpected effect from a gene known to increase diabetes risk. They assumed that the specific allele in the gene TCF7L2 which increases the risk of type 2 diabetes, impairs insulin production in response to increased insulin resistance. Some slight evidence of that was found, but more significantly the researchers discovered that this variant impaired a person's ability to balance blood sugar (glucose) by suppressing glucagon - the hormone that raises the level of glucose in the bloodstream. The findings appear in the journal Diabetes.

"This was surprising. It demonstrates a completely novel mechanism of predisposition to diabetes that could lead to novel therapies," says Adrian Vella, M.D., Mayo Clinic endocrinologist and senior author of the study. "Ultimately, this sheds new light on how this gene actually predisposes to diabetes."

Dr. Vella says more detailed clinical studies need to be done to confirm the finding as well as to better understand how this affects diabetes in more heterogeneous populations over the long term.

Comments

The opinions expressed here are the views of the writer and do not necessarily reflect the views and opinions of News Medical.
Post a new comment
Post

While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. We do not provide medical advice, if you search for medical information you must always consult a medical professional before acting on any information provided.

Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles.

Please do not ask questions that use sensitive or confidential information.

Read the full Terms & Conditions.

You might also like...
Tirzepatide significantly reduces weight and diabetes risk in patients with obesity and prediabetes