A woman checks her blood sugar level as part of a routine follow-up
A woman checks her blood sugar level as part of a routine follow-up

World (Enmaeya News) – January 6, 2025

A recent scientific study suggests that one of the most commonly prescribed treatments for type 2 diabetes may accelerate disease progression by causing insulin-producing cells to lose their functional identity.

Sulphonylurea drugs have been used to treat type 2 diabetes since the early 1950s. They remain among the most widely prescribed medications for the condition.

Common examples include glimepiride (Amaryl), glipizide (Glucotrol), and glyburide (Diabeta, Micronase). However, evidence shows their effectiveness may decline with long-term use.

Studies also indicate that these drugs may cause more side effects than several newer diabetes treatments.

A new research paper by the University of Barcelona, the Bellvitge Biomedical Research Institute (IDIBELL), Bellvitge University Hospital, and the CIBERDEM Center was published in Diabetes, Obesity and Metabolism.

The study found that sulphonylureas may interfere with the normal function of insulin-producing cells.

Researchers observed that these drugs can trigger a loss of cellular identity in pancreatic beta cells, limiting their ability to release insulin.

Laboratory tests showed that treated cells gradually lost their capacity to produce insulin. Gene activity linked to their specialized function declined, while cell death rates increased.

Scientists described this process as a “loss of functional identity,” where beta cells shift from insulin-producing cells to inactive ones, even though they remain alive.

This effect is associated with increased stress in the endoplasmic reticulum, the part of the cell responsible for producing essential proteins like insulin.

With prolonged drug use, this internal stress worsens, potentially explaining why these medications lose effectiveness over time.

This phenomenon is medically known as “secondary sulphonylurea failure.”

Despite the concerns, the findings also open new research possibilities. Since the issue involves loss of identity rather than cell death, the process may be theoretically reversible.

This could lead to future treatments aimed at restoring the natural function of beta cells.

Researchers emphasized that patients should not stop taking their medication based on this study.

Instead, the findings highlight the importance of regular medical follow-ups and treatment evaluations, particularly as newer therapeutic options become available.