Mechanism behind age-dependent diabetes found

In a significant revelation that may aid enhanced treatment of diabetes, researchers have found that ageing of insulin-secreting cells is linked to a progressive decline in signal transduction and insulin release.

The study provides a new molecular mechanism underlying age-related impairment of insulin-producing cells and diabetes.

Most 65 plus people have greater risk of developing type 2 diabetes if their insulin producing cells in the pancreas fail to compensate for insulin resistance.

A decline in insulin secretion from these beta cells is a major contributing factor causing the disease, but little has been known about why this happens.

For understanding a link between ageing, beta cell dysfunction and diabetes, they took a closer look at calcium ions.

"Calcium ions as mediators of signals in the cell play a crucial role in regulating the function and survival of insulin-producing beta cells," said Luo-Sheng Li of The Rolf Luft Research Center for Diabetes and Endocrinology at the Karolinska Institutet in Sweden.

The researchers studied three different types of mice that differed in age-induced deterioration.

The first was a genetically modified mouse that aged prematurely.

The second type of mouse represented naturally mature ageing, whereas the third was more resistant to age-induced deterioration.

The function of the mitochondria is reduced with age and this reduction of mitochondrial function in beta cells finally leads to reduced insulin release, found the investigators.

An impaired fine tuning of the free calcium concentration in the beta cell is the molecular mechanism linking mitochondrial dysfunction to impaired insulin release, showed the study.

"This is important information that may lay the foundation for a novel treatment regimen for diabetes," concluded Per-Olof Berggren, principal investigator at the Rolf Luft Research Center for Diabetes and Endocrinology.

The finding appeared in the journal Diabetes.