Stress -activated genes harm cells that produce insulin in type 2 diabetes

Stress has no one – not even the cells that produce insulin – any good.

Researchers from the Osaka Metropolitan University have identified a gene that, when activated by metabolic stress, damage the pancreatic B -cells – cells responsible for insulin production and blood sugar control – pushing them. The findings highlight a very promising new goal for early intervention in type 2 diabetes.

While many factors can contribute to type 2 diabetes, lifestyle, especially nutrition, plays an important role in its appearance. Genetics matters, but bad eating habits can significantly increase the risk of developing what is now often called a “silent epidemic”.

Type 2 diabetes occurs when pancreatic β-cells, which secrete insulin to regulate blood glucose, become weakened due to prolonged stress caused by bad dietary habits, a condition known as oxidative stress. “

Naoki Harada, Associate Professor at the School of Agriculture at the Osaka Metropolitan University and lead author of this study

But what exactly does these vital cells wear out?

Searching for an answer, the group turned to a gene that responds to stress called Redd2. These types of genes are activated when the cells are under pressure and are intended to help with the stress strain strategies. But this sometimes discovers.

“We noticed that the increased expression of this gene hurts beta cells, which in turn leads to reduced insulin secretion and the onset of diabetes,” Harada said.

The group found that Redd2 activity increased when B -cells were exposed to high levels of glucose, fatty acids and STZ – a chemical used for the diabetes model in laboratory regulations. When RedD2 levels are suppressed, beta-cells survived better and maintained their function. On the contrary, the Redd2 overactive led to increased cell death and a disturbance of a basic cell growth known as MTORC1.

Further experiments on cultivation cells and mouse models also showed that RedD2 lack of mice had better blood sugar control when fed with a high fat or exposed -in -diabetes chemicals. These mice also had a larger number of β-cell healthy and produced more insulin. Data analysis of human islands supports the negative effects of Redd2 on beta-cell capacity and insulin secretion.

“We have found that the suppression of Redd2 expression protects β-cells from damage, even in tendency to over-consumption, preventing the onset of diabetes,” Harada said.

The discovery of the RedD2 role as a key player in beta-cell damage opens new possibilities for early diagnosis and treatment of type 2 diabetes.

“We hope that Redd2 can serve as a diagnostic indicator for type 2 diabetes and pave the way for new medicines or functional foods targeting it,” Harada said.

The study was published in Newspaper of biological chemistry.