Stress destroys insulin

A team of researchers from Osaka University asked a simple but important question: what exactly causes insulin-producing cells to break down in type 2 diabetes? After all, the disease is increasingly appearing in people in adulthood — often unnoticed, against the background of stress, overeating and malnutrition.

It is this combination—an overabundance of sugar, fat, and food overload—that turns on REDD2. Normally, this gene should help cells cope with stress. But in this case, on the contrary, it harms: the cells begin to work worse, die faster, and the body loses the ability to control blood sugar levels.

When the scientists suppressed the activity of REDD2, the pancreatic cells revived. They started producing insulin in the right amounts again, even if the animals or cells were exposed to stress like a fatty diet or chemicals that mimic diabetes. And in laboratory mice in which this gene was disabled, blood sugar remained normal even after a heavy meal.

What was particularly impressive was that REDD2 affects one of the central mechanisms of cell growth and survival, the mTORC1 pathway. If this path is disrupted, the cell loses its navigator and stops functioning normally.

This discovery could be an important fulcrum for creating new ways to prevent diabetes. Scientists hope that in the future REDD2 can be used as a marker to understand in advance who is at risk of diabetes, as well as as a target for drugs or even special products that can disable the harmful activity of this gene.

“We hope that this finding will help protect people from diabetes even before it begins,” says study leader Professor Naoki Harada. “If we learn how to calm REDD2, we can protect insulin cells even under conditions of malnutrition.”

So, perhaps in the coming years, the fight against diabetes will begin not with injections of insulin, but with fine—tuning the internal biochemistry – before the disease has time to manifest itself.