Mitochondria are essential to generate energy that feeds the cells and helps them work.
However, mitochondrial defects are associated with the development of diseases such as type 2 diabetes. Patients suffering from this disorder cannot produce sufficient insulin or use insulin produced by their pancreas to maintain their blood sugar at normal levels.
Several studies have shown that β pancreatic cells insulin producing patients with diabetes have abnormal mitochondria and cannot generate energy. However, these studies could not explain why cells behaved in this way.
In a study published in ScienceResearchers at the University of Michigan used mice to show that dysfunctional mitochondria trigger an answer that affects the maturation and function of β cells.
“We wanted to determine what ways are important to maintain an adequate mitochondrial function,” said Emily M. Walker, Ph.D, an assistant teacher of internal medicine research and first author of the study.
To do so, the team damaged three components that are essential for mitochondrial function: its DNA, a path used to get rid of damaged mitochondria, and one that maintains a healthy set of mitochondria in the cell.
“In all three cases, exactly the same response to stress was activated, which caused the β cells to become immature, stop doing enough insulin and essentially cease to be β cells,” Walker said.
“Our results show that mitochondria can send signals to the nucleus and change the destination of the cell.”
The researchers also confirmed their findings in the cells of human pancreatic islets.
Mitochondrial dysfunction affects various types of cells
Their results led the team to expand their search in other cells affected during diabetes.
“Diabetes is a multi -systems disease: increases in weight, its liver produces too much sugar and its muscles are affected. That is why we also wanted to look at other fabrics,” said Scott A. Soleimanpour, MD, director of the Research Center for Research Center Michigan diabetes and main author of the study.
The team repeated its mouse experiments in liver cells and fat storage cells and saw that the same stress response was activated. Both types of cells could not mature and work properly.
“Although we have not tried all possible types of cells, we believe that our results could be applicable to all the different tissues affected by diabetes,” Soleimanpour said.
Reversing mitochondrial damage could help cure diabetes
Regardless of the type of cell, the researchers found that damage to mitochondria did not cause cell death.
This observation raised the possibility that if they could reverse the damage, the cells would function normally.
To do so, they used a medication called isib that blocked the response to stress. They discovered that after four weeks, the β cells recovered their ability to control glucose levels in mice.
“Losing their β cells is the most direct route to obtain type 2 diabetes. Through our study, we now have an explanation of what could be happening and how we can intervene and fix the root cause,” Soleimanpour said.
The team is working to dissect even more cell paths that are interrupted and hope they can replicate their results in cell samples of diabetic patients.