Mitochondria are responsible for creating energy, which fuels cells and keeps them functioning. However, mitochondrial abnormalities have been linked to the development of disorders like type 2 diabetes. Patients with this illness are unable to produce enough insulin or use the insulin produced by their pancreas to maintain normal blood sugar levels.
Researchers at the University of Michigan used mice to show that dysfunctional mitochondria trigger a response that affects the maturation and function of b-cells.
Several studies have shown that insulin-producing pancreatic b-cells of patients with diabetes have abnormal mitochondria and are unable to generate energy. Yet, these studies were unable to explain why the cells behaved this way.
“We wanted to determine which pathways are important for maintaining the proper mitochondrial function,” said Emily M. Walker, Ph.D, a research assistant professor of internal medicine and first author of the study.
To do so, the team damaged three components that are essential for mitochondrial function: their DNA, a pathway used to get rid of damaged mitochondria, and one that maintains a healthy pool of mitochondria in the cell.
“In all three cases, the exact same stress response was turned on, which caused b-cells to become immature, stop making enough insulin, and essentially stop being b-cells,” Walker said. “Our results demonstrate that the mitochondria can send signals to the nucleus and change the fate of the cell.”
The researchers also confirmed their findings in human pancreatic islet cells.
Their results prompted the team to expand their search into other cells that are affected by diabetes.
Losing your b-cells is the most direct path to getting type 2 diabetes. Through our study we now have an explanation for what might be happening and how we can intervene and fix the root cause,” said Scott A. Soleimanpour, M.D.