Mitochondrial Dysfunction Impairs β-Cell Maturation and Function in Diabetes
A study published in Science by researchers at the University of Michigan demonstrates that mitochondrial dysfunction triggers a stress response that alters the identity and function of β-cells, contributing to type 2 diabetes.
“We wanted to determine which pathways are important for maintaining 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 essential mitochondrial components: their DNA, a pathway used to eliminate damaged mitochondria, and another that maintains a healthy mitochondrial pool.
“In all three cases, the exact same stress response was turned on, which caused β-cells to become immature, stop making enough insulin, and essentially stop being β-cells,” Walker explained. “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, reinforcing the relevance of their discoveries.
Expanding their research, the scientists observed the same stress response in liver and fat-storing cells, suggesting a broader impact of mitochondrial dysfunction in diabetes. Importantly, they found that blocking this stress response with the drug ISRIB restored β-cell function in mice, offering a potential therapeutic strategy to reverse diabetes at its root cause.
Image Credit: Targeting mitochondrial dysfunction could cure diabetes / Getty Images
