Produced by the pancreas to maintain normal blood sugar levels.
Scientists at the University of Michigan conducted research using mice to demonstrate that malfunctioning mitochondria initiate a response that impacts the development and performance of B-cells.
Studying certain cells found that they had abnormal mitochondria, unable to produce energy. Despite this, researchers were unable to determine the cause of this unusual behavior.
"We sought to identify the pathways crucial for maintaining optimal mitochondrial function," said Emily M. Walker, Ph.D, a research assistant professor of internal medicine and lead author of the study.
To achieve this, the researchers impaired three vital components necessary for mitochondrial operation: their genome, a mechanism used for eliminating defective mitochondria, and a system responsible for maintaining a healthy mitochondrial pool within the cells.
And "essentially, stop being B-cells," Walker commented. "Our findings show that the mitochondria can send signals to the nucleus, which can then change the cell's fate."
The researchers also confirmed their results in human pancreatic islet cells.
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"We finally have an explanation for what's going on and know how we can address and correct the main issue," said Dr. Scott A. Soleimanpour.
"We found that in diabetes, not only muscle tissue, but other tissues such as fat and liver are also producing too much sugar, which is affecting the whole body. That's why we wanted to examine other tissues as well," says Dr. Scott A. Soleimanpour, Director of the Michigan Diabetes Research Center and lead author of the study.
The cells and fat-storing cells under stress activated the same response to stress. However, both cell types failed to mature and operate correctly.
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Although the type of cell being studied was not a factor, the researchers concluded that damage to the mitochondria failed to result in cell death.
This observation raises the possibility that if the damage can be reversed, the cells should function normally.
To achieve this, they employed a medication called ISRIB that suppressed the stress response. They determined that, following a four-week period, the b-cells regained the capacity to govern glucose levels in mice.
"We now have an explanation for what is happening and how we can address it and correct the root cause," Soleimanpour said.
The team is currently involved in further analyzing the cellular pathways that are affected and hopes to be able to replicate their findings using cell samples from diabetic patients.