The production of energy that powers cells and facilitates their operation depends on mitochondria.
On the other hand, disorders like type 2 diabetes are linked to mitochondrial abnormalities. Individuals with this condition are unable to use the insulin their pancreas produces to maintain normal blood sugar levels or create enough of it themselves.
Diabetes patients’ insulin-producing pancreatic β-cells contain aberrant mitochondria that prevent them from creating energy, according to multiple studies. However, these investigations failed to provide an explanation for the cells’ actions.
Their findings were published in the journal Science.
We wanted to determine which pathways are important for maintaining proper mitochondrial function.
Emily M. Walker
In order to accomplish this, the researchers harmed three elements that are necessary for mitochondrial function: their DNA, a mechanism that eliminates damaged mitochondria, and one that keeps the cell’s mitochondrial pool healthy.
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,
Our results demonstrate that the mitochondria can send signals to the nucleus and change the fate of the cell.
Emily M. Walker
The team’s findings led them to broaden their investigation into additional cells impacted by diabetes.
Losing your β-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,
Diabetes is a multi-system disease—you gain weight, your liver produces too much sugar and your muscles are affected. That’s why we wanted to look at other tissues as well.
Although we haven’t tested all possible cell types, we believe that our results could be applicable to all the different tissues that are affected by diabetes.
Scott A. Soleimanpour
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Upon repeating their animal tests in fat-storing and liver cells, the scientists observed that the same stress response was triggered. Both cell types failed to develop and perform as intended.
The researchers discovered that mitochondrial damage did not result in cell death, regardless of the kind of cell.
This observation raised the prospect that the cells would behave normally if the harm could be undone.
They accomplished this by blocking the stress response with a medication known as ISRIB. After four weeks, they discovered that the β-cells could once again regulate the mice’s blood sugar levels.
Losing your β-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.
Scott A. Soleimanpour
Source: University of Michigan – News
Journal Reference: Walker, Emily M., et al. “Retrograde Mitochondrial Signaling Governs the Identity and Maturity of Metabolic Tissues.” Science, 2025, DOI: 10.1126/science.adf2034.
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Graduated from the University of Kerala with B.Sc. Botany and Biotechnology. Attained Post-Graduation in Biotechnology from the Kerala University of Fisheries and Ocean Science (KUFOS) with the third rank. Conducted various seminars and attended major Science conferences. Done 6 months of internship in ICMR – National Institute of Nutrition, Hyderabad. 5 years of tutoring experience.