Mitochondria May Hold The Key To Curing Diabetes, Study Reveals New Breakthrough


New York: Mitochondria, that produce energy for the cell, holds the key to curing diabetes, researchers have learned. 

Mitochondrial defects are associated with the development of diseases such as type 2 diabetes.

Patients who suffer from this disorder are unable to produce enough insulin or use the insulin produced by their pancreas to keep their blood sugar at normal levels.

Several studies have shown that insulin-producing pancreatic 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.

In a new study published in the journal Science, researchers at the University of Michigan in the US used mice to show that dysfunctional mitochondria trigger a response that affects the maturation and function of these cells.

“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 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 pancreatic cells to become immature, stop making enough insulin, and essentially stop being pancreatic 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.

Losing your pancreatic 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 authors.

The team is working on further dissecting the cellular pathways that are disrupted and hope that they will be able to replicate their results in cell samples from diabetic patients.

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