Our bodies rely on tiny structures called mitochondria to generate energy for our cells. These structures are often described as the “powerhouses” of the cell because they turn food into energy. However, when mitochondria don’t work properly, it can lead to serious health problems, including type 2 diabetes.
Type 2 diabetes is a condition where the body cannot produce enough insulin or does not use insulin effectively. Insulin is a hormone that helps regulate blood sugar levels. Without it, sugar builds up in the blood, leading to various health complications.
Scientists have known for a while that people with diabetes have damaged mitochondria in their insulin-producing cells, called β-cells. These cells are found in the pancreas and play a crucial role in keeping blood sugar levels in check. However, researchers did not fully understand why mitochondria in these cells stopped working.
A study from the University of Michigan, published in Science, sheds light on this mystery. Researchers used mice to investigate what happens when mitochondria in β-cells become dysfunctional.
They found that when mitochondria are damaged, they send signals that make the β-cells immature. As a result, these cells stop making enough insulin, which contributes to the development of diabetes.
Dr. Emily M. Walker, the study’s lead author, explained that the team focused on three key components that help mitochondria function properly: mitochondrial DNA, a pathway that removes damaged mitochondria, and a system that keeps mitochondria healthy.
When they disrupted any of these components, the same stress response was triggered, causing β-cells to lose their ability to function.
The study also found that this process is not limited to β-cells. Since diabetes affects many parts of the body, the researchers wanted to see if the same mitochondrial stress response happened in other cells, such as liver cells and fat-storing cells.
When they conducted similar experiments on these cells, they observed the same problem—cells became immature and lost their function.
Dr. Scott A. Soleimanpour, the senior author of the study, emphasized that diabetes is a complex disease that affects multiple organs. Weight gain, high blood sugar production by the liver, and muscle issues are all linked to diabetes. This study suggests that mitochondrial problems could be a common factor in these issues.
One of the most promising discoveries from this research is that the damaged cells did not die. This means there could be a way to reverse the damage. To test this, the researchers gave the mice a drug called ISRIB, which blocked the stress response caused by mitochondrial damage.
After four weeks of treatment, the β-cells started producing insulin again, and the mice’s blood sugar levels returned to normal.
Dr. Soleimanpour highlighted that the loss of β-cells is a major cause of type 2 diabetes, and this study provides a possible explanation for why it happens. More importantly, it offers hope that scientists could find ways to restore damaged cells and potentially reverse diabetes.
The team is now working to understand the detailed mechanisms behind this process and hopes to test their findings on human cells from diabetic patients. If successful, this research could lead to new treatments that address the root cause of diabetes rather than just managing its symptoms.
If you care about diabetes, please read studies about bananas and diabetes, and honey could help control blood sugar.
For more health information, please see recent studies about Vitamin D that may reduce dangerous complications in diabetes and results showing plant-based protein foods may help reverse type 2 diabetes.
The research findings can be found in Science.
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