Diabetes is a disease for which a solid cure has not yet been discovered, although efforts are ongoing. Now a means of treatment is being sought from the mitochondria present in the cells.
Diabetes: Researchers have found in a study that mitochondria, which produce energy for the body's cells, are the key to treating diabetes. Diseases like diabetes type 2 are related to a malfunction in the "mitochondria" present within the cells. Patients suffering from this disease are unable to produce sufficient amount of insulin or are unable to use the insulin produced by their pancreas to maintain blood sugar at normal levels.
Experiments done on mice
Several studies have shown that the insulin-producing pancreatic cells of diabetic patients have abnormal mitochondria and are unable to produce energy. However, these studies have been unable to clarify why the cells behave this way. In a new study published in the journal Science, researchers from the University of Michigan conducted experiments on mice to show that malfunctioning mitochondria produce a response that affects the maturation and function of these cells.
What the researchers say
"We wanted to determine which pathways are important for maintaining proper mitochondrial function," said Emily M. Walker, PhD, research professor of internal medicine and first author of the study. The team damaged three components that are essential to the function of mitochondria: their DNA, a pathway used to get rid of damaged mitochondria, and one that maintains a healthy pool of mitochondria in the cell.
Solution to Diabetes
"In all three conditions, the body triggered the same stress response. This made the pancreatic cells immature, unable to produce enough insulin, and eventually the pancreas ceased to be cells. Our results show that mitochondria can send signals to the cell nucleus and change the way the cell works," Walker said. The researchers also confirmed their findings in human pancreatic islet cells.
The destruction of pancreatic cells is a direct cause of type 2 diabetes. This study helps us understand how this happens and how to find solutions to this problem. The team is working on further analysing the cellular pathways that are disrupted, and they hope to be able to replicate their results in cell samples from diabetic patients.
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