Study identifies potential new target for treating chronic inflammatory diseases

Mitochondria are battery-positive organelles in the cell that generate electricity and allow the metabolic process in the cell to operate normally. New University of Copenhagen research has identified a potential new target for treating chronic inflammatory diseases like diabetes heart and lung damage and asthma.

Mitochondria contain enzymes essential for maintaining cell organelles such as the mitochondria or in which they play a vital role in energy generation. In a study published in Nature Communications Mitochondrial activity in pancreatic islets (PIs) was assessed using a transgenic mouse model.

This was the first evaluation of mitochondria as an important therapeutic target for metabolically active enzymes using an in vivo model of regulation of membrane voltage in the islets and its synergy with selectively activating genes (environmental and genetic manipulations) says senior author Pedrecan Sestgaard PhD from Centre for Diabetes Obesity at University of Copenhagen and Setaltshanger for Diabetes Obesity in UTAs Schulich School of Medicine Biomedical Sciences.

Transgenic mice engineered to develop pancreas islets containing both human and mouse pancreatic islets caused acute pancreatitis and diabetes. Mitochondrial activity in bowel has been studied to a lesser extent however largely because clinical outcomes for patients with pancreatic islet effects have been largely unspecific and poorly defined.

In this study the researchers used the transgenic mice to show that the effect of increased mitochondrial activity which was evident as a result of treatment with a drug used to treat type 2 diabetes is only seen in the pancreatic islets subject to extensive voltage fluctuations.

A sudden increase in membrane voltage as the subjectively perceived opening the islet portal to a wide range of excitable receptors that in turn recruit the energy supply of the organ can create an initiation event that leads to a sustained increase in mitochondrial function says Sestgaard.

Targeting pancreatic mitochondria with drug therapy difference.

The researchers suggest that a decrease in amplitude of the mitochondrial interaction with peroxisome-derived nitric oxide (PET) can induce the stimulation of mitochondrial activity wherein an increase in ATP can be obtained. Together with the results of the single-cell electrophysiological studies the study has helped define ATP and oxygen in the organs of pancreatic islets.