Researchers at the Pennington Biomedical Research Center have revealed critical ideas about how deteriorated mitochondrial dynamics and quality control mechanisms on the influence of skeletal muscle influence insulin sensitivity in patients with type 2 or T2D diabetes. The study, entitled “Deviquitinant enzymes regulate mitochondrial quality control of skeletal muscle and insulin sensitivity in patients with type 2 diabetes”, was recently published in the Journal of Cachexia, Sarcopenia and Muscle.
The research team, led by Pennington’s Biomedic Executive Director, Dr. John Kirwan, focused on the importance of misubiquitation or DUB enzymes, in the regulation of mitochondrial dynamics within the skeletal muscle. The findings suggest that mitochondrial fragmentation can avoid defects in mythophagy, the process by which cells eliminate damaged mitochondria, to maintain quality control of skeletal muscle in patients with DA2. This adaptation can help maintain mitochondrial function despite deteriorated mythophagy.
In other words, the study shows that people with T2D have less healthy mitochondria, the parts of the cell that produce energy, because a certain protein protein related to dynamine 1, or DRP1, is working too much. In addition, it is shown that another group of protein, Dubs, interferes with a process that helps the body to clean the damaged mitochondria. This interference makes it more difficult for muscles to use insulin correctly, which is a key issue in diabetes.
The results of the investigation advance the understanding of how the deteriorated mitochondrial dynamics and the quality control can contribute to the resistance to the insulin of the skeletal muscle and the manifestation of the DA2, and also provides key evidence that Dub antagonists can play an important role in the prevention or treatment of T2D.
“Our research team examined how certain enzymes affect mitochondria in the muscle cells of people with diabetes,” said Dr. Kirwan Dr. Kirwan, Executive Director and George A. Bray, Jr., gave Super Chair in nutrition in Pennington Biomedical. “We discovered that when the normal cleaning process for damaged mitochondria does not work well, the cells adapt by breaking the mitochondria into smaller pieces. This alternative approach helps maintain muscle function despite the metabolic challenges of type 2 diabetes Metabolic. ” “