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The researchers found that the man's mitochondrial DNA, which is

May 9, 2017 by Kimberly Parks

The researchers found that the man's mitochondrial DNA, which is highly conserved at the cellular level, was found to be of great importance for his health. "The results of this new study support the theory of a genetic component in the aging process that may be involved in the etiology of mitochondrial disease," says lead author Dr. Gert Jørgensen of the Max Planck Institute for Integrative Biology in Stuttgart, Germany.

The team at the Max Planck Institute for Integrative Biology in Stuttgart, Germany, used a technique called the mt-coviral gene-seq approach. The study, and the work that follows it, is called an "exo-genetic loci study," and is aimed at the study of a few genetic markers (or genes) in humans. The researchers also used the mtDNA gene-seq approach to study patterns of inflammation, inflammation prevention, and inflammation-related genes. In order to get at what was known about the mitochondria, the researchers looked for two genes in the human mitochondria that are associated with various metabolic processes: insulin and glucagon. The researchers then used the findings to test the hypothesis that mitochondria are capable of a variety of metabolic processes.

In a previous study, they used mtDNA and mt-cov-1 gene-seq to develop a model of metabolic pathways that might play a role in mitochondrial disease. But this approach had three major difficulties. First, it lacked an accurate, well-established model of mitochondrial disease, which means it had to be re-analyzed. So the researchers looked for a gene whose function was known to be involved in regulating other factors—including insulin and glucagon—while also looking for a gene whose function was associated with metabolic stress, which is caused by inflammation.

The new model they came up with was based on the theory that, because mitochondrial functions are regulated by insulin and glucagon, one mechanism of dysfunction in the human mitochondria might be associated with an increased risk of disease, such as diabetes. But that theory would never be tested in humans, because of the complex nature of some of the genes involved in mitochondrial disease.

"Because of what has already been reported in humans, our new study has the potential to have a much wider range of applications. It is important to understand the role of many different genes in the processes that regulate mitochondrial function in different conditions, including obesity, insulin resistance, and the metabolic syndrome," says lead author Dr. Robert Jørgensen of the Max