01 February 2013

Deterioration of mitochondria can prolong life and improve health

Mitochondria are intracellular structures in which the synthesis of molecules of adenosine triphosphate (ATP), which is a source of energy for cells, takes place. Researchers at the University of Texas, working under the guidance of Professor Holly Van Remmen, have demonstrated that the health status of mice with disabled copies of the Surf1 – Surf1 gene (-/-), in whose body the corresponding protein involved in the normal functioning of mitochondria is not synthesized, is in many ways better than in animals of the control group.

In addition, the average lifespan of mice with Surf1 knockout was 20% longer than that of normal animals. According to the authors, this looks paradoxical, since, at first glance, suppression of the functioning of mitochondria should have negative consequences.

It is also interesting that one of the effects of gene modification was a decrease in animal body weight (by 15%) and adipose tissue mass (by 20%) due to an increase in the amount of fat cleaved by mitochondria.

The researchers also found that, unlike the control group animals, more new mitochondria were synthesized in the cells of the modified mice. This fact is also quite important, since in order to maintain good functionality, the cell needs constant updating, in which the renewal of the mitochondrial pool plays an important role.

Mitochondrial disorders occur as the body ages and are associated with many age-related diseases, such as type 2 diabetes, diseases of the cardiovascular system and cancer.

According to the authors, their results shed light on the fact that mitochondrial function can affect the sensitivity of cells to insulin, which is an important step towards studying the mechanisms of diabetes development.

They also note the exceptional importance of the fact that the disruption of the protein complex, including Surf1, which reduced the activity of cytochrome c oxidase protein in all animal tissues by 50-70%, which catalyzes the final stage of electron transfer to oxygen during oxidative phosphorylation during ATP synthesis by mitochondria, is accompanied by an increase in the lifespan of mice.

Previously, other groups of researchers have demonstrated this phenomenon on a number of animal models, such as roundworms and fruit flies, but in experiments on mammals, such results were obtained for the first time.

Article by Deepa et al. Improved insulin sensitivity associated with reduced mitochondrial complex IV assembly and activity is published in The FASEB Journal.

Evgeniya Ryabtseva
Portal "Eternal youth" http://vechnayamolodost.ru based on the materials of the UT Health Science Center at San Antonio:
Link found between insulin sensitivity, cells’ powerhouses.

01.02.2013

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