The study was reported in The FASEB Journal by authors from the School of Medicine at the UT Health Science Centre San Antonio and the university’s Barshop Institute for Longevity and Aging Studies. These researchers discovered that mice with a diminished activity of a protein complex involved in mitochondrial function were healthier, and their life span was 20% longer on average.
According to lead author Deepa Sathyaseelan, PhD, research assistant professor of cellular and structural biology in the School of Medicine, ‘This is an unexpected finding because you would think that something that decreases mitochondrial function would have a damaging effect, but instead we saw an increase in life span and beneficial metabolic effects. The most important thing we noticed is reduced body weight and decreased fat mass in the mice. We found that this decreased fat mass is due to increased fat utilization.’
Everything you do, from breathing to thinking, requites energy from the ATP that mitochondria produce, and study senior author Holly Van Remmen, Ph.D., professor of cellular and structural biology adds that the cellular powerhouses are a major site of fat utilization. Too much or too little fat can damage your wellness, as fat is an endocrine organ that performs many functions. The mice with the mitochondrial mutation made greater numbers of new mitochondria, in comparison to the control animals, which means their cells are constantly remodelling themselves.
As mitochondrial dysfunction often occurs with age, and age relates to many diseases such as type 2 diabetes, heart disease and cancer, Dr Van Remmen said the mice ‘are very important from an aging standpoint. We want to understand how these animals can have added longevity, yet have a 60% reduction in a protein complex involved in mitochondrial function.’
Dr Sathyaseelan added that the study ‘opens the door to new clues about how mitochondrial function might modulate insulin sensitivity’ which represents an important step for diabetes research.