Twin study reveals how obesity can dull the function of mitochondria
Scientists at the University of Helsinki have used 49 pairs of identical twins to delve into the metabolic changes that can take place in fat tissue as a result of obesity, teasing out some distinct biological processes that were linked to adverse health effects. The study highlights how obesity can negatively affect the performance of mitochondria in our fat cells, which can in turn drive inflammation and a range of obesity-related conditions.
Because identical twins share an identical genetic background, often along with many shared life events and family upbringing, they offer scientists a very useful testbed for studying how environmental factors later in life alone can impact their gene expression. A good example of this is the NASA twins study that compares the genes and biology of twins Mark and Scott Kelly, one of which spent almost a year in space and one of which did not.
The University of Helsinki team applied this methodology to identical twins that were "highly discordant" for clinical characteristics of obesity, meaning one was heavier than the other. This enabled the team to explore how environmental and lifestyle factors impacted their gene expression, particularly in relation to mitochondria, widely known as the powerhouse of cells.
“Identical twins have the same genes, and their weight is usually fairly similar," says study author Professor Kirsi Pietiläinen. "In fact, studying twins is the best way to investigate the interplay between genes and lifestyle. In spite of their identical genome, the genes and even mitochondria of twins can function on different activity levels. We utilized this characteristic in our study when looking into the effects of weight on tissue function."
The team used various analytical tools and biopsies of fat and muscle tissue to gain a picture of genome-wide gene expression in the twins. This showed that mitochondrial function in fat tissue was greatly reduced as a result of obesity. The analysis also revealed evidence that these changes in the fat tissue can drive inflammation and many of the biological processes associated with obesity, such as increased fat in the liver and changes to cholesterol, glucose and insulin metabolism. While mitochondria in muscle tissue was also found to be altered, the effects weren't as profound and weren't associated with the adverse health effects.
“If mitochondria, the cellular powerplants, are compared to the engine of a car, you could say that the power output decreases as weight increases," says Pietiläinen. "A low-powered mitochondrial engine may also generate toxic exhaust fumes, which can cause a proinflammatory state in adipose tissue and, consequently, the onset of diseases associated with obesity."
Additionally, the researchers also observed a weakening in the mitochondrial function of amino acid metabolism.
“This finding was of particular significance because the reduced breakdown of these amino acids and the resulting heightened concentration in blood have also been directly linked with prediabetic changes and the accumulation of liver fat in prior twin studies,” says Pietiläinen.
The research was published in journal Cell Reports Medicine.
Source: University of Helsinki
Please keep comments to less than 150 words. No abusive material or spam will be published.
It used to be considered a fallacy to confuse correlation with causation but in modern times it seems to have been reversed into a law of correlation equaling causation.