Obesity found to dull the function of mitochondia
Scientists at the University of Helsinki, Finland, who analysed metabolic changes that can take place in fat tissue as a result of obesity, have found that obesity can negatively affect the performance of mitochondria in fat cells and drive inflammation and a range of other obesity-related conditions.
The scientists recruited 49 pairs of identical twins because of their identical genetic background, and often have many shared life events and family upbringing. Identical twins also offer scientists a very useful testbed for studying how environmental factors later in life alone can impact their gene expression.
The identical twins in the study were “highly discordant” for clinical characteristics of obesity, meaning one was significantly heavier than the other. This enabled the scientists to explore how environmental and lifestyle factors impacted their gene expression, particularly in relation to mitochondria.
“Identical twins have the same genes, and their weight is usually fairly similar,” said Professor Kirsi Pietiläinen of the university’s Obesity Research Unit. “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 utilised this characteristic in our study when looking into the effects of weight on tissue function.”
Using various analytical tools and biopsies of fat and muscle tissue to gain a picture of genome-wide gene expression in the twins, the scientists discovered 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.
Additionally, the researchers also observed a weakening in the mitochondrial function of amino acid metabolism – the reduced breakdown of branched chain 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.
Professor Pietiläinen sums this up: “If mitochondria, the cellular powerplants, are compared to the engine of a car, you could say that the power output decreases as weight increases. 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.”
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