Mitochondria and obesity
Study of twins showed how obesity disrupts mitochondria
Georgy Golovanov, Hi-tech+
Scientists from Finland collected 49 pairs of twins to understand the metabolic changes occurring in adipose tissue as a result of obesity. They paid special attention to biological processes that negatively affect health. Researchers have found that obesity disrupts the function of mitochondria in fat cells, which leads to inflammation and a number of other adverse effects.
Since identical twins have identical genetic backgrounds, often along with the same upbringing and shared experience, they turn out to be an extremely useful test model for science to study the effects of environmental factors on gene expression.
A team of scientists from The University of Helsinki applied this method to pairs of twins, among whom one was much heavier than the other. Using a set of analytical tools and biopsy of fat and muscle tissues, they obtained a genome-wide picture of gene expression, according to a press release A twin study indicates that metabolic changes in fat tissue in obesity associated with adverse health effects – No similar link found in muscle tissue.
Article by van der Kolk et al. Molecular pathways behind acquired obesity: adipose tissue and skeletal muscle multiomics in monozygotic twin pairs discordant for BMI published in the journal Cell Reports Medicine – VM.
It turned out that mitochondrial function in adipose tissues was significantly reduced as a result of obesity. The analysis also showed that these changes in adipocytes can lead to inflammation and a number of biological processes unfavorable to health: fat deposition in the liver, changes in the metabolism of cholesterol, glucose and insulin. Although mitochondrial abnormalities were also observed in muscle tissues, they were not as extensive and dangerous to health.
"If we compare the mitochondria, the power plant of a cell, with the engine of a car, we can say that with increasing weight, the output power decreases," explained Professor Kirsi Pietilainen, the author of the article. "A low–powered mitochondrial engine can also produce exhaust gases that cause a pro-inflammatory condition in adipose tissue and, as a result, diseases associated with obesity."
In addition, scientists observed a weakening of the mitochondrial function of amino acid metabolism. This leads to an increased concentration of these amino acids in the blood, which, as was found in a previous study, is directly related to prediabetic changes and fat deposits in the liver.
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