A double study recently completed at the University of Helsinki shows that the machines responsible for handling energy in adipose tissue work poorly in obesity. In the study, a significant reduction in the activity of mitochondrial genes in obesity was observed in adipose tissue, while a similar change in genomic mitochondria was negligible at the genome level. An association with adverse health effects has only been found in the mitochondria of adipose tissue.
Researchers at the University of Helsinki Obesity Research Unit have found that obesity significantly reduces mitochondrial gene expression in adipose or adipose tissue. Mitochondria are important cellular power plants that process all of our energy input. Often times, when the pathways associated with the breakdown of nutrients are lazy, the changes can have health-related consequences.
The study carried out at the University of Helsinki involved a total of 49 pairs of identical twins who did not match in terms of body weight: their body composition and metabolism were examined in detail, and biopsies were taken from adipose and muscle tissue. Several techniques were used in the study to analyze genome-wide gene expression, proteome, and metabolome.
The study was recently published in the journal Cell Reports Medicine.
According to the findings, the pathways responsible for mitochondrial metabolism in adipose tissue were greatly reduced by obesity. Since mitochondria are the key to cellular energy production, their diminished function can sustain obesity. For the first time, the study also compared the effects of obesity specifically on the mitochondria in the muscle tissue of these identical pairs of twins: the muscle mitochondria were also out of tune, but the change was less pronounced than in adipose tissue.
The study provided strong evidence of a link between the poor performance of mitochondria in adipose tissue and a pro-inflammatory condition. In addition, the results indicate that metabolic changes in adipose tissue are associated with increased fat accumulation in the liver, prediabetic disorders of glucose and insulin metabolism and cholesterol.
If mitochondria, the cellular powerhouses, are compared to a car’s engine, it could be said that performance decreases as weight increases. A low power mitochondrial engine can also produce toxic fumes, which can cause an inflammatory condition in adipose tissue and, consequently, the occurrence of diseases associated with obesity. “
Professor Kirsi Pietiläinen, Department of Obesity Research, University of Helsinki
“What was surprising was that the mitochondrial pathways in the muscle were unrelated to these adverse health effects,” added Pietiläinen.
Obesity also affected amino acid metabolism
Changes in mitochondrial function in amino acid metabolism were also observed in the study. The metabolism of branched chain amino acids, which are essential for humans, has been weakened in the mitochondria of both adipose tissue and muscle tissue.
“This finding was of particular importance because the reduced breakdown of these amino acids and the resulting increased concentration in the blood were directly linked to prediabetic changes and the accumulation of liver fat in earlier twin studies,” says Pietiläinen.
Obesity, with its numerous associated diseases, is a widespread phenomenon, the prevalence of which is steadily increasing. While lifestyle influences the onset of obesity, genes also play a significant role.
“Identical twins share the same genes, and their weight is usually quite similar. In fact, studying twins is the best way to study the relationship between genes and lifestyle. Despite their identical genome, twins’ genes and even mitochondria can work We used this trait in our study to look at the effects of weight on tissue function, “says Pietiläinen.
Source:
Journal reference:
van der Kolk, BW et al. (2021) Molecular Pathways Behind Acquired Obesity: Adipose Tissue and Skeletal Muscle Multiomics in Monozygous Twins Mismatched for BMI. Cell reports medicine. doi.org/10.1016/j.xcrm.2021.100226.
