[Finland], April 11 (ANI): During a recent study, researchers at the University of Helsinki Obesity Research Unit found that obesity significantly reduced mitochondrial gene expression in adipose or adipose tissue.
Mitochondria are important cellular powerhouses 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 was recently published in the journal Cell Reports Medicine.
A total of 49 pairs of identical twins who did not match in terms of body weight participated in the study carried out at the University of Helsinki: their body composition and metabolism were examined in detail, and biopsies from adipose and muscle tissue were collected. Several techniques were used in the study to analyze genome-wide gene expression, proteome, and metabolome.
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 accumulation of fat in the liver, prediabetic disorders of glucose and insulin metabolism, and cholesterol. “If mitochondria, the cellular powerhouses, are compared to the engine of a car, you could say that performance decreases with increasing weight.
A low-powered mitochondrial engine can also produce toxic fumes that can cause an inflammatory state in adipose tissue and, consequently, the occurrence of obesity-related diseases, “says Professor Kirsi Pietilainen of the Obesity Research Unit at Helsinki University.” Which was surprising that the mitochondrial pathways in the muscle were unrelated to these adverse health effects, “added Pietilainen.
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, was weakened in the mitochondria of both adipose tissue and muscle tissue. “This finding was of particular importance because these amino acids were broken down less and the concentration in the blood increased was also in previous twin studies directly linked to prediabetic changes and the accumulation of liver fat,” says Pietilainen.
Obesity, with its numerous associated diseases, is a widespread phenomenon, the prevalence of which is steadily increasing. While lifestyle affects the onset of obesity, genes also play an important role. “Identical twins share the same genes and their weights are usually quite similar. In fact, studying twins is the best way to examine the relationship between genes and lifestyle. Despite their identical genome, twins’ genes and even mitochondria can be at different levels of activity We used this property in our study to look at the effects of weight on tissue function, “says Pietilainen.