During a recent study, researchers at the Obesity Research Unit of the University of Helsinki found that obesity clearly reduces mitochondrial gene expression in fat tissue or adipose tissue. A total of 49 pairs of identical twins discordant for bodyweight participated in the study conducted at the University of Helsinki: their body composition and metabolism were studied in detail, and biopsies from adipose and muscle tissue were collected. Multiple techniques for analysing the genome-wide gene expression, the proteome, and the metabolome were used in the study. According to the findings, the pathways responsible for mitochondrial metabolism in adipose tissue were greatly reduced by obesity. Since mitochondria are key to cellular energy production, their reduced function can maintain obesity. The study provided strong evidence of a connection between the low performance of adipose tissue mitochondria and a proinflammatory state. A low-powered mitochondrial engine may also generate toxic exhaust fumes, which can cause a pro-inflammatory state in adipose tissue and, consequently, the onset of diseases associated with obesity," says Professor Kirsi Pietilainen from the Obesity Research Unit, University of Helsinki."What was surprising was that the mitochondrial pathways in muscle had no association with these adverse health effects," Pietilainen adds. Obesity also affected amino acid metabolism. In the study, changes in mitochondrial function were also seen in amino acid metabolism. The metabolism of branched-chain amino acids, which are essential to humans, was weakened in the mitochondria of both adipose tissue and muscle tissue.