Obesity is a major risk factor for various metabolic diseases such as diabetes, fatty liver, cardiovascular disease, and cancer, and the prevalence of obesity in South Koreans stood at 34.8% as of 2016, resulting in 11.5 trillion won a year in socioeconomic losses. Obesity due to the disproportionate increase in fat tissue will undergo remodeling, accompanied by increased size of fat cells and changes in replacement rate, which causes dysfunction and metabolic diseases in fat tissues.
Researchers at Seoul National University’s College of Natural Sciences, Kim Jae-beom, proposed a new possibility of controlling metabolic diseases such as insulin resistance caused by accumulation of fat cells by identifying new control mechanisms to inhibit the formation of fat cells.
Professor Kim’s research team first identified that DNMT1 gene, which mediates DNA methylation, inhibits the formation of large fat cells through chromosomal restructuring in fat cells and mediates the constancy of systemic energy metabolism. Unlike normal mice, mice with DNMT1 gene defects have large fat cells, and if these mice eat high fat, their body fat increases accelerated and metabolic disease indicators such as insulin resistance deteriorated.
The findings suggest that the DNMT1 gene could be a new target for the development of treatments for obesity and metabolic diseases.
The implications of this study are as follows: 1) The team identified chromosomal structural regulation mechanisms that inhibit obesity and metabolic diseases; 2) the first link between DNA methylation and chromosomal regulation in fat cells; and 3) an anti-obesity mechanism was proposed. This study provided an important academic foundation for overcoming obesity and developing treatments.