- Low energy expenditure is linked to long-term weight gain.
- THNSL2 gene in skeletal muscle is associated with energy expenditure and weight gain.
- Targeting the gene THNSL2 could be the new treatment for obesity, claims a new study.
Obesity affects people of all ages, gender, and its prevalence has significantly increased in the recent years. Researchers have been conducting experiments to combat obesity, which increases the risk of metabolic disorders and death. For the first time, a study explored the link between genetics and calorie burn or energy expenditure. Researchers have identified a new potential pathway in the muscle tissue to improve the rate of energy expenditure.
"Obesity research continues to show that our ability to gain or lose weight may not be completely reliant on individual behaviors, but perhaps our genetic traits," says lead author Paolo Piaggi, Ph.D., National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), part of the National Institutes of Health.
‘Increased expression of a gene called THNSL2 in human skeletal muscle is associated with lower energy expenditure and weight gain.’
"This new study is one of the first to identify a particular genetic pathway in our muscle tissue that we may be able to harness to develop new treatments for obesity."
The researchers at NIDDK's Phoenix Epidemiology and Clinical Research Branch performed an exome-wide gene expression study in skeletal muscle biopsies. The study involved 219 healthy individuals. The skeletal muscle biopsies of the individuals measured at rest and over 24 hours were analyzed by the Affymetrix Human Exon 1.0 ST array. The researchers analyzed the long-term weight change over seven years.
Researchers found that the expression of the THNSL2 gene in skeletal muscle tissue had the strongest association between lower energy expenditure and weight gain.
The gene THNSL2 is bimodally expressed, and an mRNA splice variant, a key player in translating a gene to a protein, impacts the production of the osteoclastogenic factor of activated T cells (SOFAT), a cytokine secreted by T-cells that stimulates the production of interleukin 6. The study suggests that SOFAT may influence energy expenditure through the inflammatory pathways related to energy expenditure and obesity.
"The research brings us one step closer to better understanding the variation in weight gain among individuals, particularly when on similar diets," said Anthony Comuzzie, PhD, spokesperson for The Obesity Society and Scientist at Texas Biomedical Research Institute.
"We know that there are ties between our genes and energy expenditure, and this study offers several potentially important extensions to that work, in particular by implicating a specific pathway for treatment," added Comuzzie.