The team’s findings, published in the European scientific journal Molecular Metabolism, showed that different versions of the PGC-1a protein are produced in skeletal muscle when people exercise. The greater the production of this protein, the more energy people expend.

The team, comprising researchers from the Kobe University Graduate School of Medicine and other institutions, found that mice lacking these variants “manifest impaired energy expenditure during exercise, leading to the development of obesity and hyperinsulinemia”.

When the team examined skeletal muscle in humans, they found that other PGC-1a variants also increased during exercise. They thus suggest that production of variants differs by individual, leading to a gap in weight loss even when people do the same exercise.

While drugs that suppress appetite are often prescribed in treating obesity, the latest findings could lead to new drugs that induce or increase those variants independently of exercise.

“Obesity-linked illnesses are a significant healthcare target, and if new drugs can eliminate obesity, it could help treat various diseases,” said Wataru Ogawa, a Kobe University professor on the team.