Scientists from Tokyo Medical University in Japan looked at the synoviolin gene (SYVN1), which is known to be linked to levels of white adipose tissue - a key factor in obesity.
Mice bred to be lacking the gene lost weight and did not accumulate as much fat as mice with the gene, researchers found. SYVN1 influences the number and activity of mitochondria within cells, so fat tissue 'used up' more energy in the mutant mice.
The team then tested a drug, dubbed LS-102, which inhibits the enzyme coded for by SYVN1.
When trialled in obese mice, LS-102 decreased the animals' weight by 85% even though they did not eat less and were absorbing the same amount of nutrients from their food.
The researchers think that LS-102 will have fewer side effects than previously trialled drugs for obesity.
Obesity is linked to inflammatory diseases such as RA, and the SYVN1 gene is known to be linked to RA.
'Obesity is a known risk factor for other chronic disorders,' said Professor Toshihiro Nakajima, who led the study. 'Our findings indicate that synoviolin may be a key for understanding the common features of obesity and chronic inflammatory disease such as RA.'
Mice given LS-102 also had decreased blood glucose levels. 'Although further studies are needed to clarify the role of SYVN1 in glucose metabolism, SYVN1 is an important drug candidate for obesity and associated metabolic diseases,' the study authors wrote.
The study comes as a Lancet report suggests that progress in tackling obesity levels is now 'unacceptably slow'.
The National Obesity Forum has said there is a strong argument for new QOF targets for GPs to provide advice on weight management.
It has said the current QOF target for practices to keep a register of obese patients is counterproductive and effectively penalises GPs for helping patients to lose weight.