Some people could be fatter than others even when they eat similar food because of genes which encourage fat storage, according to a new study.
Scientists compared fat tissue from mice that had been selectively bred.
Researchers at Edinburgh University have found a number of genes in fat tissue which could lead to weight being retained unnecessarily in the body.
They hope the discovery could eventually lead to the development of medicines targeting obesity.
The researchers then pinpointed genes that prevented the breakdown of fat, which were more prevalent in the fat tissue of the overweight mice compared to lean mice.
Mice were then bred from one overweight parent and one lean parent.
The offspring that turned out to be overweight were found to have the same active genes as the fatter parent mouse, suggesting that hereditary factors play a role in fat storage and can increase the likelihood of putting on weight.
Dr Nik Morton, a Wellcome Trust research career development fellow at the University of Edinburgh's Centre for Cardiovascular Science, said: "While genes controlling appetite are known to be important in determining our fatness, our study shows that genes switched on in the fat tissue itself can play a role in determining why some people tend to hang onto their fat more easily than others.
"While this supports the idea that genetic factors are linked to obesity, exercise and diet are still important for healthy lifestyles and can prevent most people from becoming obese.
"If we can identify the genes and proteins that are controlling how fat we get, we may be able to target them with medicines to try and target the obese or the consequences of obesity."
The research also found that the thin mice offspring had an added protection against weight-gain.
When both sets of mice were given fatty foods, the thin offspring appeared able to break down fatty tissue more easily than the heavier mice, suggesting they had inherited elusive "lean genes".
The research was funded by the Wellcome Trust and published in the journal PLoS One.