Nearly six per cent of morbidly obese patients have a genetic defect which prevents them from feeling full, regardless of how much they have eaten.
Researchers at the University of Florida have discovered that mutations of a certain hunger-regulating gene, the melanocortin-4 receptor, cause the receptor to miss signals from molecules that tell the body when to stop eating.
Mutations of this particular gene are known to be the most common cause of genetic obesity and the latest discovery brings scientists a step closer to correcting the defects.
The researchers have already isolated a molecule which appears to help overcome the mutation, revealed Dr Carrie Haskell-Luevano, associate professor of medicinal chemistry and lead author of the study, which is published in Biochemistry journal.
"If you administer these compounds, it's a potential anti-obesity agent because you feel full," she said. "It directly controls the desire to eat."
Dr Sadaf Farooqi, one of the team of British scientists who made the original connection between the mutation and human obesity, said that the study "provides more detail and it starts to put some of the pieces of the puzzle together".
She added: "Understanding this pathway is really important to understanding obesity. It's an important part of getting to the next step."
Admittedly, only a fraction of obese children and adults have genetic conditions or mutations that are linked to obesity.
However, "Genetics is a very strong component of obesity," said Dr Haskell-Luevano.
"As a scientist and a researcher, what I like to focus on is seeing if we can design some molecule or drug that can fix this."