A gene linked to eating disorders resulted in abnormal behavior and feeding in mice, which were given the gene mutation, according to research published Thursday. However, the study found that the gene mutation affected only female mice.

Researchers looked into histone deacetylase 4 (HDAC4) — a transcriptional repressor that turns off other genes. For the study published in the journal Biological Psychiatry, researchers developed a mouse model to examine the behavioral effects the gene mutation.

“The mutated female mice have several behaviors relevant to eating disorders,” Michael Lutter, psychiatrist at the Eating Recovery Center of Dallas and study author, said in a statement. “In particular, they work less hard to obtain high-calorie food when they are hungry, which is important because failure to increase food intake in response to hunger is a core feature of anorexia nervosa. Also, they have compulsive grooming, which is considered a model of obsessive-compulsive disorder in mice. OCD-like behaviors are very common in patients with anorexia nervosa as well,” he said.

According to the researchers, the study results support a role of the HDAC4 mutation in leading to eating disorders in people.

After placing genetically mutated female mice in a group, researchers found that the rodents exhibited more anxiety and irritability. The mice did not find the social situation to be rewarding, according to the findings.

Researchers also identified genes controlled by HDAC4. The study results showed that the HDAC4 mutation caused a decline in the expression of genes involved in synthesis of the neurotransmitter glutamate.

“This is important because glutamate has previously been implicated in feeding, obsessive-compulsive disorder (OCD), and depression,” Lutter explained. “So this one observation could explain a whole array of behavioral deficits.”

“This is the first biological pathway that's been identified as being associated with the risk of developing an eating disorder," Huxing Cui, a scientist at University of Iowa, noted. "This work will open new avenues of research to understand the neurobiological basis of eating disorders and identify new opportunities for development of medications to treat eating disorders.”

Researchers said that the mouse model they developed could also be used to monitor potential drugs to treat eating disorders.