At present, researchers have discovered that a genetic mutation associated with an increased risk of eating disorders in humans can also cause mice to exhibit several behavioral abnormalities that look very similar to patients with anorexia nervosa. Recently, the relevant research results published in the journal Cell-Communication may provide a new direction for reversing behavioral problems related to eating disorders.
"For a long time, we have known that 50% to 70% of the risk of eating disorders comes from heredity, but the characteristics of genes that can regulate this risk are still unknown." The corresponding author of the paper and the University of Iowa Carver School of Neurology The scientist Michael Lutter said.
In previous studies, Lutter and colleagues sequenced the genomes of two families with multiple members affected by eating disorders, and found that the estrogen-related receptor alpha (ESRRA) genes or effects of family members with eating disorders Other genes expressed by ESRRA have rare mutations. These mutations reduced the activity of ESRRA protein expression. Although it is known that this protein is expressed in the brain, little is known about its function in nerve cells.
Through mouse research, researchers have now discovered that the level of ESRRA protein in the brain is controlled by energy reserves. Moreover, those mice that were genetically bred to lack the protein exhibited obsessive-compulsive neurosis-like behavior and social disorders and a reduced interest in eating high-fat foods when hungry.
"The study identified that the estrogen-related receptor alpha may increase the risk of anorexia nervosa or bulimia nervosa," Lutter said. "Clear social factors—especially the Western concept of “slimming for beauty”, This increases the remaining'non-hereditary' risk. We know that the prevalence of eating disorders has continued to increase over the past few decades. This may be due to social factors rather than genetic factors."
At present, the Lutter research team plans to study the mechanism of estrogen-related receptor alpha in the brain and test whether the new therapy can reverse the behavioral problems in the mouse model.