基因突变,饮食障碍 z-bio 2021-06-18 507

　　Researchers have now discovered that genetic mutations associated with an increased risk of eating disorders in humans cause mice to develop many behavioral disorders that are very similar to those of patients with anorexia nervosa. The findings recently published in the journal Cell-Communication may provide new directions for reversing behavioral problems related to eating disorders.

　　"It has long been known that the risk of eating disorders is 50 70 hereditary, but the characteristics of genes that can regulate this risk are not yet known." Hospital neurologist Michael Latter said. In a previous study, Lutter et al. sequenced the genomes of two families with multiple members affected by eating disorders and the estrogen-related receptor alpha (ESRRA) genes of families with eating disorders. Genes that affect the expression of ESRRA. These mutations reduce the activity of ESRRA protein expression. This protein is known to be expressed in the brain, but little is known about its function in nerve cells. By right

　　In the study of mice, researchers found that the level of ESRRA protein in the brain is regulated by energy storage. In addition, mice genetically raised due to protein deficiency showed obsessive-compulsive disorder-like behavior and social disorders, reducing the interest in eating high-fat foods on an empty stomach.

　　"This study found that estrogen-related receptor alpha may increase the risk of anorexia nervosa or bulimia nervosa," Lutter said. Especially in the West, we know that the concept of "slim is beautiful" is still a "non-genetic risk". The prevalence of eating disorders has continued to increase in the past few decades. "This may be due to social factors rather than genetic factors."

　　Currently, Lutter’s research team is planning to study the mechanism of estrogen-related receptor α in the brain and new therapies to test whether this method can reverse behavioral problems in mouse models.