Researchers Recreate Conditions That Contribute To Anorexia In Mice
A team of researchers from Columbia University Medical Center say they have uncovered how a combination of genetic and environmental factors can trigger anorexia using mice in a recent study.
According to the report published in the journal Translational Psychiatry, researchers have long believed the risk of anorexia is connected to a number of genetic, biological, psychological, and sociocultural factors, but they have been unable to establish animal models that recreate the pattern of disease onset in humans.
Lead researcher on the new study, Lori Zeltser, Ph.D., says the previous animal models of anorexia included some factors, but they failed to incorporate the social stress and genetic components of anxiety and anorexia that most likely contribute to the development of anorexia in humans.
To incorporate these factors, the team of researchers exposed adolescent mice to a gene variant linked with anorexia and anxiety in both mice and humans, known as the BDNF gene. Then, the mice were placed on a calorie-restricted diet similar the dieting humans do preceding anorexia. The overall caloric intake was reduced by 20-30%.
“One driver of anorexia in humans is peer pressure, specifically the desire to be thin,” says Zeltser.
“People assumed that you couldn’t replicate that in a mouse,” she continues. “We decided to take peer pressure out of the equation and focus on social stress, which can be accomplished by housing mice alone, instead of in groups.”
When the young mice with the gene variant were placed in isolated housing to replicate social stress, along with a restricted diet, the researchers saw they were more likely to avoid eating. However, this change in behavior was not found when researchers imposed the environmental variables on adult mice.
When the team imposed just social stress or reduced diet – but not both conditions – on the adolescent mice given the gene variant, the mice showed little change in eating behavior.
“Our findings show that having the at-risk genotype alone is not sufficient to cause anorexia-like behavior, but it confers susceptibility to social stress and dieting, especially during adolescence,” said Zeltser. “You need all of these variables in place to see this robust effect on eating.”
The researchers concede “there will always be questions about the extent to which a mouse model can fully capture a disorder as complex as [anorexia nervosa].” But, they believe their model incorporates many key components that “accurately reflect the conditions thought to promote eating disorders.”
“In the end, we’ve achieved a model that closely replicates the factors that elicit anorexic behavior in humans,” concludes study author Moneek Madra, Ph.D., also from CUMC.