UC San Diego

In modern society, an increased availability of palatable food has promoted obesity, leading some to diet and restrict oneself from certain “desired” foods. This restriction leads to under-acceptance of alternative diets, followed by an overconsumption of palatable food when one can no longer withstand dieting. Here, we modeled this behavior of “fasting” and “binging” in mice, based off our previous free-feeding rat model. In this mouse model, female mice were assigned one of three diet groups (ad libitum chow diet, ad libitum palatable, sucrose-rich, chocolate-flavored diet, and intermittent access to chocolate diet). To assess binge eating behavior, the mice in these three diet groups were compared on operant-self administration (fixed/progressive ratio), and daily energy consumption. Operant self-administration results revealed that intermittent mice were significantly more motivated and compulsive than ad libitum mice, and demonstrated significant rejection of non-palatable chow diet, showing that intermittent access to a palatable diet promotes compulsive eating behavior, allowing for the establishment of a mouse binge eating model. Binge eating has been shown by various studies to cause neurological changes in the brain, similar those caused by drug addiction. The following studies on the mouse model tested the hypothesis that compulsive eating may alter various neurological mechanisms in a similar manner as drugs of addiction. BBP-02, a sigma-1 receptor antagonist, was treated in mice but showed no effect on self-administration, suggesting that sigma-1 by itself may not play a role in the modulation of compulsive eating. Another drug, 14-methyoxymetoponin, a mu-opioid receptor agonist, resulted in a significant decrease in self administration with intermittent mice at the two highest doses, suggesting that the opioid system may be altered in mice with compulsive eating behavior.