The Role of Beta-Endorphin in Food Deprivation-Mediated Increases in Food Intake and Binge-Eating

Abstract

Food deprivation and binge eating represent significant public health concerns. Previous studies have implicated that hypothalamic opioids are affected following food deprivation. However, the role of each opioid peptide is not fully understood. Therefore, we investigated the role of endogenous beta-endorphin in food deprivation-mediated increases in food intake and binge eating. Male mice lacking beta-endorphin and their respective controls were subjected to 24 h food deprivation and then were randomly assigned to receive a regular diet (RD) or a high-fat diet (HFD). After four to five weeks, animals were re-exposed to an HFD to assess if previous exposure to HFD would enhance binge-eating behavior. We report that food deprivation significantly increases food intake; however, beta-endorphin may not be involved in this process. In addition, our findings suggest that prior exposure to an HFD promotes binge-eating behavior in wildtype mice, and that these effects were modestly decreased in beta-endorphin knockout mice. Overall, our results support that beta-endorphin may play a modest role in mediating palatability-driven feeding, but not hunger-associated feeding. A better understanding of neural mechanisms involved in binge eating and deprivation-induced increases in food intake may inspire new prevention or treatment options to decrease the burden of eating disorders.

Keywords: beta-endorphin; binge-eating; food deprivation; high-fat diet.

Figure 1

Schematic diagram of the food deprivation protocol.

Figure 2

Cumulative Food consumption (A) and caloric intake (B) in deprived beta-endorphin knockout mice and their wildtype littermates/controls (n = 9/group). Animals were randomly assigned to receive HFD or RD following a 24 h deprivation period. Food and caloric intake were measured on day 1 (baseline: at 1, 2, 4, and 24 h) and day 3 (after deprivation: at 49, 50, 52, and 72 h). A three-way ANOVA revealed an interaction between time and food assignment in caloric intake. All data are expressed as mean ± SEM. No significant differences were found between mice of the two genotypes.

Figure 3

Cumulative (A) Food and (B) Caloric Intake of non-deprived beta-endorphin knockout mice and their wildtype littermates/controls (n = 6 per group). After baseline (day 2), food measurements were taken (at 1, 2, 4, and 24 h); all animals were maintained on RD for the next 24 h (day 2), then randomly assigned to receive HFD or RD for 24 h (day 3). Food and caloric intake were measured and recorded. All data are expressed as mean ± SEM. **** p < 0.01 by three-way ANOVA/Fisher’s LSD post hoc test.

Figure 4

Comparison of food intake of wildtype (left half of the panel) and beta-endorphin knockout (right half) mice following 24 h food deprivation compared to their non-deprived controls at the end of the first (49 h, A), second (50 h, B), fourth (52 h, C) and twenty-fourth (72 h, D). * p < 0.05, ** p < 0.001, and *** p < 0.0001 signify a difference between deprived and non-deprived mice; # p < 0.05, and ## p < 0.01 signify a difference between HFD vs. RD group.

Figure 5

HFD consumption in non-deprived and deprived beta-endorphin knockout mice and their wildtype littermates/controls during the test for binge-eating. Food intake (g) was measured in non-deprived and deprived mice exposed to HFD for one hour and compared to their initial HFD intake, as measured in Figure 2 (deprived group) and Figure 3 (non-deprived group). All data are expressed as mean ± SEM of 6-9 mice per group. * p < 0.05; *** p < 0.0001, mixed-effect analysis/Fisher’s LSD.