An interaction between sex and endogenous beta-endorphin in food intake in mice fed a high-fat diet.
Location
Philadelphia, PA
Start Date
17-4-2026 1:30 PM
End Date
17-4-2026 2:30 PM
Description
Background: The prevalence of obesity and obesity-related disease continue to rise worldwide, classifying obesity as a global epidemic. The endogenous opioid signalling has been implicated in regulating both homeostatic and hedonic aspects of feeding behaviour. However, the role of individual opioid peptides is only partially characterized.
Objective: Therefore, we assessed the role of proopiomelanocortin (POMC)-derived peptide beta-endorphin (β-END) in food intake, and glucose homeostasis, and sex as a biological variable in this process.
Methods: Male and female mice lacking the ability to produce β-END and their respective controls were subjected to a 12-week HFD consumption to determine the role of the opioid peptide in food intake and glucose homeostasis. Body weight and food intake were measured weekly for twelve weeks. At weeks 6 and 12, glucose tolerance was analyzed using the oral glucose tolerance test.
Results: We found that male β-END–deficient mice gained significantly more weight and consumed more calories compared to wildtype male controls during HFD feeding. In contrast, this genotype-dependent difference was not observed in female mice. Interestingly, female mice, regardless of genotype, consumed more calories relative to body weight compared to males, despite having lower absolute body weights. In addition, differences in glucose levels between wildtype and β-END–deficient mice were observed at week 6 but were no longer present at week 12, suggesting a time-dependent effect of β-END deficiency on glucose homeostasis during diet-induced obesity.
Conclusion: Taken together, these findings suggest that endogenous β-END contributes to the regulation of feeding behavior and metabolic function, particularly in male mice, and highlight potential sex-specific differences in opioid-mediated metabolic regulation. Further investigation into the mechanisms underlying these sex-dependent effects may provide insight into novel therapeutic targets for obesity and metabolic disease.
Embargo Period
5-20-2026
An interaction between sex and endogenous beta-endorphin in food intake in mice fed a high-fat diet.
Philadelphia, PA
Background: The prevalence of obesity and obesity-related disease continue to rise worldwide, classifying obesity as a global epidemic. The endogenous opioid signalling has been implicated in regulating both homeostatic and hedonic aspects of feeding behaviour. However, the role of individual opioid peptides is only partially characterized.
Objective: Therefore, we assessed the role of proopiomelanocortin (POMC)-derived peptide beta-endorphin (β-END) in food intake, and glucose homeostasis, and sex as a biological variable in this process.
Methods: Male and female mice lacking the ability to produce β-END and their respective controls were subjected to a 12-week HFD consumption to determine the role of the opioid peptide in food intake and glucose homeostasis. Body weight and food intake were measured weekly for twelve weeks. At weeks 6 and 12, glucose tolerance was analyzed using the oral glucose tolerance test.
Results: We found that male β-END–deficient mice gained significantly more weight and consumed more calories compared to wildtype male controls during HFD feeding. In contrast, this genotype-dependent difference was not observed in female mice. Interestingly, female mice, regardless of genotype, consumed more calories relative to body weight compared to males, despite having lower absolute body weights. In addition, differences in glucose levels between wildtype and β-END–deficient mice were observed at week 6 but were no longer present at week 12, suggesting a time-dependent effect of β-END deficiency on glucose homeostasis during diet-induced obesity.
Conclusion: Taken together, these findings suggest that endogenous β-END contributes to the regulation of feeding behavior and metabolic function, particularly in male mice, and highlight potential sex-specific differences in opioid-mediated metabolic regulation. Further investigation into the mechanisms underlying these sex-dependent effects may provide insight into novel therapeutic targets for obesity and metabolic disease.