Location
Philadelphia, PA
Start Date
17-4-2026 1:30 PM
End Date
17-4-2026 2:30 PM
Description
Background: The rate of obesity and obesity-related diseases has continued to increase worldwide, classifying obesity as a global epidemic. Obesity is characterized by excessive accumulation of adipose tissue or body fat, predominantly caused by a long-term energy imbalance between energy input and energy expenditure. There are two known complementary systems known to regulate food intake: the homeostatic pathway, which maintains energy balance via hypothalamic signaling, and the hedonic pathway, which mediates reward-driven eating through mesolimbic circuitry.
Objective: To review current literature on the role of endogenous opioids and opioid receptor signaling in regulating food intake, with emphasis on homeostatic and hedonic feeding.
Methods: A narrative review of peer-reviewed studies conducted on PubMed, specifically research on opioid peptides, opioid receptor signaling, and hypothalamic melanocortin pathways, mesolimbic dopamine circuity, and feeding behavior.
Results: The endogenous opioid peptides composed of endorphins, enkephalins, and dynorphins which act through three different receptors, μ (MOP), δ (DOP), and κ (KOP). These receptors are widely expressed throughout the central nervous system, including regions involved in homeostatic regulation (hypothalamus) and hedonic control of feeding (nucleus accumbens and ventral tegmental area). Pharmacologic studies have demonstrated that the activation of opioid receptors, particularly MOP, increases food intake and enhances consumption of palatable energy dense food. Conversely, administration of opioid antagonists such as naloxone or naltrexone reduces overall intake and attenuates hedonic feeding behaviors. In addition to their role in reward-driven eating, endogenous opioids also contribute to homeostatic regulation of feeding. Although the precise interaction between central opioid and melanocortin systems remains incompletely understood, the expression of opioid receptors on proopiomelanocortin (POMC) neurons supports a functional interaction between these pathways.
Conclusion: Taken together, current evidence suggests a significant role of endogenous opioid signaling in both the homeostatic and hedonic aspects of food intake. Although the role of opioids in regulating feeding behavior has been widely studied, our understanding is still incomplete. These findings highlight the interrelationship between homeostatic and hedonic aspect of feeding modulated by the opioid system and suggest that dysregulation of this network may contribute to the pathophysiology of obesity and obesity-related metabolic disorders. A better understanding of these mechanisms may elucidate the development of targeted therapeutic strategies for obesity and obesity-related metabolic orders. Further research is needed to clarify receptor-specific actions and translational implications in human populations.
Embargo Period
6-3-2026
Included in
Endogenous Opioid Signaling in the Regulation of Food Intake: A Literature Review
Philadelphia, PA
Background: The rate of obesity and obesity-related diseases has continued to increase worldwide, classifying obesity as a global epidemic. Obesity is characterized by excessive accumulation of adipose tissue or body fat, predominantly caused by a long-term energy imbalance between energy input and energy expenditure. There are two known complementary systems known to regulate food intake: the homeostatic pathway, which maintains energy balance via hypothalamic signaling, and the hedonic pathway, which mediates reward-driven eating through mesolimbic circuitry.
Objective: To review current literature on the role of endogenous opioids and opioid receptor signaling in regulating food intake, with emphasis on homeostatic and hedonic feeding.
Methods: A narrative review of peer-reviewed studies conducted on PubMed, specifically research on opioid peptides, opioid receptor signaling, and hypothalamic melanocortin pathways, mesolimbic dopamine circuity, and feeding behavior.
Results: The endogenous opioid peptides composed of endorphins, enkephalins, and dynorphins which act through three different receptors, μ (MOP), δ (DOP), and κ (KOP). These receptors are widely expressed throughout the central nervous system, including regions involved in homeostatic regulation (hypothalamus) and hedonic control of feeding (nucleus accumbens and ventral tegmental area). Pharmacologic studies have demonstrated that the activation of opioid receptors, particularly MOP, increases food intake and enhances consumption of palatable energy dense food. Conversely, administration of opioid antagonists such as naloxone or naltrexone reduces overall intake and attenuates hedonic feeding behaviors. In addition to their role in reward-driven eating, endogenous opioids also contribute to homeostatic regulation of feeding. Although the precise interaction between central opioid and melanocortin systems remains incompletely understood, the expression of opioid receptors on proopiomelanocortin (POMC) neurons supports a functional interaction between these pathways.
Conclusion: Taken together, current evidence suggests a significant role of endogenous opioid signaling in both the homeostatic and hedonic aspects of food intake. Although the role of opioids in regulating feeding behavior has been widely studied, our understanding is still incomplete. These findings highlight the interrelationship between homeostatic and hedonic aspect of feeding modulated by the opioid system and suggest that dysregulation of this network may contribute to the pathophysiology of obesity and obesity-related metabolic disorders. A better understanding of these mechanisms may elucidate the development of targeted therapeutic strategies for obesity and obesity-related metabolic orders. Further research is needed to clarify receptor-specific actions and translational implications in human populations.