MON-669 Hunger By Proxy: Social Influence On Food Intake In Mice Via Dopamine Signaling

Abstract Disclosure: X. Xu: None. H. Liu: None. Y. Xu: None. Background: Unwanted weight gain, leading to overweight and obesity, is now recognized as a chronic disease. Appetite can be influenced by non-nutritive factors, including social context and sensory cues, which can drive food intake even in the absence of hunger. The role of cognitive brain mechanisms in obesity cannot be overlooked. A previous human study demonstrated a significant association between external eating behaviors and watching eating show. However, this phenomenon has not been validated in a murine model. This study aims to address this gap. Objective: To evaluate whether satiated mice increase food intake when observing a peer’s binge-like eating behavior, even in the absence of hunger, using a hunger transmission protocol. Additionally, we aim to determine whether dopamine signaling plays a role in this phenomenon. Methods: 14 male mice were divided into two groups: Group A mice were either fed or fasted overnight before testing, while Group B mice were always fed prior to testing. Mice were paired based on genetic and parental information and placed in separate but adjacent chambers, allowing visual and olfactory interaction without physical contact. Food intake was measured hourly for four hours across different test days, using chow, high-fat, and sucrose diets. In a follow-up experiment, Group B mice received intraperitoneal injections of either 0.1 ml of 0.9% saline, a D1 dopamine receptor (DRD1) inhibitor (SCH23390, 0.1 mg/kg), or a D2 dopamine receptor (DRD2) inhibitor (Eticlopride, 1 mg/kg) 15 minutes before testing, and food intake was measured. Results: Satiated mice did not have significant increased intake of chow or high-fat diets, when observing a fasted peer consume diets. However, they exhibited a significant increase in sucrose diet intake during the first hour when observing a fasted peer (p = 0.0043 in the initial test, p = 0.0154 in the repeated test). This effect persisted after saline injection (p = 0.0057) but was abolished following administration of DRD1 or DRD2 inhibitors (p = 0.2153 and p = 0.0811, respectively). Conclusion: Our findings confirm that social observation influences food intake in mice, but only for palatable foods such as sucrose diet. Dopamine signaling appears to regulate, or at least partially mediate, this hunger transmission effect. Establishing this animal model provides a foundation for future studies on the neurobiological mechanisms underlying cognitive-driven food intake and may contribute to the development of targeted therapeutic strategies for obesity. Presentation: Monday, July 14, 2025

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Journal
Journal of the Endocrine Society
Published
2025-10-01
DOI
https://doi.org/10.1210/jendso/bvaf149.009
Primary Topic
Diet and metabolism studies
Type
article
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article

MON-669 Hunger By Proxy: Social Influence On Food Intake In Mice Via Dopamine Signaling

Yong Xu, Hesong Liu, Xu Xu
Journal of the Endocrine Society
Diet and metabolism studies
article

MON-669 Hunger By Proxy: Social Influence On Food Intake In Mice Via Dopamine Signaling

Yong Xu, Hesong Liu, Xu Xu
article en

Abstract

Abstract Disclosure: X. Xu: None. H. Liu: None. Y. Xu: None. Background: Unwanted weight gain, leading to overweight and obesity, is now recognized as a chronic disease. Appetite can be influenced by non-nutritive factors, including social context and sensory cues, which can drive food intake even in the absence of hunger. The role of cognitive brain mechanisms in obesity cannot be overlooked. A previous human study demonstrated a significant association between external eating behaviors and watching eating show. However, this phenomenon has not been validated in a murine model. This study aims to address this gap. Objective: To evaluate whether satiated mice increase food intake when observing a peer’s binge-like eating behavior, even in the absence of hunger, using a hunger transmission protocol. Additionally, we aim to determine whether dopamine signaling plays a role in this phenomenon. Methods: 14 male mice were divided into two groups: Group A mice were either fed or fasted overnight before testing, while Group B mice were always fed prior to testing. Mice were paired based on genetic and parental information and placed in separate but adjacent chambers, allowing visual and olfactory interaction without physical contact. Food intake was measured hourly for four hours across different test days, using chow, high-fat, and sucrose diets. In a follow-up experiment, Group B mice received intraperitoneal injections of either 0.1 ml of 0.9% saline, a D1 dopamine receptor (DRD1) inhibitor (SCH23390, 0.1 mg/kg), or a D2 dopamine receptor (DRD2) inhibitor (Eticlopride, 1 mg/kg) 15 minutes before testing, and food intake was measured. Results: Satiated mice did not have significant increased intake of chow or high-fat diets, when observing a fasted peer consume diets. However, they exhibited a significant increase in sucrose diet intake during the first hour when observing a fasted peer (p = 0.0043 in the initial test, p = 0.0154 in the repeated test). This effect persisted after saline injection (p = 0.0057) but was abolished following administration of DRD1 or DRD2 inhibitors (p = 0.2153 and p = 0.0811, respectively). Conclusion: Our findings confirm that social observation influences food intake in mice, but only for palatable foods such as sucrose diet. Dopamine signaling appears to regulate, or at least partially mediate, this hunger transmission effect. Establishing this animal model provides a foundation for future studies on the neurobiological mechanisms underlying cognitive-driven food intake and may contribute to the development of targeted therapeutic strategies for obesity. Presentation: Monday, July 14, 2025

Journal of the Endocrine SocietyVol. 9(Supplement_1)
SUNY Upstate Medical University (US), Texas Children's Hospital (US)
Openalex Percentile: Top 62%
Diet and metabolism studies
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