Why do these obese mice eat so often?
Enhanced 2-arachidonoyl glycerol-dependent CB1 activation contributes to feeding dysregulation in KK-Ay mice.
Not medical advice. For informational purposes only. Always consult a healthcare professional. Terms
Systematic Reviews & Meta-Analyses
Max 100Randomized Controlled Trials
Max 90Cohort Studies
Max 72Case-Control Studies
Max 58Cross-Sectional Studies
Max 44Case Reports & Case Series
Max 30Expert Opinion & Narrative Reviews
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Evidence Score
Groups of people are followed over time to see who develops an outcome. Strong for identifying risk factors and associations, but cannot prove causation as firmly as RCTs.
Not medical advice. For informational purposes only. Always consult a healthcare professional. Terms
Systematic Reviews & Meta-Analyses
Max 100Randomized Controlled Trials
Max 90Cohort Studies
Max 72Case-Control Studies
Max 58Cross-Sectional Studies
Max 44Case Reports & Case Series
Max 30Expert Opinion & Narrative Reviews
Max 58 / 72
Evidence Score
Groups of people are followed over time to see who develops an outcome. Strong for identifying risk factors and associations, but cannot prove causation as firmly as RCTs.
Publication
Journal
The British journal of nutrition
Year
2026
Authors
Miki Igarashi, Kensuke Iwasa, Shinji Yamamoto, Takayo Ohto-Nakanishi, Ikuo Kimura, K. Yoshikawa
Related Content
Claims (6)
Consuming linoleic acid, a type of fat found in certain oils, leads to the production of molecules that bind to CB1 receptors in the brain, which can lead to an increase in hunger.
In a specific strain of obese mice, overeating occurs because they eat more frequently, not because they eat larger meals or wait longer between meals. This suggests that the biological signals controlling hunger, not fullness, are altered.
Blocking the enzyme cyclooxygenase-2 decreases eating behavior in KK-Ay mice, suggesting that prostaglandins, along with endocannabinoids, play a role in driving excessive food intake in this genetically obese mouse strain.
In a specific strain of obese mice, higher levels of a fat-related molecule in the intestine correlate with more frequent eating, and blocking a specific receptor in the gut reduces food intake, suggesting this molecular pathway plays a role in overeating.
In mice with a genetic form of obesity, certain signaling molecules derived from arachidonic acid are found at higher concentrations in the intestines compared to lean mice, suggesting a change in how these fat-related compounds are processed in the gut.