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LEAP2: from feeding regulation to its implications in eating disorders
Francesca Mariuz1, Tatiana Landré2, Chloé Tezenas du Montcel3
1Université Paris Cité, Institute of Psychiatry and Neuroscience of Paris, INSERM U1266, Team "Vulnerability to Psychiatric and Addictive Disorders", F-75014 Paris, France.
Physiology & Behavior
|July 6, 2025
Summary
Liver-Expressed Antimicrobial Peptide 2 (LEAP2) antagonizes ghrelin, impacting food intake and energy balance. LEAP2 variants and its role in obesity and anorexia nervosa offer new therapeutic targets.
Area of Science:
- Endocrinology
- Metabolism
- Neuroscience
Background:
- Ghrelin, a Growth Hormone Secretagogue (GHS), stimulates appetite and is produced in the stomach.
- LEAP2 (Liver-Expressed Antimicrobial Peptide 2) is an endogenous antagonist to ghrelin.
- The ghrelin receptor is known as GHSR.
Purpose of the Study:
- To review LEAP2's role as an antimicrobial peptide and ghrelin antagonist.
- To examine ghrelin and LEAP2 regulation by energy balance and nutrient intake.
- To discuss LEAP2 variants and their implications in eating disorders and obesity.
Main Methods:
- Literature review of ghrelin and LEAP2 research.
- Analysis of regulatory mechanisms of ghrelin and LEAP2.
- Discussion of LEAP2 variants and associated pathologies.
Main Results:
- LEAP2 opposes ghrelin's effects on food intake, GH secretion, and energy homeostasis.
- Ghrelin and LEAP2 levels are regulated by energy balance and meal intake.
- LEAP2 variants may influence eating behaviors and are implicated in obesity and anorexia nervosa.
Conclusions:
- Ghrelin and LEAP2, acting via GHSR, are crucial targets for metabolic and eating disorder therapies.
- Understanding LEAP2's function provides new insights into energy balance regulation.
- LEAP2 represents a potential therapeutic target for obesity and related feeding disorders.
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