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New Fluorescent Probe Based on Ghrelin's Natural Blocker LEAP2 Maps Hunger Receptor in the Brain

evidence
The takeaway

A fluorescent version of the ghrelin-blocking peptide LEAP2 was developed that retains its biological activity, reduces ghrelin-induced food intake in mice, and can visually map ghrelin receptor locations in the brain.

Surface vs intracellular labeling

F-LEAP2 labeled ghrelin receptors on the cell surface while fluorescent ghrelin was internalized — revealing that the natural blocker and the natural agonist trigger fundamentally different receptor trafficking.

What the researchers found

The fluorescent LEAP2 analogue (F-LEAP2) displayed binding affinity and inverse agonism to GHSR similar to native LEAP2. Notably, F-LEAP2 labeled GHSR on the cell surface, while fluorescent ghrelin was mainly observed inside cells — revealing different receptor trafficking patterns for agonists versus antagonists.

When centrally injected in mice, F-LEAP2 reduced ghrelin-induced food intake with efficacy similar to native LEAP2 and specifically labeled cells in GHSR-expressing brain areas. This dual functionality — biological activity plus fluorescent visualization — makes F-LEAP2 a uniquely valuable research tool.

Why it matters

The ghrelin system is a prime target for appetite-suppressing drugs, but studying it has been limited by a lack of good visualization tools. F-LEAP2 solves this by letting researchers see exactly where ghrelin receptors are and how they behave when blocked — critical information for developing anti-obesity drugs that target ghrelin signaling. The observation that LEAP2 and ghrelin cause different receptor trafficking could reveal new pharmacological strategies.

How the study worked

Researchers synthesized F-LEAP2 based on the N-terminal LEAP2 sequence conjugated to a fluorescent tag. In vitro binding affinity and inverse agonism were assessed in GHSR-expressing cell lines. Cell surface versus intracellular labeling patterns were compared between F-LEAP2 and fluorescent ghrelin. In vivo studies in C57BL/6 mice tested F-LEAP2's ability to block ghrelin-induced food intake and label GHSR-expressing brain regions following central (intracerebroventricular) injection.

What this study cannot tell us

F-LEAP2 was injected centrally (directly into the brain) rather than peripherally, so its ability to cross the blood-brain barrier is unknown. The fluorescent tag could potentially alter peptide behavior in contexts not tested. Only acute effects on food intake were measured, not chronic appetite regulation. The tool's utility is primarily for research rather than therapeutic application.

How to read the evidence

This is a tool-development study with supporting in vitro and in vivo validation. It provides proof-of-concept for a new research probe rather than testing a therapeutic hypothesis. The biological validation (food intake reduction, brain area labeling) is convincing but limited to acute central injection.

When this study was published

Published in 2019, shortly after LEAP2's identification as a ghrelin antagonist, this was among the first studies to develop practical research tools for studying the LEAP2-ghrelin system.

The bigger picture

LEAP2 was only recently identified as an endogenous ghrelin antagonist, making it one of the newest players in appetite regulation. Creating a functional fluorescent version is a crucial step for understanding the LEAP2-ghrelin balance. The finding that LEAP2 stays on the cell surface while ghrelin gets internalized suggests fundamentally different signaling dynamics — agonists pull the receptor inside while antagonists stabilize it at the surface — which has implications for drug design.

Questions still open

  • Could the different receptor trafficking patterns of LEAP2 (surface) versus ghrelin (internalized) be exploited to design better anti-obesity drugs?
  • Does the inverse agonist property of LEAP2 mean it could suppress appetite even when ghrelin levels are low?
  • Can F-LEAP2 be used to map changes in ghrelin receptor distribution in obesity or eating disorders?

Common questions

What is LEAP2 and why make a fluorescent version?
LEAP2 is a naturally occurring peptide that blocks the ghrelin (hunger) receptor. Making a fluorescent version allows scientists to see exactly where ghrelin receptors are located in the brain and body, and to watch in real time how these receptors behave when blocked. This visual information is essential for developing drugs that target the ghrelin system to reduce appetite.
What does 'inverse agonist' mean in the context of the ghrelin receptor?
The ghrelin receptor has a unique property: it's partially active even without ghrelin bound to it (called constitutive activity). An inverse agonist like LEAP2 doesn't just block ghrelin from activating the receptor — it actually reduces the receptor's baseline activity below its normal resting level. This is stronger than simple blocking and could be important for suppressing appetite.

Read the original research

Development of a novel fluorescent ligand of growth hormone secretagogue receptor based on the N-Terminal Leap2 region.

Molecular and cellular endocrinology, 498, 110573

Citation

Barrile, Franco; M'Kadmi, Céline; De Francesco, Pablo N; Cabral, Agustina; García Romero, Guadalupe; Mustafá, Emilio R; Cantel, Sonia; Damian, Marjorie; Mary, Sophie; Denoyelle, Séverine; Banères, Jean-Louis; Marie, Jacky; Raingo, Jesica; Fehrentz, Jean-Alain; Perelló, Mario. (2019). Development of a novel fluorescent ligand of growth hormone secretagogue receptor based on the N-Terminal Leap2 region.. Molecular and cellular endocrinology, 498, 110573. https://doi.org/10.1016/j.mce.2019.110573