The Science

A naturally occurring molecule at the heart of satiety.

Oleoylethanolamide (OEA) is a lipid mediator produced in the small intestine after eating. It is one of the body's own signals in the regulation of appetite, energy balance and metabolic wellbeing.

From capsule to small intestine

How OLEACORE™ is designed to work

Diagram showing the OLEACORE capsule journey from ingestion through the oesophagus and stomach to release in the duodenum, where ultramicronised OEA is delivered in an olive oil lipid matrixClick to zoom

Educational visualization: the ultramicronised OEA is suspended in a refined olive oil lipid carrier for delivery in the duodenum, where OEA is naturally produced after meals.

Satiety signalling

How OEA signals appetite regulation

Once released, OEA joins one of the body's own post-meal conversations — from the gut lining, to the PPAR-α receptor, to the brain via the vagal pathway.

Infographic showing how OEA signals satiety: olive oil fats from a meal, OEA production in the small intestine villi, activation of the PPAR-alpha receptor, and a vagal nerve signal travelling from the gut to the brainClick to zoom

Educational visualization of published research on OEA signalling. OLEACORE® is a dietary supplement, not a treatment for any disease.

1. Produced after eating

Cells lining the small intestine synthesise OEA from dietary fats, particularly oleic acid — the main lipid in olive oil.

2. Activates PPAR-α

OEA binds the PPAR-α receptor, a key regulator of fatty-acid oxidation and metabolic gene expression in liver, muscle and fat tissue.

3. Signals satiety

It communicates with the brain via afferent nerves to support the natural feeling of fullness and healthy eating patterns.

Research foundation

Two decades of peer-reviewed OEA science.

OEA wasn't invented by a supplement brand. It was discovered in academic laboratories and characterised across more than twenty years of published research into satiety signalling, appetite regulation and gut–brain communication.

2001

First discovery

5

Landmark papers

10

Leading researchers

4

Countries

Study type labels:In vivoAnimal model researchIn vitroCell/tissue researchReviewLiterature synthesisHumanHuman participant study
  1. 2001Nature 414, 209–212In vivoPeer-reviewed

    Rodríguez de Fonseca F, et al. An anorexic lipid mediator regulated by feeding.

    First discovery that intestinal OEA is regulated by feeding.

    DOI: 10.1038/35102582
  2. 2003Neuropsychopharmacology 28, 1311–1316In vivoPeer-reviewed

    Gaetani S, Oveisi F, Piomelli D. Modulation of meal pattern in the rat by the anorexic lipid mediator oleoylethanolamide.

    Showed OEA changes meal patterns by increasing satiety.

    DOI: 10.1038/sj.npp.1300166
  3. 2003Nature 425, 90–93In vivoPeer-reviewed

    Fu J, Gaetani S, et al. Oleylethanolamide regulates feeding and body weight through activation of the nuclear receptor PPAR-α.

    Identified PPAR-α as the key receptor mediating OEA's effects on appetite.

    DOI: 10.1038/nature01921
  4. 2005Cellular and Molecular Life Sciences 62, 708–716ReviewPeer-reviewed

    Lo Verme J, et al. Regulation of food intake by oleoylethanolamide.

    Comprehensive review of OEA biology, metabolism and research potential.

  5. 2014PNAS 111, 11527–11532In vivoPeer-reviewed

    Provensi G, et al. Satiety factor oleoylethanolamide recruits the brain histaminergic system to inhibit food intake.

    Demonstrated a central pathway linking gut-derived OEA to reduced food intake.

Prof. Daniele Piomelli

MD, PhD · University of California, Irvine · Italian Institute of Technology

Led the work establishing OEA as a satiety molecule acting through the PPAR-α receptor.

Fu J, Gaetani S, et al. (2003). Nature 425, 90–93.

Dr. Jin Fu

PhD · University of California, Irvine

First author of the landmark discovery paper linking OEA, feeding and body weight to PPAR-α.

Fu J, et al. (2003). Nature 425, 90–93.

Prof. Silvana Gaetani

MD, PhD · Sapienza University of Rome

Showed OEA delays meal initiation and prolongs satiety without causing illness or malaise.

Gaetani S, Oveisi F, Piomelli D. (2003). Neuropsychopharmacology 28, 1311–1316.

Dr. Jesse Lo Verme

PhD · University of California, Irvine

Authored the comprehensive review of OEA pharmacology, metabolism and appetite regulation.

Lo Verme J, et al. (2005). Cell Mol Life Sci 62, 708–716.

Prof. Fernando Rodríguez de Fonseca

MD, PhD · University of Córdoba · Hospital Carlos Haya, Spain

First identified OEA as an endogenous lipid whose intestinal levels rise after feeding.

Rodríguez de Fonseca F, et al. (2001). Nature 414, 209–212.

Prof. Maria Beatrice Passani

PhD · University of Florence

Demonstrated that OEA recruits the brain histaminergic system to inhibit food intake.

Provensi G, et al. (2014). PNAS 111, 11527–11532.

Dr. Gustavo Provensi

PhD · University of Florence

First author describing a central nervous system mechanism for OEA-induced satiety.

Provensi G, et al. (2014). PNAS 111, 11527–11532.

Prof. Patrizio Blandina

MD · University of Florence

Co-author on the histaminergic satiety pathway work, expanding gut–brain understanding.

Provensi G, et al. (2014). PNAS 111, 11527–11532.

Prof. Wolfgang Langhans

PhD · ETH Zurich

Clarified how peripheral OEA signalling contributes to meal termination and appetite control.

Karimian Azari E, et al. (2014). Langhans laboratory.

Dr. Myrtha Arnold

PhD · ETH Zurich

Published extensively on nutrient sensing and OEA-mediated control of feeding behaviour.

Gut–brain communication research programme, ETH Zurich.

Citations are provided for educational reference. These researchers and institutions are not affiliated with, and do not endorse, OLEACORE®. Much of the published work described above was conducted in animal models; OLEACORE® is a dietary supplement and is not intended to diagnose, treat, cure or prevent any disease.

OLEACORE softgel capsules

Why ultramicronised

Formulated for advanced absorption.

OLEACORE™ uses an ultramicronised form of OEA suspended in a refined olive-oil lipid matrix. Smaller particle size and a natural lipid carrier are designed to support consistent, comfortable daily use.

Daily serving

300 mg

Per bottle

120 softgels

Ingredient philosophy

Everything essential. Nothing extra.

Ultramicronised OEA

The core active — 150 mg per softgel.

Refined olive oil

Natural lipid carrier for smooth, consistent delivery.

Sunflower lecithin

Supports emulsification and absorption.

Mixed tocopherols

Naturally derived vitamin E for oxidative stability.

Softgel capsule

Gelatin, purified water, calcium carbonate.

*These statements have not been evaluated by any regulatory authority. This product is not intended to diagnose, treat, cure or prevent any disease. Formulated to support healthy appetite, satiety and metabolic wellness as part of a balanced diet and lifestyle.

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