Olive Oil, GLP-1 and Appetite: What the Mechanism Really Shows

A claim circulating on social media says olive oil "pulls the same levers as" the GLP-1 drug semaglutide. Part of the pharmacology behind it is documented. In human studies, digesting olive oil forms 2-oleoylglycerol (2-OG), which activates the GPR119 receptor, and an olive-oil meal raises GLP-1, the gut hormone that semaglutide is built to mimic. In rodents, oleoylethanolamide (OEA), a lipid made from oleic acid, reduces food intake through the nuclear receptor PPAR-alpha. The equivalence with the drug is not supported: native GLP-1 has a plasma half-life of one to two minutes, semaglutide's is about a week, and drugs aimed at the same pathway — GPR119 agonists and DPP-4 inhibitors — have already been tested in people. This page sets out each step, says which evidence is human and which is animal, and notes the energy content of the oil: in the body-weight studies cited here, olive oil was compared against another oil or a control diet, not added on top of an unchanged diet.

Table of Contents

  1. GLP-1: A Hormone the Gut Already Makes
  2. 2-Oleoylglycerol and the GPR119 Switch
  3. Where the “2 Grams of 2-OG” Figure Comes From
  4. The Copenhagen Carrot Studies
  5. Oleoylethanolamide and PPAR-alpha
  6. Why a Knockout Beats a Correlation
  7. CCK, PYY and Slower Gastric Emptying
  8. Olive Oil Is Not Semaglutide: Where the Comparison Breaks
  9. This Pathway Was Already Tested as a Drug — Twice
  10. Energy Content: Addition Versus Substitution
  11. "Fat Loss 80% Higher" — Relative Versus Absolute
  12. The EU Polyphenol Health Claim
  13. Where the Claim Circulates and What the Research Says
  14. What the Existing Studies Did Not Test
  15. Evidence Ledger
  16. Summary of the Findings
  17. Key Research Papers
  18. Connections
  19. Featured Videos

GLP-1: A Hormone the Gut Already Makes

Glucagon-like peptide-1 (GLP-1) is a 30-amino-acid hormone made from proglucagon by the endocrine L-cells of the intestinal lining and released in response to meal intake. Its main actions are to stimulate insulin secretion — the incretin effect — and to inhibit glucagon secretion, which limits the rise in blood glucose after a meal. It also slows gastrointestinal motility as part of the "ileal brake," and appears to be a physiological regulator of appetite and food intake (Holst, 2007).

That the body makes GLP-1 is textbook physiology and the reason the drug class exists. The detail that matters for the comparison with the drug is how long the hormone lasts.

Native GLP-1 has a plasma half-life of one to two minutes. It is degraded by the enzyme dipeptidyl peptidase-4 (DPP-4) and eliminated, mainly by the kidneys, too fast to be useful as a drug (Nauck and Meier, 2019); much of it is inactivated before it has even left the gut (Holst, 2007). A meal's effect on GLP-1 is therefore short-lived, and that is the hinge of the comparison with semaglutide. The drug class is covered on the GLP-1 receptor agonists page.

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2-Oleoylglycerol and the GPR119 Switch

Dietary fat arrives as triacylglycerol: glycerol carrying three fatty acids. Digestion by pancreatic lipase releases free fatty acids and a 2-monoacylglycerol — glycerol with the middle fatty acid still attached (Hansen and colleagues, 2011). Most of olive oil's fat is oleic acid (see the Olive Oil Benefits hub), and the 2-monoacylglycerol in question is 2-oleoylglycerol (2-OG).

In cells engineered to carry human GPR119, 2-OG and other 2-monoacylglycerols raised intracellular cyclic AMP (for 2-OG, half-maximal at 2.5 µM). In eight healthy volunteers, 2 g of 2-OG delivered directly into the jejunum raised plasma GLP-1 over the first 25 minutes compared with an equimolar dose of oleic acid or with the glycerol vehicle, and GIP, the other incretin hormone, also rose. The authors conclude that 2-monoacylglycerols formed during fat digestion can activate GPR119 and cause incretin release from the human intestine, that this mechanism is likely to contribute to dietary fat's known effect on incretin secretion, and that GPR119 acts as a fat sensor (Hansen and colleagues, 2011).

L-cells are not spread evenly along the gut. In an immunohistochemical study of rat, pig and human intestine, GLP-1 cells were numerous in the distal jejunum and ileum, and their density rose along the colon to the highest numbers in the rectum. The authors read this as L-cells being positioned to sense nutrients that escape absorption in the upper small intestine (Eissele and colleagues, 1992).

Oleoylethanolamide is also a GPR119 ligand. A 2006 study identified OEA as an endogenous ligand of GPR119 and suggested that OEA's effects on food intake in rats may be mediated at least in part through that receptor (Overton and colleagues, 2006). The two mechanisms on this page therefore overlap at the same receptor, with OEA also acting on PPAR-alpha.

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Where the “2 Grams of 2-OG” Figure Comes From

The circulating claim says that digesting 5 mL of olive oil — one teaspoon — produces about 2 g of 2-OG. The figure comes from the research literature: Hansen and colleagues (2011) state that digestion of 5 mL of olive oil with pancreatic lipase will result in formation of approximately 2 g of 2-OG and 3.2 g of oleic acid. In the same study, 2 g of 2-OG was the dose placed directly into the jejunum of the volunteers.

It is a theoretical yield, not a measured amount at a receptor. The same research group later described the 2-OG expected from 19 g of olive oil as a theoretical 7.7 g formed during digestion (Mandøe and colleagues, 2018). How much of it reaches L-cells intact was not reported in these abstracts.

2-OG is also not unique to olive oil. Every dietary triacylglycerol yields a 2-monoacylglycerol on digestion, and in the cell experiments other 2-monoacylglycerols activated GPR119 as well (Hansen and colleagues, 2011). What differs between fats is which fatty acid that monoacylglycerol carries.

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The Copenhagen Carrot Studies

The main human evidence is a randomised, single-blinded crossover study from Copenhagen (Mandøe and colleagues, 2015, American Journal of Clinical Nutrition 102:548–555). Twelve healthy white men (mean age 24, mean BMI 22) ate four meals on four different days: 200 g of carrots alone; carrots with 6.53 g of tributyrin, which yields the short-chain fatty acid butyrate; carrots with 13.15 g of a designed oil, 1,3-dioctanoyl-2-oleoyl glycerol ("C8-dietary oil"), which is digested to medium-chain octanoic acid and 2-OG; and carrots with 19 g of olive oil. The lipid doses were matched at 0.0216 mol.

Results. The olive-oil and C8-oil meals gave the same GLP-1 response (incremental area under the curve 538 ± 71 and 583 ± 101 pmol/L × 120 min; P = 0.733), and peptide YY (PYY) and neurotensin followed the same pattern. The GIP response was higher with olive oil than with the C8 oil (3293 ± 404 versus 1674 ± 270 pmol/L × 120 min), and only olive oil released cholecystokinin (CCK). Tributyrin and carrots alone produced no increase in any of the hormones measured. The authors conclude that, under their study conditions, 2-OG and GPR119 activation can fully explain olive oil's effect on GLP-1, PYY and neurotensin, that both oleic acid and 2-OG contributed to the GIP response, and that olive oil's oleic acid appears fully responsible for its CCK response.

The design isolates the 2-OG step: the C8 oil delivers 2-OG without long-chain fatty acids and matched olive oil's GLP-1 response, while tributyrin delivers a short-chain fatty acid without 2-OG and produced none.

A follow-up in type 2 diabetes. The same group gave 13 overweight people with type 2 diabetes 19 g of olive oil, 10.7 g of a butyrate-based test oil designed to yield the same amount of 2-OG, or carrots alone, each with 200 g of carrots, and measured hormones over 180 minutes. Both oils raised GLP-1 and GIP more than carrots alone (GLP-1 incremental area 645 ± 194 and 702 ± 97 pM × min, against 7 ± 103 for carrots), with similar responses between the two oils. The authors conclude that the test oil is a more effective incretin releaser than olive oil per unit of energy (Mandøe and colleagues, 2018).

What the studies measured, and what they did not:

  1. The endpoint is a hormone concentration, not an outcome. Both studies measured blood hormones for two to three hours after one meal. Neither weighed anyone or measured food intake on later days. Reading a postprandial GLP-1 curve as a fat-loss result is endpoint substitution.
  2. The samples are small. The first study enrolled 12 young, lean, healthy men; the second, 13 overweight adults with type 2 diabetes.
  3. One meal, no follow-up. Whether the response persists, fades or is compensated for with daily use over weeks was not studied.

The carrot-only meal. Versions of the claim say that the plain carrot meal did not trigger GLP-1 release. The study supports that: carrots alone produced no increase in any of the hormones measured (Mandøe and colleagues, 2015), and in the 2018 study the carrot meal's GLP-1 response was close to zero.

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Oleoylethanolamide and PPAR-alpha

The second mechanism involves oleoylethanolamide (OEA) — spelled oleylethanolamide in much of the primary literature — a naturally occurring lipid structurally related to the endocannabinoid anandamide that does not bind cannabinoid receptors (Fu and colleagues, 2003).

In rats, food deprivation markedly reduces OEA production in the small intestine, and giving OEA causes a potent and persistent decrease in food intake and in body-mass gain. The effect is behaviourally selective and is associated with activation of brain regions involved in satiety, the paraventricular hypothalamic nucleus and the nucleus of the solitary tract. OEA does not affect food intake when injected into the brain ventricles, and its effect is prevented when peripheral sensory fibres are removed with capsaicin; the authors conclude that OEA acts in the peripheral regulation of feeding (Rodríguez de Fonseca and colleagues, 2001).

Its main identified target is PPAR-alpha, a nuclear receptor that regulates several aspects of lipid metabolism. OEA bound PPAR-alpha with high affinity, and it produced satiety and reduced body-weight gain in normal mice but not in mice lacking PPAR-alpha (Fu and colleagues, 2003). In freshly isolated rat fat cells, OEA stimulated the release of glycerol and fatty acids, and it increased fatty-acid oxidation in skeletal-muscle strips, liver cells and cultured heart-muscle cells; given to animals, it produced lipolysis in rats and normal mice but not in PPAR-alpha-deficient mice (Guzmán and colleagues, 2004).

The human evidence for this arm is one small meal study. Fifteen volunteers each ate, on three occasions in random order, a meal of 30 g of bread with 30 mL of sunflower oil, high-oleic sunflower oil or virgin olive oil. After the high-oleic sunflower oil and the olive oil, circulating OEA was significantly higher than after ordinary sunflower oil, and energy intake over the following 24 hours was significantly lower (Mennella and colleagues, 2015).

Because high-oleic sunflower oil did the same as olive oil in that study, the finding concerns the oleic-acid content of the meal rather than olive oil specifically. The Olive Oil overview and the avocado pages on monounsaturated fats and fibre and satiety cover related material on monounsaturated fat.

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Why a Knockout Beats a Correlation

The OEA-to-PPAR-alpha link rests on a knockout experiment (Fu and colleagues, Nature, 2003). Why that design is a different tier of evidence applies well beyond olive oil.

An observational finding — people who eat more olive oil are leaner — is compatible with explanations that have nothing to do with olive oil, such as income, vegetable intake or smoking. A postprandial hormone rise is better, because the timing fits and the comparison is within the same person, but it still shows only two things moving together. A receptor knockout tests causation directly: if OEA reduces feeding through PPAR-alpha, an animal lacking PPAR-alpha should not respond to it. If the same dose works in a normal mouse and not in a PPAR-alpha-null mouse, the receptor is required for the effect, not merely associated with it.

What the knockout studies show is narrower than the circulating summary. That summary says "no receptor and nothing happened — zero lipolysis, zero fat burning." The published studies say:

So the knockout shows that OEA's effects in these experiments required PPAR-alpha — not that fat cannot be used without it. All of the OEA and PPAR-alpha experiments above were done in rodents or rodent cells; the human evidence is the 15-person meal study described in the previous section.

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CCK, PYY and Slower Gastric Emptying

A fatty meal is filling for reasons that do not depend on GPR119.

A review of the human evidence describes intestinal fat — especially long-chain free fatty acids — acting through cholecystokinin (CCK) as a physiological satiety pathway. CCK stimulates gallbladder contraction and pancreatic secretion, inhibits gastric emptying and inhibits appetite, limiting the amount eaten in a meal; fat digestion products also release peptide YY (Beglinger and Degen, 2004). GLP-1 itself inhibits gastrointestinal motility as part of the "ileal brake" (Holst, 2007). In the Copenhagen study, olive oil released CCK and the 2-OG test oil did not (Mandøe and colleagues, 2015).

Gastrointestinal effects are also the commonest side effects of the drug: in the STEP 1 trial of semaglutide 2.4 mg, nausea and diarrhoea were the most common adverse events, typically transient and mild to moderate, and 4.5% of the semaglutide group, against 0.8% on placebo, stopped treatment because of gastrointestinal events (Wilding and colleagues, 2021). Two conditions in which fat and gastric emptying come up:

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Olive Oil Is Not Semaglutide: Where the Comparison Breaks

The circulating claim is that olive oil pulls "not a similar lever — the same one." At the level of the receptor, both end in GLP-1 receptor signalling. The differences are in duration and in the size of the effect.

Duration

Semaglutide is not GLP-1 itself but a GLP-1 analogue with two amino-acid substitutions and an attached fatty-acid chain, designed for high albumin affinity and full stability against metabolic degradation (Lau and colleagues, 2015). Its half-life in people is about one week, the basis of once-weekly dosing (Ikushima and colleagues, 2018); native GLP-1's is one to two minutes (Nauck and Meier, 2019). A meal-driven GLP-1 rise lasts only as long as the hormone survives; the weekly drug stays in circulation between doses.

Effect size, and a longer pathway

In STEP 1, 1,961 adults with obesity, or overweight with a weight-related condition, and without diabetes were randomised to semaglutide 2.4 mg weekly or placebo, both with lifestyle intervention, for 68 weeks. Mean body-weight change was −14.9% with semaglutide and −2.4% with placebo (Wilding and colleagues, 2021). In the off-treatment extension, participants regained two-thirds of their prior weight loss within a year of stopping (Wilding and colleagues, 2022). More on the drug class is on the GLP-1 receptor agonists page. The olive-oil body-weight figures cited on this page are of a different order: −0.92 kg against control diets in a meta-analysis of 11 trials, and a fat loss of 2.4 kg against 1.3 kg in a nine-week trial, both described below.

Semaglutide binds the GLP-1 receptor directly. Olive oil acts several steps upstream: digestion, 2-OG formation, GLP-1 secretion from L-cells, and then a hormone that DPP-4 begins inactivating at once (Holst, 2007). On the question of whether people with type 2 diabetes respond less, a meta-analysis of 22 trials found that they do not, in general, show reduced GLP-1 secretion after an oral glucose or meal test, although worse glycaemic control may be associated with lower secretion (Calanna and colleagues, 2013).

In short: olive oil nudges a pathway that the drug saturates. The mechanism is real in human postprandial studies, and its documented size and duration differ from the drug's. No study cited here tested olive oil as an alternative to GLP-1 drug therapy; decisions about medicines belong with a prescriber.

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This Pathway Was Already Tested as a Drug — Twice

A further check on a mechanism is whether drugs aimed at the same target have been tested. Two classes have.

GPR119 agonists

In rats, a synthetic GPR119 agonist suppressed food intake and, with subchronic oral dosing in high-fat-fed rats, reduced body-weight gain and white fat deposition (Overton and colleagues, 2006). A 2024 review reports that this success in rodent models of type 2 diabetes and obesity failed to translate to early-stage clinical trials in patients with type 2 diabetes; one later compound, DS-8500a, showed increased efficacy with acute and chronic dosing but was discontinued, and the review describes the remaining candidates as preclinical or early-phase (Hryciw and colleagues, 2024).

DPP-4 inhibitors

DPP-4 inhibitors — the gliptins — block the enzyme that inactivates native GLP-1 rather than adding hormone, which makes them a test of "raise the body's own GLP-1." In a 2007 meta-analysis of randomised trials in type 2 diabetes, DPP-4 inhibitors lowered HbA1c by 0.74 percentage points compared with placebo and were weight neutral, while GLP-1 analogues produced weight loss (1.4 kg against placebo). All but three of the included trials lasted 30 weeks or less (Amori and colleagues, 2007). These trials were in people with type 2 diabetes and do not show what the same approach does in people without diabetes.

These results do not bear on olive oil's other documented effects, which are covered on the pages on heart health and polyphenols and oleocanthal. What they show is narrower: in these drug trials, enhancing the body's own GLP-1 with a DPP-4 inhibitor was weight neutral, and GPR119 agonists did not reproduce their rodent results in people.

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Energy Content: Addition Versus Substitution

Olive oil is almost entirely fat. The USDA FoodData Central record for olive oil (entry 171413, "Oil, olive, salad or cooking") lists 884 kcal and 100 g of fat per 100 g, and gives the weight of one tablespoon as 13.5 g. Versions of the claim that describe adding olive oil to most meals do not address that energy.

Whether added fat is offset by eating less later was not measured at those intakes in any study cited here. The Copenhagen meal studies measured hormones for two to three hours after 19 g of oil (Mandøe and colleagues, 2015 and 2018). The one study that measured later intake found lower energy intake over 24 hours after a single meal with 30 mL of high-oleic oil than after ordinary sunflower oil (Mennella and colleagues, 2015). In modelling work on energy balance, the body-weight response to a change in energy intake is slow, with half times of about a year, and larger in people with more body fat (Hall and colleagues, 2011).

The substitution distinction

The two body-weight studies cited on this page compared olive oil against something else. In a nine-week trial in 41 women with excess body fat, daily breakfasts contained 25 mL of either extra-virgin olive oil or soybean oil within an energy-restricted diet (Galvão Cândido and colleagues, 2018) — the olive oil replaced another oil inside a calorie-reduced plan. A 2018 systematic review and meta-analysis of 11 randomised trials lasting at least 12 weeks found that olive-oil-enriched diets reduced body weight by 0.92 kg, waist circumference by 0.60 cm and BMI by 0.90 more than control diets, with the benefit seen when the oil was taken in its natural liquid form and not as capsules (Zamora Zamora and colleagues, 2018). That abstract does not state whether olive oil replaced other fat in each included trial. PREDIMED, covered on the heart health page, tested Mediterranean dietary patterns against a control diet for cardiovascular events.

None of the studies cited here tested olive oil added on top of an unchanged diet. Related pages: energy density and the science of satiety.

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"Fat Loss 80% Higher" — Relative Versus Absolute

The figure comes from a randomised, double-blinded, placebo-controlled trial in Brazil. Forty-one adult women with excess body fat (mean age 27, mean body fat 46.8%) ate daily high-fat breakfasts containing 25 mL of soybean oil (control, n = 20) or extra-virgin olive oil (n = 21) for nine consecutive weeks, as part of an energy-restricted, normal-fat diet (−2090 kJ a day, about 32% of energy from fat). Body composition was assessed by anthropometry and dual-energy X-ray absorptiometry (Galvão Cândido and colleagues, 2018).

The authors report that fat loss was about 80% higher with olive oil: −2.4 ± 0.3 kg against −1.3 ± 0.4 kg (P = 0.037). Diastolic blood pressure fell by 5.1 mmHg with olive oil and rose by 0.3 mmHg in the control group (P = 0.011).

"80% higher" and "2.4 kg against 1.3 kg over nine weeks" describe the same result; the absolute figures show its size. In this trial the olive oil replaced soybean oil inside a calorie-reduced diet — a substitution design, not an addition. Whenever a percentage improvement is quoted without the two numbers it was computed from, those two numbers are the missing facts. The realistic expectations page covers the wider weight-loss literature.

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The EU Polyphenol Health Claim

Versions of the claim discuss whether a given bottle contains meaningful polyphenols. The EU has one regulated measure. Commission Regulation (EU) No 432/2012, based on a 2011 EFSA opinion, authorises the claim "Olive oil polyphenols contribute to the protection of blood lipids from oxidative stress" only for olive oil that contains at least 5 mg of hydroxytyrosol and its derivatives (e.g. oleuropein complex and tyrosol) per 20 g of olive oil, and requires that the consumer be told the beneficial effect is obtained with a daily intake of 20 g of olive oil. The chemistry belongs to the polyphenols and oleocanthal page.

What kind of instrument this is matters, because regulatory claims are often quoted as if they were trial results:

The "close to 90%" figure. Versions of the claim say that "close to 90%" of supermarket olive oil "probably does nothing." The laboratory finding usually behind such statements is narrower. In the UC Davis Olive Center's April 2011 report, 73% of the samples from the five top-selling imported "extra virgin" brands in the United States failed the International Olive Council's sensory standards for extra-virgin oil, as judged by two IOC-accredited panels, while all samples passed the IOC chemistry standards for free fatty acids, fatty-acid profile and peroxide value. Those are grade failures — mostly sensory defects — on oils bought in California, not a finding that the oils "do nothing."

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Where the Claim Circulates and What the Research Says

The idea that olive oil works like a GLP-1 drug circulates in social-media health videos, some of which also promote olive-oil products or programmes. The commercial context does not settle whether the pharmacology is right; the studies do. Set against the research cited on this page:

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What the Existing Studies Did Not Test

The question most relevant to the claim — whether adding olive oil to an unchanged diet changes body composition — was not tested by any study cited on this page. The cited abstracts leave these gaps open:

  1. Addition versus substitution. No cited trial compared olive oil added on top of a usual diet with the same oil replacing other fat, with body fat measured — for example by dual-energy X-ray absorptiometry, as in the nine-week trial.
  2. Repeated exposure. The Copenhagen studies were single meals; whether the GLP-1 response to olive oil persists or changes with daily use over weeks was not studied.
  3. Compensation. One study measured later energy intake, over 24 hours after a single meal (Mennella and colleagues, 2015); none measured it over weeks of habitual use.
  4. Oleic acid versus polyphenols. The EUROLIVE trial compared three olive oils that were otherwise similar but had low (2.7 mg/kg), medium (164 mg/kg) or high (366 mg/kg) phenolic content, 25 mL a day for three weeks each in 200 healthy men; its endpoints were blood lipids and oxidative-stress markers, not appetite or body weight (Covas and colleagues, 2006).

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Evidence Ledger

The strongest evidence sits at the mechanism end and the weakest at the outcome end — the opposite of how the claim is usually presented.

Established, in humans

Established, but in animals or cells

Small human studies

Not tested in the studies cited here

Tested as drugs

Checked and clear

The core human GLP-1 studies used ordinary olive oil eaten with food, by mouth, in people — no species, route or preparation substitution. The substitution that is present is endpoint substitution — a postprandial hormone result standing in for a fat-loss result — plus species substitution in the OEA arm, where the decisive experiments are in mice and rats.

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Summary of the Findings

  1. Substitution, not addition. In the body-weight studies cited here, olive oil replaced another oil or was compared with a control diet; none tested it as an addition to an unchanged diet. Olive oil is 884 kcal per 100 g.
  2. The GLP-1 response comes from digesting the oil within a meal. 2-OG is formed when lipase digests the fat; in the Copenhagen studies the oil was eaten with carrots.
  3. Not a drug-like effect. Native GLP-1 lasts one to two minutes, semaglutide about a week; no cited study tested olive oil as an alternative to prescribed treatment. Decisions about a GLP-1 receptor agonist belong with a prescriber.
  4. Product claims. The EU claim requires 5 mg of hydroxytyrosol and its derivatives per 20 g of oil and concerns blood-lipid oxidation only; the UC Davis 73% figure concerns sensory grade failures. The extra virgin quality page covers grades and testing.
  5. Gastroparesis and gallstones. The ACG guideline's dietary recommendation for gastroparesis is a small-particle diet, and small-particle, low-fat diets were better tolerated in the review it cites; a 1991 review of controlled studies concluded that biliary colic is not induced by fatty meals.
  6. Where the stronger evidence is. The cardiovascular evidence on the heart health page is more extensive than the GLP-1 evidence on this one.

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Key Research Papers

  1. Mandøe MJ, Hansen KB, Hartmann B, et al. (2015). The 2-monoacylglycerol moiety of dietary fat appears to be responsible for the fat-induced release of GLP-1 in humans. American Journal of Clinical Nutrition 102(3):548–555. — PubMed PMID: 26178726
  2. Mandøe MJ, Hansen KB, Windeløv JA, et al. (2018). Comparing olive oil and C4-dietary oil, a prodrug for the GPR119 agonist, 2-oleoyl glycerol, less energy intake of the latter is needed to stimulate incretin hormone secretion in overweight subjects with type 2 diabetes. Nutrition & Diabetes 8(1):2. — PubMed PMID: 29330461
  3. Hansen KB, Rosenkilde MM, Knop FK, et al. (2011). 2-Oleoyl glycerol is a GPR119 agonist and signals GLP-1 release in humans. Journal of Clinical Endocrinology and Metabolism 96(9):E1409–E1417. — PubMed PMID: 21778222
  4. Eissele R, Göke R, Willemer S, et al. (1992). Glucagon-like peptide-1 cells in the gastrointestinal tract and pancreas of rat, pig and man. European Journal of Clinical Investigation 22(4):283–291. — PubMed PMID: 1499644
  5. Overton HA, Babbs AJ, Doel SM, et al. (2006). Deorphanization of a G protein-coupled receptor for oleoylethanolamide and its use in the discovery of small-molecule hypophagic agents. Cell Metabolism 3(3):167–175. — PubMed PMID: 16517404 (Rat study.)
  6. Rodríguez de Fonseca F, Navarro M, Gómez R, et al. (2001). An anorexic lipid mediator regulated by feeding. Nature 414(6860):209–212. — PubMed PMID: 11700558 (Rat study.)
  7. Fu J, Gaetani S, Oveisi F, et al. (2003). Oleylethanolamide regulates feeding and body weight through activation of the nuclear receptor PPAR-alpha. Nature 425(6953):90–93. — PubMed PMID: 12955147 (Mouse study.)
  8. Guzmán M, Lo Verme J, Fu J, et al. (2004). Oleoylethanolamide stimulates lipolysis by activating the nuclear receptor peroxisome proliferator-activated receptor alpha (PPAR-alpha). Journal of Biological Chemistry 279(27):27849–27854. — PubMed PMID: 15123613 (Rat and mouse study.)
  9. Mennella I, Savarese M, Ferracane R, et al. (2015). Oleic acid content of a meal promotes oleoylethanolamide response and reduces subsequent energy intake in humans. Food & Function 6(1):204–210. — PubMed PMID: 25347552
  10. Kersten S, Seydoux J, Peters JM, et al. (1999). Peroxisome proliferator-activated receptor alpha mediates the adaptive response to fasting. Journal of Clinical Investigation 103(11):1489–1498. — PubMed PMID: 10359558 (Mouse study.)
  11. Zimmermann R, Strauss JG, Haemmerle G, et al. (2004). Fat mobilization in adipose tissue is promoted by adipose triglyceride lipase. Science 306(5700):1383–1386. — PubMed PMID: 15550674
  12. Holst JJ (2007). The physiology of glucagon-like peptide 1. Physiological Reviews 87(4):1409–1439. — PubMed PMID: 17928588
  13. Nauck MA, Meier JJ (2019). Management of endocrine disease: Are all GLP-1 agonists equal in the treatment of type 2 diabetes? European Journal of Endocrinology 181(6):R211–R234. — PubMed PMID: 31600725
  14. Lau J, Bloch P, Schäffer L, et al. (2015). Discovery of the once-weekly glucagon-like peptide-1 (GLP-1) analogue semaglutide. Journal of Medicinal Chemistry 58(18):7370–7380. — PubMed PMID: 26308095
  15. Ikushima I, Jensen L, Flint A, et al. (2018). A randomized trial investigating the pharmacokinetics, pharmacodynamics, and safety of subcutaneous semaglutide once-weekly in healthy male Japanese and Caucasian subjects. Advances in Therapy 35(4):531–544. — PubMed PMID: 29536338
  16. Wilding JPH, Batterham RL, Calanna S, et al.; STEP 1 Study Group (2021). Once-weekly semaglutide in adults with overweight or obesity. New England Journal of Medicine 384(11):989–1002. — PubMed PMID: 33567185
  17. Wilding JPH, Batterham RL, Davies M, et al.; STEP 1 Study Group (2022). Weight regain and cardiometabolic effects after withdrawal of semaglutide: the STEP 1 trial extension. Diabetes, Obesity and Metabolism 24(8):1553–1564. — PubMed PMID: 35441470
  18. Amori RE, Lau J, Pittas AG (2007). Efficacy and safety of incretin therapy in type 2 diabetes: systematic review and meta-analysis. JAMA 298(2):194–206. — PubMed PMID: 17622601
  19. Hryciw DH, Patten RK, Rodgers RJ, et al. (2024). GPR119 agonists for type 2 diabetes: past failures and future hopes for preclinical and early phase candidates. Expert Opinion on Investigational Drugs 33(3):183–190. — PubMed PMID: 38372052
  20. Calanna S, Christensen M, Holst JJ, et al. (2013). Secretion of glucagon-like peptide-1 in patients with type 2 diabetes mellitus: systematic review and meta-analyses of clinical studies. Diabetologia 56(5):965–972. — PubMed PMID: 23377698
  21. Beglinger C, Degen L (2004). Fat in the intestine as a regulator of appetite — role of CCK. Physiology & Behavior 83(4):617–621. — PubMed PMID: 15621067
  22. Camilleri M, Kuo B, Nguyen L, et al. (2022). ACG Clinical Guideline: Gastroparesis. American Journal of Gastroenterology 117(8):1197–1220. — PubMed PMID: 35926490
  23. Egbert AM (1991). Gallstone symptoms: myth and reality. Postgraduate Medicine 90(5):119–126. — PubMed PMID: 1924000
  24. Galvão Cândido F, Xavier Valente F, da Silva LE, et al. (2018). Consumption of extra virgin olive oil improves body composition and blood pressure in women with excess body fat: a randomized, double-blinded, placebo-controlled clinical trial. European Journal of Nutrition 57(7):2445–2455. — PubMed PMID: 28808791
  25. Zamora Zamora F, Martínez Galiano JM, Gaforio Martínez JJ, et al. (2018). Olive oil and body weight: systematic review and meta-analysis of randomized controlled trials [in Spanish]. Revista Española de Salud Pública 92:e201811083. — PubMed PMID: 30461730
  26. Hall KD, Sacks G, Chandramohan D, et al. (2011). Quantification of the effect of energy imbalance on bodyweight. Lancet 378(9793):826–837. — PubMed PMID: 21872751
  27. Covas MI, Nyyssönen K, Poulsen HE, et al.; EUROLIVE Study Group (2006). The effect of polyphenols in olive oil on heart disease risk factors: a randomized trial. Annals of Internal Medicine 145(5):333–341. — PubMed PMID: 16954359
  28. EFSA Panel on Dietetic Products, Nutrition and Allergies (NDA) (2011). Scientific Opinion on the substantiation of health claims related to polyphenols in olive and protection of LDL particles from oxidative damage (ID 1333, 1638, 1639, 1696, 2865) and other claims pursuant to Article 13(1) of Regulation (EC) No 1924/2006. EFSA Journal 9(4):2033. — doi:10.2903/j.efsa.2011.2033
  29. Commission Regulation (EU) No 432/2012 of 16 May 2012, list of permitted health claims (olive oil polyphenols: at least 5 mg of hydroxytyrosol and its derivatives per 20 g of olive oil; daily intake of 20 g). — EUR-Lex 32012R0432
  30. EFSA Panel on Nutrition, Novel Foods and Food Allergens (NDA) (2025). Phenolic compounds naturally present in olive oil and lowering of blood LDL-cholesterol and systolic blood pressure, therefore reducing the risk of coronary heart disease: evaluation of a health claim pursuant to Article 14 of Regulation (EC) No 1924/2006. EFSA Journal 23(5):e9470. — PubMed PMID: 40416788 (Cause-and-effect relationship not established.)
  31. EFSA Panel on Nutrition, Novel Foods and Food Allergens (NDA) (2025). Olive oil polyphenols and the maintenance of normal HDL-cholesterol concentrations: evaluation of a health claim pursuant to Article 13(5) of Regulation (EC) No 1924/2006. EFSA Journal 23(5):e9372. — PubMed PMID: 40321163 (Evidence insufficient.)
  32. Frankel EN, Mailer RJ, Wang SC, et al. (2011). Evaluation of extra-virgin olive oil sold in California. UC Davis Olive Center report, April 2011. — UC Davis Olive Center report (PDF)
  33. U.S. Department of Agriculture, Agricultural Research Service. FoodData Central, SR Legacy entry 171413, "Oil, olive, salad or cooking." — USDA FoodData Central 171413

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