Following studies carried out in the 80s, it was observed that, by performing an oral tolerance curve with a glucose solution and, by measuring blood sugar levels with blood samples taken at time intervals (time zero, after 60 and 120 minutes), this test was used to measure the glycemic response and diagnose forms of diabetes or reduced carbohydrate tolerance (prediabetes).
An observation from that period had shown that, by administering glucose "in vein" or "orally", the two load curves were different and staggered over time as if there were the secretion of a molecule (intestinal hormone) capable of stimulating a "further" secretion of insulin.
This molecule, produced by intestinal endocrine cells, following a meal, is the “glucagon-like peptide 1” (GLP-1 o Glucagon-Like Peptide-1), that is, an intestinal hormone that stimulates endogenous insulin secretion, also capable of reduce glucagon, and capable of increase the feeling of satiety as well as of slow down digestion.
This type of hormone has been called “incretins”. The name incretin comes from the contraction of "intestinal secretion” (intestinal secretion). Today we know that there are actually two peptides GLP-1 and GIP (Glucose-dependent Insulinotropic Polypeptide).
"The incretin effect”, it has been shared as the phenomenon according to which the oral intake of glucose leads to a greater insulin response than that which would occur with the intravenous administration of glucose, that is, specifically the intervention of incretins, released into circulation in response to the meal, contribute to maintaining normal blood glucose levels through an increase in the secretion of insulin by pancreatic β-cellsa whirlpool bath, decreased glucagon secretion by pancreatic α-cells and a slowing of gastric emptying, with a consequent reduced appetite.
All the research agreed that this hormonal secretion did not occur by administering glucose intravenously, but only by ingesting food.
Further studies have shown that the GLP-1 has a short lifespan (half-life 2 minutes) as it is degraded by a enzyme with protease activity, Dipeptidyl-peptidase 4 (acronym DPP-4).
The research has produced antidiabetic (and anti-obesity) drugs belonging to the class of inhibitors of the activity of the enzyme DiPeptidyl-Peptidase 4 and drugs belonging to the class of GLP-1 receptor agonists (they bind to the GLP-1 receptor, i.e., the GLP-1R).
Since 2006, antidiabetic drugs (type 2 diabetes, T2DM) based on DPP-4 inhibition such as sitagliptin have been on the market in the USA, followed later by vildagliptin, saxagliptin and linagliptin, and others.
In an attempt to solve the problem of native GLP-1 degradation, new approaches have been implemented two different strategies. The first involves the use of GLP-1 receptor agonists, resistant to degradation by DPP-4, and for this purpose several molecules resistant to this action have been developed. The second approach consists in the inhibition of DPP-4 in order to reduce the degradation of endogenous GLP-1.
Having said this, it has been seen that olive oil has a favourable action on glycemic effects as monounsaturated fatty acids (MUFA, Monounsaturated Fatty Acids) (as oleic acid of olive oil, value between 55-85%, national median 74,6%) can stimulate the secretion of glucagon-like peptide 1 more than saturated fatty acids, (1, 2, 3) “probably” influencing the rate of gastric emptying.
This may be one of the reasons why olive oil lowers the glycemic index of a meal containing carbohydrates (simple and complex).
This hypothesis is supported by the favorable glycemic effects shown from canola oil (Erucic acid-free rapeseed oil, variety Brassica) also rich in MUFA, like olive oil (4)
Olive oil also has a beneficial effect on type 2 diabetes through: reduction of pro-inflammatory interleukins (IL-6, IL-7, IL-8), the increase in incretins (GLP-1), a inhibition of the enzyme that inactivates incretins (DPP-4), an inhibition of diabetic microangiopathy genes and prothrombotic mechanisms, finally a reduction of 22-40% of the risk to develop “type 2 diabetes” (5).
Francesco Violi suggests that EVO oil also improves post-prandial glycemia and LDL cholesterol (6).
Oleuropein, a phenolic compound in EVO olive oil, promotes glucose-stimulated insulin secretion (GSIS, Glucose-Stimulated Insulin Secretion) in β cells. The effect is dose-dependent and stimulates the ERK/MAPK signaling pathway (Extracellular signal-Regulated Kinase and Mitogen-Activated Protein Kinase).
[MAPK/ERK is a cellular signaling cascade that transmits signals from cell-surface receptors to the nucleus, regulating key processes such as cell proliferation, differentiation, survival, and death, involving a sequential series of protein kinases that phosphorylate downstream targets, including transcription factors, altering gene expression.]
Furthermore Oleuropein inhibits amyloid-induced cytotoxicity of amylin, a hallmark of type 2 diabetes. Two are the structure-specific functions: the 3-hydroxytyrosol portion of oleuropein is responsible for amyloid inhibition, while the GSIS function requires the entire structure of the molecule (7, 8).
In the early stages of type 2 diabetes, hypersecretion of amylin (in response to insulin resistance) can lead to formation of amyloid deposits in the pancreas, contributing to cellular damage.
To conclude, remembering that extra virgin olive oil of healthy quality is not a drug, but that it has a pleiotropic action on type 2 diabetes, in fact following the Mediterranean Diet, rich in vegetable fibres, these lower the glycemic index and in this sense we have a synergistic action by combining an EVO oil, with a high content of oleic acid and a healthy content of phenolic compounds (EU Regulation 432/2012) (9).
Bibliography
- https://pubmed.ncbi.nlm.nih.gov/10357731/
- https://pubmed.ncbi.nlm.nih.gov/12081840/
- https://pubmed.ncbi.nlm.nih.gov/12600850/
- https://pubmed.ncbi.nlm.nih.gov/24929428/
- https://pubmed.ncbi.nlm.nih.gov/36343558/
- https://pubmed.ncbi.nlm.nih.gov/26192450/
- https://pubs.acs.org/doi/10.1021/acs.biochem.7b00199
- https://pubmed.ncbi.nlm.nih.gov/35586621/
- https://doi.org/10.2337/dc15-2189

















