European Journal of Nutrition

, Volume 58, Issue 8, pp 3091–3107 | Cite as

High dietary intake of palm oils compromises glucose tolerance whereas high dietary intake of olive oil compromises liver lipid metabolism and integrity

  • Youzan Ferdinand Djohan
  • Eric BadiaEmail author
  • Beatrice Bonafos
  • Gilles Fouret
  • Céline Lauret
  • Anne-Marie Dupuy
  • Edith Pinot
  • Thibault Sutra
  • Sylvie Gaillet
  • Karen Lambert
  • Fabrice Raynaud
  • Nathalie Gayrard
  • Bernard Jover
  • Absalome Aké Monde
  • Jean Paul Cristol
  • Charles Coudray
  • Christine Feillet-Coudray
Original Contribution



Palm (PO) and olive oils (OO) are the two most consumed and/or used oils in the world for food elaboration. These oils should not be confused with the solid palm stearin which is widely used in pastry making. Large number of studies was reported dealing with adverse/beneficial cardiovascular effects of PO and OO, whereas few studies were conducted to compare their potential effects on hepatic steatosis and liver lipid metabolism. The aim of this study was to compare the metabolic effects of high intake of POs (both crude and refined) and virgin OO on surrogate parameters of glucose tolerance, hepatic lipid metabolism and liver integrity.


Thirty-two young male Wistar rats were divided into four equal groups and fed either control diet (11% energy from fat) or three high-fat diets rich in crude or refined POs or in OO (56% energy from fat), during 12 weeks. Systemic blood and liver biochemical parameters linked to glucose and lipid metabolism as well as hepatic steatosis and liver fatty acid composition were explored. The inflammation and oxidative stress status as well as the expression of several genes/proteins were also analyzed.


The major effects of POs intake concerned glucose metabolism and liver fatty acid composition, whereas the major effects of OO intake concerned hepatic TG accumulation, inflammation, and cytolysis.


In conclusion, high dietary intake of PO compromises glucose tolerance whereas high dietary intake of OO compromises hepatic lipid composition and liver integrity. However, adverse hepatic effects of OO observed in this study may not be transposed to human since, (a) the rodent model could lead to different effects than those observed in humans and (b) the average normal OO amounts ingested in the population are lower than those corresponding to a high-fat diet. So, further studies are needed to determine a maximum non-invasive dietary intake of OO.


Palm oil Olive oil High fat intake Liver steatosis Oxidative stress 



Acetyl-CoA carboxylase


Alanine aminotransferase


AMP-activated protein kinase


Aspartate aminotransferase


Area under the curve


Cholesterol esters


Crude palm oil


Carnitine palmitoyltransferase-1A


Olive oil


Fatty acid


Fatty acid-binding protein


Fatty acid synthase


Fatty acid transporter/cluster of differentiation 36


Cluster of differentiation 68




Glutamate-cysteine ligase catalytic subunit


Glutathione peroxidase




Oxidized gluthatione


β-hydroxyacyl-CoA dehydrogenase


HDL cholesterol


High-fat diet


Heme oxygenase 1


Homeostasis model assessment-insulin resistance




Intraperitoneal glucose tolerance test


Inhibitor kappa B alpha


Monocyte chemoattractant protein 1


Monounsaturated fatty acids


Nuclear factor “kappa-light-chain-enhancer” of activated β-cells


NADH quinone oxidoreductase-1


Nuclear factor E2-related factor 2 (gene coding for Nrf2)


Peroxisome proliferator activator receptor γ coactivator-1α (gene coding for PGC-1α)


Peroxisome proliferator-activated receptor alpha


Peroxisome proliferator-activated receptor gamma


Polyunsaturated fatty acids


Red blood cell


Reactive oxygen species


Refined palm oil


60S acidic ribosomal protein P0


Saturated fatty acids


Superoxide dismutase


Thiobarbituric acid reactive substances




Tumor necrosis factor alpha



We gratefully acknowledge Dr C Notarnicola, Dr V Scheuermann. Designed research (JPC, EB, CFC, CC, AM); wrote the paper (BE, CC, CFC); conducted research (YFD, GF, CL, AMD, EP, TS, SG, KL, NG, BJ), analyzed data or performed statistical analysis (EB, CC, CFC). All authors have read and approved the final manuscript.


Except YFD (who received help from University of Cocody and a modest grant from SANIA company), the authors have not received any funding or benefits from industry to conduct this study.

Supplementary material

394_2018_1854_MOESM1_ESM.docx (414 kb)
Supplementary material 1 (DOCX 413 KB)


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Copyright information

© Springer-Verlag GmbH Germany, part of Springer Nature 2018

Authors and Affiliations

  • Youzan Ferdinand Djohan
    • 1
  • Eric Badia
    • 1
    Email author
  • Beatrice Bonafos
    • 2
  • Gilles Fouret
    • 2
  • Céline Lauret
    • 1
  • Anne-Marie Dupuy
    • 3
  • Edith Pinot
    • 3
  • Thibault Sutra
    • 3
  • Sylvie Gaillet
    • 2
  • Karen Lambert
    • 1
  • Fabrice Raynaud
    • 1
  • Nathalie Gayrard
    • 4
  • Bernard Jover
    • 1
  • Absalome Aké Monde
    • 5
  • Jean Paul Cristol
    • 3
  • Charles Coudray
    • 2
  • Christine Feillet-Coudray
    • 2
  1. 1.PhyMedExp, Univ. Montpellier, INSERM U1046, CNRS UMR 9214MontpellierFrance
  2. 2.DMEM, INRA, Univ. MontpellierMontpellierFrance
  3. 3.Laboratoire de Biochimie, CHU-LapeyronieMontpellierFrance
  4. 4.EA7288, Univ. MontpellierMontpellierFrance
  5. 5.Laboratoire de Biochimie, CHU, Univ. Félix Houphouët-BoignyCocodyCôte d’Ivoire

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