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

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Abstract

Purpose

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.

Methods

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.

Results

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.

Conclusions

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.

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Abbreviations

ACC:

Acetyl-CoA carboxylase

ALAT:

Alanine aminotransferase

AMPK:

AMP-activated protein kinase

ASAT:

Aspartate aminotransferase

AUC:

Area under the curve

CE:

Cholesterol esters

cPO:

Crude palm oil

CPT-1A:

Carnitine palmitoyltransferase-1A

OO:

Olive oil

FA:

Fatty acid

Fabp1 :

Fatty acid-binding protein

FAS:

Fatty acid synthase

Fat/Cd36 :

Fatty acid transporter/cluster of differentiation 36

CD68:

Cluster of differentiation 68

DAPI:

4′,6-diamidino-2-phenylindole

Gclc :

Glutamate-cysteine ligase catalytic subunit

GPx:

Glutathione peroxidase

GSH:

Gluthatione

GssG:

Oxidized gluthatione

β-HAD:

β-hydroxyacyl-CoA dehydrogenase

HDL-C:

HDL cholesterol

HFD:

High-fat diet

HO-1:

Heme oxygenase 1

HOMA-IR:

Homeostasis model assessment-insulin resistance

IL-6:

Interleukin-6

IPGTT:

Intraperitoneal glucose tolerance test

Iκb-α :

Inhibitor kappa B alpha

Mcp-1 :

Monocyte chemoattractant protein 1

MUFA:

Monounsaturated fatty acids

Nf-κb :

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

Nqo-1 :

NADH quinone oxidoreductase-1

Nfe2l2 :

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

Ppargc-1α :

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

Ppar-α :

Peroxisome proliferator-activated receptor alpha

Ppar-γ :

Peroxisome proliferator-activated receptor gamma

PUFA:

Polyunsaturated fatty acids

RBC:

Red blood cell

ROS:

Reactive oxygen species

rPO:

Refined palm oil

Rplp0 :

60S acidic ribosomal protein P0

SFA:

Saturated fatty acids

SOD:

Superoxide dismutase

TBARS:

Thiobarbituric acid reactive substances

TG:

Triglycerides

Tnf-α :

Tumor necrosis factor alpha

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Acknowledgements

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.

Funding

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.

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Correspondence to Eric Badia.

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Djohan, Y.F., Badia, E., Bonafos, B. et al. High dietary intake of palm oils compromises glucose tolerance whereas high dietary intake of olive oil compromises liver lipid metabolism and integrity. Eur J Nutr 58, 3091–3107 (2019). https://doi.org/10.1007/s00394-018-1854-3

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  • DOI: https://doi.org/10.1007/s00394-018-1854-3

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