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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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.
KeywordsPalm oil Olive oil High fat intake Liver steatosis Oxidative stress
AMP-activated protein kinase
Area under the curve
Crude palm oil
Fatty acid-binding protein
Fatty acid synthase
Fatty acid transporter/cluster of differentiation 36
Cluster of differentiation 68
Glutamate-cysteine ligase catalytic subunit
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
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.
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