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. 2022 Sep 4;15(9):1103.
doi: 10.3390/ph15091103.

The Impact of Dietary Consumption of Palm Oil and Olive Oil on Lipid Profile and Hepatocyte Injury in Hypercholesterolemic Rats

Affiliations

The Impact of Dietary Consumption of Palm Oil and Olive Oil on Lipid Profile and Hepatocyte Injury in Hypercholesterolemic Rats

Tarfa Albrahim et al. Pharmaceuticals (Basel). .

Abstract

A metabolic disease called hypercholesterolemia is connected to both oxidative damage and inflammation. The goal of the current investigation was to determine if olive oil and palm oil could prevent hypercholesterolemia-induced oxidative stress in the liver of rats fed a high-cholesterol diet (HCD). The experimental mice were given HCD for three months while also receiving 0.5 mL/kg of either palm or olive oil. Serum triglycerides, total cholesterol, LDL cholesterol, vLDL cholesterol, and the atherogenic index all significantly increased in HCD-fed rats, while HDL cholesterol significantly dropped. Additionally, HCD caused a notable rise in proinflammatory cytokines and serum transaminases in liver tissue. Additionally, HCD significantly increased the production of nitric oxide and lipid peroxidation in the liver while decreasing antioxidant enzymes. Treatment with palm and olive oils dramatically reduced the levels of pro-inflammatory cytokines and lipid peroxidation, improved antioxidant defenses, and considerably improved liver function indicators. Additionally, the examined oils dramatically decreased the expression of fatty acid synthase (FAS) in the liver of rats receiving HCD. In conclusion, HCD-fed rats exhibit significant antihyperlipidemic and cholesterol-lowering benefits from palm and olive oils. The improved antioxidant defenses, lower inflammation and lipid peroxidation, and altered hepatic FAS mRNA expression were the main mechanisms by which palm and olive oils produced their advantageous effects.

Keywords: FAS; hypercholesterolemia; inflammation; olive oil; oxidative stress; palm oil.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
(A) Body weight and (B) serum glucose level following treatment with palm oil (PO), olive oil (OO), or atorvastatin (AV) in high-cholesterol diet-induced hypercholesterolemia in rats. Data are expressed as the mean ± SD (n = 7). Letters a and b indicate statistically significant differences between control rats and hypercholesterolemia rats, respectively, at p < 0.05.
Figure 2
Figure 2
Serum transaminases ((A) ALT and (B) AST) following treatment with palm oil (PO), olive oil (OO), or atorvastatin (AV) in high-cholesterol diet-induced hypercholesterolemia in rats. Data are expressed as the mean ± SD (n = 7). Letters a and b indicate statistically significant differences between control rats and hypercholesterolemia rats, respectively, at p < 0.05.
Figure 3
Figure 3
Serum levels of (A) triglyceride, (B) cholesterol, (C) HDL, (D) LDL, and (E) vLDL following treatment with palm oil (PO), olive oil (OO), or atorvastatin (AV) in high-cholesterol diet-induced hypercholesterolemia in rats. Data are expressed as the mean ± SD (n = 7). Letters a and b indicate statistically significant differences between control rats and hypercholesterolemia rats, respectively, at p < 0.05.
Figure 4
Figure 4
(A) Atherogenic index and (B) fatty acid synthase expression following treatment with palm oil (PO), olive oil (OO), or atorvastatin (AV) in high-cholesterol diet-induced hypercholesterolemia in rats.Data are expressed as the mean ± SD (n = 7). Letters a and b indicate statistically significant differences between control rats and hypercholesterolemia rats, respectively, at p < 0.05.
Figure 5
Figure 5
Hepatic levels of oxidative stress markers ((A) lipid peroxidation, (B) nitric oxide, and (C) glutathione) following treatment with palm oil (PO), olive oil (OO), or atorvastatin (AV) in high-cholesterol diet-induced hypercholesterolemia in rats.Data are expressed as the mean ± SD (n = 7). Letters a and b indicate statistically significant differences between control rats and hypercholesterolemia rats, respectively, at p < 0.05.
Figure 6
Figure 6
Hepatic levels of oxidative stress markers ((A) superoxide dismutase, (B) catalase, (C) glutathione peroxidase, and (D) glutathione reductase) following treatment with palm oil (PO), olive oil (OO), or atorvastatin (AV) in high-cholesterol diet-induced hypercholesterolemia in rats.Data are expressed as the mean ± SD (n = 7). Letters a and b indicate statistically significant differences between control rats and hypercholesterolemia rats, respectively, at p < 0.05.
Figure 7
Figure 7
Hepatic levels of pro-inflammatory cytokines ((A) IL-1β and (B) TNF-α) following treatment with palm oil (PO), olive oil (OO), or atorvastatin (AV) in high-cholesterol diet-induced hypercholesterolemia in rats. Data are expressed as the mean ± SD (n = 7). Letters a and b indicate statistically significant differences between control rats and hypercholesterolemia rats, respectively, at p < 0.05.

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