Research article
Different palm oil preparations reduce plasma cholesterol concentrations and aortic cholesterol accumulation compared to coconut oil in hypercholesterolemic hamsters

https://doi.org/10.1016/j.jnutbio.2005.03.007Get rights and content

Abstract

Several studies have reported on the effect of refined, bleached and deodorized palm oil (RBD-PO) incorporation into the diet on blood cholesterol concentrations and on the development of atherosclerosis. However, very little work has been reported on the influence of red palm oil (RPO), which is higher in carotenoid and tocopherol content than RBD-PO. Thus, we studied the influence of RPO, RBD-PO and a RBD-PO plus red palm oil extract (reconstituted RBD-PO) on plasma cholesterol concentrations and aortic accumulation vs. hamsters fed coconut oil. Forty-eight F1B Golden Syrian hamsters (Mesocricetus auratus) (BioBreeders, Watertown, MA) were group housed (three/cage) in hanging polystyrene cages with bedding in an air-conditioned facility maintained on a 12-h light/dark cycle. The hamsters were fed a chow-based hypercholesterolemic diet (HCD) containing 10% coconut oil and 0.1% cholesterol for 2 weeks at which time they were bled after an overnight fast and segregated into four groups of 12 with similar plasma cholesterol concentrations. Group 1 continued on the HCD, Group 2 was fed the HCD containing 10% RPO in place of coconut oil, Group 3 was fed the HCD containing 10% RBD-PO in place of coconut oil and Group 4 was fed the HCD with 10% reconstituted RBD-PO for an additional 10 weeks. Plasma total cholesterol (TC) and non-high-density lipoprotein-cholesterol (HDL-C) (very low- and low-density lipoprotein) concentrations were significantly lower in the hamsters fed the RPO (−42% and −48%), RBD-PO (−32% and −36%) and the reconstituted RBD-PO (−37% and −41%) compared to the coconut oil-fed hamsters. Plasma HDL-C concentrations were significantly higher by 14% and 31% in hamsters fed the RBD-PO and RPO compared to the coconut oil-fed hamsters. Plasma triglyceride (TG) concentrations were significantly lower in hamsters fed RBD-PO (−32%) and the reconstituted RBD-PO (−31%) compared to the coconut oil-fed hamsters. The plasma γ-tocopherol concentrations were higher in the coconut oil-fed hamsters compared to the hamsters fed the RPO (60%), RBD-PO (42%) and the reconstituted RBD-PO (49%), while for plasma α-tocopherol concentrations, the coconut oil-fed hamsters were significantly higher than only the RPO-fed hamsters (21%). The coconut oil-fed hamsters also had significantly higher plasma lipid hydroperoxide concentrations compared to RBD-PO (112%) and the reconstituted RBD-PO (485%). The hamsters fed the coconut oil diet excreted significantly more fecal total neutral sterols and cholesterol compared to the hamsters fed the RBD-PO (158% and 167%, respectively). The coconut oil-fed hamsters had significantly higher levels of aortic total, free and esterified cholesterol compared to the hamsters fed the RPO (74%, 50% and 225%, respectively), RBD-PO (57%, 48% and 92%, respectively) and the reconstituted RBD-PO (111%, 94% and 94%, respectively). Also, aortic free/ester cholesterol ratio in the aortas of hamsters fed RPO was significantly higher than in those fed the coconut oil (124%). In conclusion, hamsters fed the three palm oil preparations had lower plasma TC and non-HDL-C and higher HDL-C concentrations while accumulating less aortic cholesterol concentrations compared to hamsters fed coconut oil.

Introduction

The oil obtained initially upon harvesting the fruit of the oil palm is red due to its content of carotene, tocopherol and tocotrienols. The palm oil generally available for use (refined, bleached and deodorized or RBD-PO) has been processed to remove the carotene and tocopherols. This fractionation brings about an increase in monounsaturated oleic acid with the concomittant reduction of palmitic acid, the major saturated fatty acid [1], [2]. Palm oil contains a higher proportion of palmitic acid as well as considerable quantities of oleic and linoleic acids, which give it a higher unsaturated fatty acid content than coconut oil and palm kernel oil [3], [4], [5], [6]. Throughout the world, 90% of palm oil is used for edible purposes (e.g., margarine, deep fat frying, shortening, ice creams, cocoa butter substitutes in chocolate) [7], [8].

Red palm oil (RPO) contains 50% saturated, 40% monounsaturated and 10% polyunsaturated fatty acids [9]. Red palm oil is the richest food source of carotenoids (500–750 mg/L) [4] and a very good source of vitamin E (tocopherols and tocotrienols) (560–100 ppm) [2], [10], [11]. The carotenoids, together with tocopherols and tocotrienols, ascorbic acid, enzymes and proteins, are members of the biological antioxidant network [12], [13] converting highly reactive radicals and free peroxy radicals to less active species, thus protecting against oxidative damage to cells [14].

Previous work has shown that tocopherol and tocotrienols may be anti-atherogenic, although they may have no effect on plasma cholesterol concentrations. Tocopherols have been reported to inhibit atherosclerosis in rabbits [15], [16] and in monkeys [17]. Antioxidants have been shown to reduce the risk of atherosclerosis in human populations [18], [19]. Tocotrienols have been reported to be natural inhibitors of cholesterol synthesis [20], [21]. The tocopherols and tocotrienols promote an antithrombotic state by reducing platelet aggregation and modulating prostanoid synthesis [21], [22], [23], [24]. Based on this information, one might then expect RPO to be less atherogenic than RBD-PO. Kritchevsky et al. [25] have shown this to be the case in studies of experimental atherosclerosis in rabbits. To further investigate the role that the carotenoids and tocopherols of RPO may play in its comparative protective action, Kritchevsky et al. [26] have compared atherogenicity in cholesterol-fed (0.1%) rabbits of RPO, RBD-PO and RBD-PO to which the antioxidant components of RPO have been added (reconstituted RPO). RBD-PO was shown to be 58% more atherogenic than RPO and 13% more atherogenic than the reconstituted RBO.

In this manuscript, we describe the atherogenic effects of RPO, RBD-PO and reconstituted RBD-PO when substituted for coconut oil in the hamster model, which has been previously described [27].

Section snippets

Animals and experimental design

Forty-eight F.B. Golden Syrian hamsters (Mesocricetus auratus) (BioBreeders, Watertown, MA) were used. They were group housed (three/cage) in hanging polystyrene cages with bedding in a temperature-controlled room (25°C) maintained on a 12-h light/dark cycle. Hamsters were given food and water ad libitum. Hamsters were fed Purina Hamster Chow (Ralston Purina, St. Louis, MO) for 1 week in order to acclimate them to the facility. The hamsters were then fed a nonpurified hypercholesterolemic diet

Results

All hamsters in each group survived the entire length of the study. No significant differences were observed between dietary treatments for initial body weight; however, by the end of the 10-week treatment period, the hamsters fed the coconut oil diet and the 50:50 mixture oil diet had gained 10% more body weight than the hamsters fed the RBD-PO (P<.05) (data not shown). At the same time, no significant difference for food consumption between the treatment diets was observed (data not shown).

Discussion

Palm oil has been stigmatized as a hypercholesterolemic fat because of its palmitic acid (16:0) content. In this study, coconut oil was the most hyperlipidemic of the test fats. Red palm oil was somewhat less cholesterolemic (10–20%) than either RBD-PO or the reconstituted RBD-PO resulting in a lower total to HDL-cholesterol ratio. Plasma triglyceride concentrations in hamsters fed RPO were almost as high as those in hamsters fed coconut oil and about 33% higher than in hamsters fed either

Acknowledgment

The palm oil preparations were a gift of the Malaysian Palm Oil Board, Kuala Lumpur, Malaysia. The authors would like to thank Monica McIntyre, Julie Desjardins, Anthony DeSimone, Catherine Jones and Ben Woolfrey for their technical assistance, and Maureen Faul for her administrative assistance.

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    The work was supported, in part, by a Research Career Award (HL 00734) to Dr. David Kritchevsky from the National Institute of Health (USA).

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