Palm Oil – A Desired Ingredient for European Food Manufacturers to Avoid Dangerous Trans Fats

Palm Oil has seen increasing demand in Europe over the last twenty years. It is needed in food preparation to supplement insufficient local production of oils and fats. Nett imports of oils and fats by the EU amount to 8 to 10 million tonnes per year making up one third of annual consumption and most of these imports are made up of palm oil.

In recent years, the Europeans have been fed with misinformation through negative campaigns by environmental NGOs.  Most customers of palm oil are secretly praying that  the current controversy over this popular  commodity will be resolved soon. They want to continue concentrating on their core business of producing products where palm oil is a desirable component because of its superior techno-economic attributes. They need palm oil to enable them to make profitable and affordable products for the depressed European economy.

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Loss of miR-29b following acute ischemic stroke contributes to neural cell death and infarct size

Khanna S, Rink C, Ghoorkhanian R, Gnyawali S, Heigel M, Wijesinghe DS, Chalfant CE, Chan YC, Banerjee J, Huang Y, Roy S, Sen CK.

J Cereb Blood Flow Metab. 2013 May 1. doi: 10.1038/jcbfm.2013.68. [Epub ahead of print]

Glutathione depletion and 12-lipoxygenase-dependent metabolism of arachidonic acid are known to be implicated in neurodegeneration associated with acute ischemic stroke. The objective of this study was to investigate the significance of miR-29 in neurodegeneration associated with acute ischemic stroke. Neural cell death caused by arachidonic acid insult of glutathione-deficient cells was preceded by a 12-lipoxygenase-dependent loss of miR-29b. Delivery of miR-29b mimic to blunt such loss was neuroprotective. miR-29b inhibition potentiated such neural cell death. 12-Lipoxygenase knockdown and inhibitors attenuated the loss of miR-29b in challenged cells. In vivo, stroke caused by middle-cerebral artery occlusion was followed by higher 12-lipoxygenase activity and loss of miR-29b as detected in laser-captured infarct site tissue. 12-Lipoxygenase knockout mice demonstrated protection against such miR loss. miR-29b gene delivery markedly attenuated stroke-induced brain lesion. Oral supplementation of α-tocotrienol, a vitamin E 12-lipoxygenase inhibitor, rescued stroke-induced loss of miR-29b and minimized lesion size. This work provides the first evidence demonstrating that loss of miR-29b at the infarct site is a key contributor to stroke lesion. Such loss is contributed by activity of the 12-lipoxygenase pathway providing maiden evidence linking arachidonic acid metabolism to miR-dependent mechanisms in stroke.Journal of Cerebral Blood Flow & Metabolism advance online publication, 1 May 2013; doi:10.1038/jcbfm.2013.68.

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Granulocyte colony-stimulating factor antibody abrogates radioprotective efficacy of gamma-tocotrienol, a promising radiation countermeasure.

Kulkarni S, Singh PK, Ghosh SP, Posarac A, Singh VK.

Cytokine. 2013 May;62(2):278-85. doi: 10.1016/j.cyto.2013.03.009. Epub 2013 Apr 3

This study aimed to determine the role of granulocyte colony-stimulating factor (G-CSF), induced by a promising radiation countermeasure, gamma tocotrienol (GT3), in protecting mice from lethal doses of ionizing radiation. CD2F1 mice were injected with an optimal dose of GT3 and a G-CSF antibody, and their 30-d survival was monitored. An appropriate antibody isotype was used as a control. Multiplex Luminex was used to analyze GT3-induced cytokines. G-CSF neutralization by exogenous administration of a G-CSF antibody was confirmed by analyzing serum cytokine levels. Our results demonstrate that GT3 significantly protected mice against ionizing radiation, and induced high levels of G-CSF in peripheral blood 24h after administration. Injection of a G-CSF neutralizing antibody to the GT3-treated mice resulted in complete neutralization of G-CSF and abrogation of its protective efficacy. Administration of a G-CSF antibody did not affect levels of other cytokines induced by GT3. Histopathology of bone marrow from GT3-treated and -irradiated mice demonstrated protection of the hematopoietic tissue, and also that such protection was abrogated by administering a G-CSF antibody. Our results suggest that induction of high levels of G-CSF by GT3 administration is responsible for its protective efficacy against radiation injury.

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Gamma-tocotrienol modulated gene expression in senescent human diploid fibroblasts as revealed by microarray analysis

Makpol S, Zainuddin A, Chua KH, Mohd Yusof YA, Ngah WZ.

Oxid Med Cell Longev. 2013;2013:454328. doi: 10.1155/2013/454328. Epub 2013 Mar 24.

The effect of γ -tocotrienol, a vitamin E isomer, in modulating gene expression in cellular aging of human diploid fibroblasts was studied. Senescent cells at passage 30 were incubated with 70  μ M of γ -tocotrienol for 24 h. Gene expression patterns were evaluated using Sentrix HumanRef-8 Expression BeadChip from Illumina, analysed using GeneSpring GX10 software, and validated using quantitative RT-PCR. A total of 100 genes were differentially expressed (P < 0.001) by at least 1.5 fold in response to γ -tocotrienol treatment. Amongst the genes were IRAK3, SelS, HSPA5, HERPUD1, DNAJB9, SEPR1, C18orf55, ARF4, RINT1, NXT1, CADPS2, COG6, and GLRX5. Significant gene list was further analysed by Gene Set Enrichment Analysis (GSEA), and the Normalized Enrichment Score (NES) showed that biological processes such as inflammation, protein transport, apoptosis, and cell redox homeostasis were modulated in senescent fibroblasts treated with γ -tocotrienol. These findings revealed that γ -tocotrienol may prevent cellular aging of human diploid fibroblasts by modulating gene expression.

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Palm tocotrienol-rich fraction improves vascular proatherosclerotic changes in hyperhomocysteinemic rats

Ku-Zaifah Norsidah, Ahmad Yusof Asmadi, Ayob Azizi, Othman Faizah, and Yusof Kamisah

Evid Based Complement Alternat Med. 2013; 2013: 976967.

This study investigated the effects of palm tocotrienol-rich fraction (TRF) on aortic proatherosclerotic changes in rats fed with a high methionine diet. Forty-two male Wistar rats were divided into six groups. The first group was the control (fed with a basal diet). Another five groups were fed with 1% methionine diet for 10 weeks. From week 6 onward, folate (8 mg/kg diet) or palm TRF (30, 60, and 150 mg/kg diets) was added into the diet of the last four rat groups, respectively. The high methionine diet raised the plasma total homocysteine and aortic lipid peroxidation, which were reduced by the palm TRF and folate supplementations. Plasma nitric oxide was reduced in the high methionine group compared to the control (3.72 ± 0.57 versus 6.65 ± 0.53  μ mol/L, P < 0.05), which reduction was reversed by the palm TRF (60 and 150 mg/kg) and folate supplementations. The increased aortic vascular cell adhesion molecule-1 expression in the methionine group (2.58 ± 0.29) was significantly reduced by the folate (1.38 ± 0.18) and palm TRF at 150 mg/kg (1.19 ± 0.23). Palm TRF was comparable to folate in reducing high methionine diet-induced plasma hyperhomocysteinemia, aortic oxidative stress, and inflammatory changes in rats.

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Pure tocotrienol concentrate protected rat gastric mucosa from acute stress-induced injury by a non-antioxidant mechanism

Rodzian MN, Ibrahim IA, Fahami NA, Ismail NM

Pol J Pathol. 2013 Mar;64(1):52-8

Stress has been implicated as a risk factor of various major health problems, such as stress-induced gastric mucosal injury. This study was performed to investigate the action of a pure preparation of tocotrienol (T3) concentrate, made up of 90% -tocotrienol and 10% γ-tocotrienol, on gastric injury of rats induced by water-immersion restraint stress (WIRS). Fourteen male Sprague-Dawley rats (200-250 g) were divided into two equal groups: a control group and a treated group. The treatment group received T3 concentrate at 60 mg/kg body weight daily for 28 days. The body weights of rats were recorded daily before the treatment was given. At the end of the treatment period, all rats were subjected to WIRS for 3.5 hours, following which the rats were euthanized. The stomachs were isolated and opened along the greater curvature for the examination of lesions and measurements of gastric malondialdehyde (MDA) and prostaglandin E2 (PGE2) contents. The mean gastric mucosal lesion index in the treated rats was significantly lower than that in the control rats. This suggests that the T3 concentrate has the ability to confer protection to the gastric mucosa against gastric injury induced by acute stress. No significant difference was observed for changes in body weight before and after the treatment. The gastric PGE2 content in both groups was comparable. However, the gastric MDA content was significantly higher in the treated group compared to the control group, indicating that the T3 supplementation was not able to reduce the lipid peroxidation process. This study concludes that the T3 concentrate has the ability to protect the gastric mucosa from stress-induced injury by a non-antioxidant mechanism.

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Studies Targeting α-Glucosidase Inhibition, Antiangiogenic Effects, and Lipid Modification Regulation: Background, Evaluation, and Challenges in the Development of Food Ingredients for Therapeutic Purposes

Nakagawa K

Biosci Biotechnol Biochem. 2013 May 7. [Epub ahead of print]

Since the discovery of α-glucosidase inhibitors and their inhibitory effects on the digestion of carbohydrates, promising results have been obtained as to the antidiabetic effects of this family of compounds. Antiangiogenic compounds have been identified that suppress tumor growth via a unique mechanism, confirming that such compounds can act as clinically applicable anticancer agents. Lipid peroxidation and lipid glycation have been suggested to play roles in food deterioration and in the pathophysiology of human diseases such as atherogenesis and diabetes, and antioxidative and antiglycative compounds can potentially be used in the prevention of food deterioration as well as to treat disease. On this basis, this review describes studies of α-glucosidase inhibition by mulberry 1-deoxynojirimycin, antiangiogenic effects of rice bran tocotrienol, and membrane lipid peroxidation/glycation and its inhibitors. These studies are ongoing in our work, with an emphasis on analytical techniques.

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Gamma-tocotrienol eliminates breast cancer stem cells

Cancer (2)Drug-resistant human breast cancer cells express high levels of Stat-3 signalling mediators essential for enrichment of cancer stem cells.  Alone or in combination with simvastatin , low doses of gamma-tocotrienol eliminates human breast cancer stem cells  via inhibition of the mevalonate pathway and activation of the novo ceramide synthesis pathways.

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Tocotrienol ameliorates biomarkers of fatty liver disease in animal models

Tocotrienol exerts a synergistic effect with alpha-tocopherol on rat liver2models of steatohepatitis (fatty liver).  Results have shown that lipid peroxide levels in the liver are lower and signs of increased liver damage are controlled after combined intake of tocotrienol and alpha-tocopherol. High levels of inflammatory cytokines mRNA suppression were observed and particularly, the gamma-isoform of tocotrienol significantly inhibited mRNA expression of TGF-beta1.

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Effects of tocotrienol on tumor necrosis factor-alpha/d-galactosamine-induced steatohepatitis in rats

Yachi, R., Muto, C., Ohtaka, N., Aoki, Y., Koike, T., Igarashi, O., Kiyose, C.

J Clin Biochem Nutr 2013;52(2):146-53

It has been reported that alpha-tocopherol (alpha-Toc), a vitamin E analog, is effective for treatment of non-alcoholic steatohepatitis (NASH). However, it is unknown whether or not other vitamin E analogs are effective. Therefore we designed a new rat model of steatohepatitis induced by tumor necrosis factor-alpha (TNF-alpha) stimulation, and used it to investigate the effects of vitamin E analogs. The rat liver triglyceride content increased with the dosage of TNF-alpha/d-galactosamine (GalN), but was suppressed by intake of both tocotrienol (T3) and alpha-tocopherol. Moreover, lipid peroxides (thiobarbituric acid-reactive substances) level in the liver level was also lower in both groups after tocotrienol and alpha-Toc intake. Intake of both tocotrienol and alpha-tocopherol also tended to control the increase of liver damage marker activity. In the tocotrienol and alpha-tocopherol groups, increases of inflammatory cytokines mRNA expression in the liver were inhibited, and these effects were considered to contribute to improvement of inflammation and fibrosis. The expression of mRNAs for inflammatory cytokines in rat primary hepatocytes was increased by TNF-alpha stimulation, but was inhibited by addition of alpha-tocotrienol and gamma-tocotrienol. Transforming growth factor-beta1 mRNA expression in particular was significantly inhibited by gamma-tocotrienol. These findings suggest that tocotrienol species are effective for amelioration of steatohepatitis, and that tocotrienol and alpha-tocopherol exert a synergistic effect.