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. 2018 Feb 13:15:15.
doi: 10.1186/s12986-018-0252-4. eCollection 2018.

Dietary canolol protects the heart against the deleterious effects induced by the association of rapeseed oil, vitamin E and coenzyme Q10 in the context of a high-fat diet

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Dietary canolol protects the heart against the deleterious effects induced by the association of rapeseed oil, vitamin E and coenzyme Q10 in the context of a high-fat diet

Thibault Leger et al. Nutr Metab (Lond). .

Abstract

Background: Obesity progressively leads to cardiac failure. Omega-3 polyunsaturated fatty acids (PUFA) have been shown to have cardio-protective effects in numerous pathological situations. It is not known whether rapeseed oil, which contains α-linolenic acid (ALA), has a similar protective effect. Omega-3 PUFAs are sensitive to attack by reactive oxygen species (ROS), and lipid peroxidation products could damage cardiac cells. We thus tested whether dietary refined rapeseed oil (RSO) associated with or without different antioxidants (vitamin E, coenzyme Q10 and canolol) is cardio-protective in a situation of abdominal obesity.

Methods: Sixty male Wistar rats were subdivided into 5 groups. Each group was fed a specific diet for 11 weeks: a low-fat diet (3% of lipids, C diet) with compositionally-balanced PUFAs; a high-fat diet rich in palm oil (30% of lipids, PS diet); the PS diet in which 40% of lipids were replaced by RSO (R diet); the R diet supplemented with coenzyme Q10 (CoQ10) and vitamin E (RTC diet); and the RTC diet supplemented with canolol (RTCC diet). At the end of the diet period, the rats were sacrificed and the heart was collected and immediately frozen. Fatty acid composition of cardiac phospholipids was then determined. Several features of cardiac function (fibrosis, inflammation, oxidative stress, apoptosis, metabolism, mitochondrial biogenesis) were also estimated.

Results: Abdominal obesity reduced cardiac oxidative stress and apoptosis rate by increasing the proportion of arachidonic acid (AA) in membrane phospholipids. Dietary RSO had the same effect, though it normalized the proportion of AA. Adding vitamin E and CoQ10 in the RSO-rich high fat diet had a deleterious effect, increasing fibrosis by increasing angiotensin-2 receptor-1b (Ag2R-1b) mRNA expression. Overexpression of these receptors triggers coronary vasoconstriction, which probably induced ischemia. Canolol supplementation counteracted this deleterious effect by reducing coronary vasoconstriction.

Conclusion: Canolol was found to counteract the fibrotic effects of vitamin E + CoQ10 on cardiac fibrosis in the context of a high-fat diet enriched with RSO. This effect occurred through a restoration of cardiac Ag2R-1b mRNA expression and decreased ischemia.

Keywords: Antioxidant; Canolol; Heart; Obesity; Rapeseed oil; ω3 PUFAs.

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Conflict of interest statement

All experiments followed European Union guidelines concerning the care and use of laboratory animals for experimental and scientific purposes. All procedures involving animals and their care were approved by the INSA–Lyon Institutional Animal Care and Use Committee.All the authors have given the manuscript approval if accepted for publication in Nutrition & Metabolism.The authors declare that they have no competing interests.Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Figures

Fig. 1
Fig. 1
Influence of the different diets on myocardial mRNA levels for angiotensin 2 (panel a), angiotensin 2 receptor-1a (Ag2R-1a, panel b) and angiotensin 2 receptor-1b (Ag2R-1a, panel c). Figures are averages of 12 rats per group. C: rats fed the control diet; PS: rats fed with the high-fat diet rich in saturated and monounsaturated fatty acids; R: rats fed the high-fat diet rich in rapeseed oil; RTC: rats fed with the same diet as R, but enriched with vitamin E and CoQ10; RTCC: rats fed the same diet as RTC, but enriched with canolol; a,b: In a given panel, histograms without a common letter are significantly different
Fig. 2
Fig. 2
Myocardial contents of collagen (panel a), TGF-β1 (panel b) and MMP9 (panel c). Averages of 12 rats per group. C: rats fed the control diet; PS: rats fed the high-fat diet rich in saturated and monounsaturated fatty acids; R: rats fed with high-fat diet rich in rapeseed oil; RTC: rats fed with the same diet as R, but enriched with vitamin E and CoQ10; RTCC: rats fed the same diet as RTC, but enriched with canolol; TGF-b1: transforming growth factor-β1; MMP9: matrix metallopeptidase 9; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; a,b,c,d,e: In a given panel, histograms without a common letter are significantly different
Fig. 3
Fig. 3
Myocardial apoptosis estimated as the amount of cleaved caspase 3 (panel a), caspase 3 activity (panel b) and p53 mRNA level (panel c). Figures are averages of 12 rats per group. C: rats fed the control diet; PS: rats fed the high-fat diet rich in saturated and monounsaturated fatty acids; R: rats fed the high-fat diet rich in rapeseed oil; RTC: rats fed the same diet as R, but enriched with vitamin E and CoQ10; RTCC: rats fed with the same diet as RTC, but enriched with canolol; Δ O.D.: change in optical density. a,b,c: In a given panel, histograms without a common letter are significantly different
Fig. 4
Fig. 4
Mitochondrial biogenesis estimated as PGC-1α mRNA expression. Figures are averages of 12 rats per group. C: rats fed the control diet; PS: rats fed the high-fat diet rich in saturated and monounsaturated fatty acids; R: rats fed the high-fat diet rich in rapeseed oil; RTC: rats fed the same diet as R, but enriched with vitamin E and CoQ10; RTCC: rats fed the same diet as RTC, but enriched with canolol; PGC-1α: peroxisome proliferator activated receptor alpha; a,b: In a given panel, histograms without a common letter are significantly different

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