Abstract

BackgroundObesity 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.MethodsSixty 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.ResultsAbdominal 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.ConclusionCanolol 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.

Highlights

  • Each group was nourished with a specific diet for 11 weeks: a low-fat diet (3% of lipids, C diet) with compositionally-balanced polyunsaturated fatty acids (PUFA); a high-fat diet rich in palm oil (30% of lipids, Palm oil/ sunflower oil (PS) diet); the palm-oil-rich high-fat diet (PS diet) in which 40% of lipids were replaced by rapeseed oil (RSO) (R diet); the R diet supplemented with coenzyme Q10 (CoQ10) and vitamin E (RTC diet); and the Rapeseed oil + α-tocopherol + coenzyme Q10 (RTC) diet supplemented with canolol (RTCC diet)

  • Our results indicated that the palm-oil-rich high-fat diet (PS diet) used here decreased cardiac oxidative stress, due to the increased accumulation of arachidonic acid in membrane phospholipids which, according to previous results collected in our laboratory, stimulates coronary perfusion and cardiac mechanical activity

  • The cyclooxygenase products derived from these fatty acids can have similar dilatation effects on coronary micro-circulation to the cyclooxygenase products formed from arachidonic acid (AA)

Read more

Summary

Introduction

Omega-3 polyunsaturated fatty acids (PUFA) have been shown to have cardio-protective effects in numerous pathological situations. A preliminary step that increases cardiac mechanical function leads to increased proportion of arachidonic acid (C20:4ω6 or AA) in the cardiac membrane and increased coronary microvessel vasodilatation capacities [5]. This status is transient: heart failure inexorably develops [6] due to the progressive development of post-prandial hyperglycemia and oxidative stress. These changes alter coronary microvessel function [7], reduce myocardial perfusion and decrease cardiac mechanical function

Objectives
Methods
Results
Discussion
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call