Rapeseed oil fortified with micronutrients can reduce glucose intolerance during a high fat challenge in rats

Abstract Background Better choices of dietary lipid sources and substitution of refined by fortified oils could reduce the intake of saturated fatty acids (FA) and increase the intake of omega 3 FA concomitantly to healthy bioactive compounds. Methods The development of obesity and metabolic disturbances was explored in rats fed during 11 weeks with a high fat diet (HFD) in which the amount of saturated and polyunsaturated FA was respectively reduced and increased, using rapeseed oil as lipid source. This oil was used in a refined form (R) or fortified (10 fold increase in concentration) with endogenous micronutrients (coenzyme Q10 + tocopherol only (RF) only and also with canolol (RFC)). The effect of substituting palm by rapeseed oil was analysed using a student t test, oil fortification was analysed using ANOVA statistical test. Results Despite a similar weight gain, diets R, RF and RFC improved glucose tolerance (+ 10%) of the rats compared to a standard HFD with palm and sunflower oils as lipid source. Plasma glucose was lowered in RF and RFC groups (− 15 and 23% respectively), although triacylglycerol level was only reduced in group RFC (− 33%) compared to R. The fortification with canolol promoted the activation of Akt and AMP-activated protein kinase (AMPK) in skeletal muscle and subcutaneous adipose tissue respectively. Canolol supplementation also led to reduce p38 MAPK activation in skeletal muscle. Conclusions This study suggests that the presence of endogenous micronutrients in rapeseed oil promotes cellular adaptations to reverse glucose intolerance and improve the metabolism of insulin sensitive tissues

Le site des Bossats à Ormesson (Seine-et-Marne): un campement solutréen dans le Bassin Parisien

International audienceLe site des Bossats à Ormesson (Seine-et-Marne): un campement solutréen dans le Bassin Parisien

The Site of Les Bossats in Ormesson (Seine-et-Marne, France): A Vast Solutrean Campsite in the Paris Basin

International audienc

Additional file 1: of Rapeseed oil fortified with micronutrients can reduce glucose intolerance during a high fat challenge in rats

Figure S1. Ferric Reducing Antioxidant Power (FRAP) in plasma. Data are mean ± SEM for n = 12 per group (*P < 0.05 vs Chow). Abbreviations: PS palm/sunflower oil group, R rapeseed oil group, RF rapeseed oil fortified with α-tocopherol and Co-Q group, RFC rapeseed oil fortified with α-tocopherol, Co-Q and canolol group. (TIFF 241 kb

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

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