We hypothesize that defatting is an important factor that can determine the beneficial effects of flaxseeds on rats with diet-induced disorders. The experiment lasts 8 weeks and is conducted on Wistar rats allocated to four groups as follows: a control group fed with a standard diet; a high-fat (HF) group fed with a diet containing 21% fat and 0.1% cholic acid as a stimulator of lipid absorption; an HF group fed a diet supplemented with 1% native flaxseeds; and an HF group fed a diet supplemented with 1% defatted flaxseeds. In the HF group, several unfavourable changes in the gut and lipid metabolism are observed. Supplementation of the HF diet with native flaxseeds prevent an increase in colonic β-glucuronidase activity, whereas dietary defatted flaxseeds increase mucosal disaccharidase activities in the small intestine (sucrose, maltase and lactase). Regardless of the form of supplementation, dietary flaxseeds increase bacterial glycolytic activity in the distal intestine and decrease hepatic fat, especially triglyceride, accumulation. Both flaxseed forms decrease lipid peroxidation in the kidneys and increase the blood HDL cholesterol concentration with the native form being more efficient in the former and the defatted form being more efficient in the latter. The lipid-modulating effects of defatted flaxseeds are associated with reduced hepatic expression of peroxisome proliferator-activated receptor α, which is not the case in terms of native flaxseeds. Dietary supplementation with a relatively small amount of flaxseeds can exert beneficial effects on gut functions and lipid metabolism in rats, and these effects are affected by defatting to some extent.
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