ABSTRACT
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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Key Findings
The aim of this study was to compare the effects of a high-fat (HF) diet supplemented with native or defatted flaxseeds on gastrointestinal tract, liver and kidney functions as well as lipid metabolism in rats. A HF diet rich in saturated fatty acids and supplemented with cholic acid, as a stimulator of lipid absorption, was used to induce metabolic disorders in rats. After 8 weeks of experimental feeding, a significantly higher body weight was observed in the HF group compared to the C group. The HF diet also increased hepatic cholesterol and triglyceride levels by approximately four and two times, respectively (compared with the C group). Both flaxseed forms affected the intestinal functions of rats but in a slightly different manner. Specifically, the addition of defatted flaxseeds, but not native seeds, to the HF diet had stimulatory effects on disaccharidase activity in the small intestinal mucosa (sucrose, maltase and lactase). A soluble fibre fraction of flaxseeds, mainly mucilage, may have been responsible for these changes. The HF diet increased colonic β-glucuronidase activity, whereas the native flaxseed supplementation prevented that increase. Generally, the suppression of bacterial β-glucuronidase activity is considered beneficial for the body because this enzyme releases some toxic or even carcinogenic substances that are excreted together with bile to the intestinal tract. Dietary flaxseeds, especially defatted flaxseeds, elevated the serum HDL cholesterol concentration, which was significantly decreased by the HF diet. In conclusion, an HF diet containing cholic acid leads to a number of unfavourable changes in the gastrointestinal tract and lipid metabolism of rats, such as colonic disruption of bacterial enzyme activities or increase in the accumulation of lipids in the liver, especially cholesterol and also triglycerides, together with the increase in the PPARα expression. Dietary supplementation with a relatively small amount of flaxseeds can exert beneficial effects on intestinal tract functions and lipid metabolism in rats, which are, to some extent, affected by defatting. Dietary supplementation with native flaxseeds prevented the increase of colonic β-glucuronidase activity, whereas dietary defatted flaxseeds increased mucosal disaccharidase activities in the small intestine. Regardless of the form of supplementation, dietary flaxseeds increased bacterial glycolytic activity in the distal intestine and decreased hepatic fat accumulation, especially triglyceride accumulation. Both flaxseed forms decreased lipid peroxidation in the kidneys and increased the blood HDL cholesterol concentration. However, the native flaxseed form was more efficient in the former, whereas the defatted flaxseed form was more efficient in the latter. The lipid-modulating effects of defatted flaxseeds, but not of native flaxseeds, was associated with a reduced hepatic expression of PPARα. Overall, these findings indicated that both native and defatted flaxseeds are a valuable dietary factor for the prevention and treatment of diet-related metabolic disorders.