Abstract
BackgroundIn an effort to identify new alternatives for long-chain n-3 polyunsaturated fatty acids (LC n-3 PUFA) supplementation, the effect of three sources of omega 3 fatty acids (algae, fish and Echium oils) on lipid profile and inflammation biomarkers was evaluated in LDL receptor knockout mice.MethodsThe animals received a high fat diet and were supplemented by gavage with an emulsion containing water (CON), docosahexaenoic acid (DHA, 42.89%) from algae oil (ALG), eicosapentaenoic acid (EPA, 19.97%) plus DHA (11.51%) from fish oil (FIS), and alpha-linolenic acid (ALA, 26.75%) plus stearidonic acid (SDA, 11.13%) from Echium oil (ECH) for 4 weeks.ResultsAnimals supplemented with Echium oil presented lower cholesterol total and triacylglycerol concentrations than control group (CON) and lower VLDL than all of the other groups, constituting the best lipoprotein profile observed in our study. Moreover, the Echium oil attenuated the hepatic steatosis caused by the high fat diet. However, in contrast to the marine oils, Echium oil did not affect the levels of transcription factors involved in lipid metabolism, such as Peroxisome Proliferator Activated Receptor α (PPAR α) and Liver X Receptor α (LXR α), suggesting that it exerts its beneficial effects by a mechanism other than those observed to EPA and DHA. Echium oil also reduced N-6/N-3 FA ratio in hepatic tissue, which can have been responsible for the attenuation of steatosis hepatic observed in ECH group. None of the supplemented oils reduced the inflammation biomarkers.ConclusionOur results suggest that Echium oil represents an alternative as natural ingredient to be applied in functional foods to reduce cardiovascular disease risk factors.
Highlights
In an effort to identify new alternatives for long-chain n-3 polyunsaturated fatty acids (LC n-3 Long-chain n-3 polyunsaturated fatty acids (PUFA)) supplementation, the effect of three sources of omega 3 fatty acids on lipid profile and inflammation biomarkers was evaluated in Receptor deficient mice (LDL) receptor knockout mice
Echium oil provided the best results in terms of Very low density lipoprotein (VLDL) and total cholesterol reduction and contributed to the attenuation of hepatic steatosis
VLDL levels after Echium oil supplementation without changes in peroxisome proliferator activated receptor α (PPARα) and liver X receptor α (LXRα) expression. These results suggest that Echium oil can exert its beneficial effect on lipid metabolism and hepatic steatosis via mechanisms other than those reported for marine oils
Summary
In an effort to identify new alternatives for long-chain n-3 polyunsaturated fatty acids (LC n-3 PUFA) supplementation, the effect of three sources of omega 3 fatty acids (algae, fish and Echium oils) on lipid profile and inflammation biomarkers was evaluated in LDL receptor knockout mice. The scientific evidence concerning the beneficial effects of the LC N-3 PUFA on lipid profile and inflammation were obtained from several studies using animal and human models These effects and the mechanisms by which they occur are restricted to the action of EPA and DHA [8]. In an effort to identify new alternatives for LC N-3 PUFA supplementation, the objective of this study was to compare the effects of three sources of N-3 FA (algae, fish and Echium oil) on lipid composition and some inflammatory biomarkers using LDL receptor deficient mice (LDLr knockout mice) as model
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
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 callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
