Key Findings
Evidence is emerging that C18 n-3 LCPUFA, stearidonic acid SDA —an intermediate metabolite between ALA and EPA is efficiently converted to EPA in the body. In this study, on the basis of the possibility of converting ALA and SDA to EPA and DHA, it is hypothesized that plants rich in ALA and SDA can counteract the undesirable health effects of a hypercaloric diet based on milk fat (typical Western diet). It was shown that (EPA and DHA)-rich FO and (SDA+ALA)-rich BUG diets have a hypocholesterolemic effect. Regarding VLDL-cholesterol, FO and LIN produced the largest effect (a reduction of over 30%). The n-3 VLCPUFA contents, particularly DHA did not benefit from ALA- or (SDA+ALA)-rich diets. Whereas the liver tissue displayed the highest number of significant differences, the brain tissue remained quite impervious to the diet changes. A TNF-α reduction indicates an anti-inflammatory effect, which has been related to dietary intake of n-3 PUFA and gene expression of TNF-α was also reduced in LIN and BUG fed rats. Ths study, that assessed the potential of ALA- and (SDA+ALA)-rich lipid sources as counteracting factors in an unhealthy diet based on milk fat and compared them with FO, showed that ALA and SDA have an important impact on rats’ lipid metabolism and health condition. The unbalance in the plasma biochemical profile, resulting from the hypercaloric diet, was mitigated. The most positive impact of ALA and SDA substitution was the reduction of total lipids (from 395 ± 3 to 352–361 mg/dL), VLDL-cholesterol (from 21.8 ± 0.2 to 14.1–17.8 mg/dL), and triacylglycerols (from 109 ± 1 to 71–89 mg/dL) in both ALA- and (SDA+ALA)-rich diets. In the case of SDA combined with ALA (BUG diet), the impact was almost as positive as with FO.
ABSTRACT
In this study, we hypothesized that terrestrial plant oils, rich in alpha linolenic acid (ALA) and stearidonic acid (SDA) relative to fish oil, rich in eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), prevent negative effects on cardiovascular and neurological function using a rat model fed a hypercaloric diet. Results showed effects on the FA profile, namely, eicosapentaenoic, EPA, and docosahexaenoic, DHA, levels. There were also effects on neural aspects (cAMP response element-binding protein, CREB, gene expression, at least, doubled) and the pro-inflammatory/anti-inflammatory balance (TNF-α, tumor necrosis factor alpha reduced by 30-50%). The most positive impact of ALA and SDA was the beneficial reduction of total lipids (from 395 ± 3 to 352-361 mg/dL), VLDL-cholesterol (from 21.8 ± 0.2 to 14.1-17.8 mg/dL), and triacylglycerols (from 109 ± 1 to 71-89 mg/dL) in both LIN (diet enriched in linseed oil) and BUG (diet enriched in Buglossoides oil) groups. Overall, data indicate that ALA- and SDA-rich lipid sources may counteract the undesirable cardiovascular effects of a hypercaloric diet based on milk fat.
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