Abstract
Long-chain polyunsaturated fatty acids (LCPUFA) which are synthesized mainly in the liver have relevant functions in the organism. A diet high in fat (HFD) generates an increase in the levels of fat and induces oxidative stress (lipo-peroxidation) in the liver, along with a reduction in tissue n-3 and n-6 LCPUFA. Extra virgin olive oil (EVOO) is rich in anti-oxidants (polyphenols and tocopherols) which help to prevent the development of oxidative stress. This study evaluated the role of EVOO in preventing the induction of fat deposition and oxidative stress in the liver and in the depletion of LCPUFA in the liver, erythrocytes and brain generated by a HFD in C57BL/6J mice. Four experimental groups (n = 10/group) were fed a control diet (CD) or a HFD for 12 weeks and were respectively supplemented with EVOO (100 mg/day). The group fed HFD showed a significant increase (p < 0.05) in fat accumulation and oxidative stress in the liver, accompanied by a reduction in the levels of n-3 and n-6 LCPUFA in the liver, erythrocytes and brain. Supplementation with EVOO mitigated the increase in fat and oxidative stress produced by HFD in the liver, along with a normalization of LCPUFA levels in the liver, erythrocytes and brain. It is proposed that EVOO supplementation protects against fat accumulation, and oxidative stress and normalizes n-3 and n-6 LCPUFA depletion induced in mice fed a HFD.
Highlights
The physiological and biochemical functions of n-3 and n-6 long-chain polyunsaturated fatty acids (LCPUFA) such as n-3 eicosapentaenoic acid (C20:5 n-3, EPA) and docosahexaenoic acid (C22:6 n-3, DHA) and n-6 arachidonic acid (C20:4 n-6, AA) are solidly documented (Valenzuela, 2009; De Caterina, 2011; Bazinet and Layé, 2014)
Values for the High Fat Diet (HFD)+Extra virgin olive oil (EVOO) were far from those obtained for the control diet (CD)+EVOO supplementation, showing that EVOO improved the modification of liver parameters induced by the HFD, but did not restore these parameters to the levels observed for the CD groups (Table 2-B)
Liver fat accumulation and oxidative stress would be linked to the reduction of the n-3 and n-6 LCPUFA observed in the liver, erythrocytes and the brain (Tables 4 to 6), effects that may be directly linked to the increase in systemic and hepatic oxidative stress parameters previously observed in the mice fed the HFD (Valenzuela et al, 2015)
Summary
The physiological and biochemical functions of n-3 and n-6 long-chain polyunsaturated fatty acids (LCPUFA) such as n-3 eicosapentaenoic acid (C20:5 n-3, EPA) and docosahexaenoic acid (C22:6 n-3, DHA) and n-6 arachidonic acid (C20:4 n-6, AA) are solidly documented (Valenzuela, 2009; De Caterina, 2011; Bazinet and Layé, 2014). EPA, DHA and AA are formed through elongation and de-saturation of the respective precursor carried out by elongase and desaturase enzymes (Valenzuela et al, 2012; Valenzuela et al, 2014). The conversion of ALA to EPA and DHA is very low in mammals (rodents and humans) (Valenzuela et al, 2014; Gibson et al, 2011) it is estimated to be sufficient to obtain the physiological levels of EPA required in erythrocytes and the liver and of DHA in the brain and visual tissues (Gerster, 1998; Brenna et al, 2009). A diet high in saturated fat, containing palmitic acid (C16:0), increases liver oxidative stress reducing n-3 and n-6 LCPUFA (EPA, DHA and AA) in different tissues, such as erythrocytes, brain, heart, liver and adipose tissue (Valenzuela et al, 2015)
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