2015
DOI: 10.1016/j.plefa.2015.04.002
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Reduction in the desaturation capacity of the liver in mice subjected to high fat diet: Relation to LCPUFA depletion in liver and extrahepatic tissues

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Cited by 81 publications
(65 citation statements)
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“…Another interesting aspect of EVOO is its high content of 18:1 n-9, which, although it is more stable to lipo-oxidation compared to PUFAs, can be also oxidized in low quantity, which could generate a protective response as an increase in cellular antioxidant defenses (Haeiwa et al, 2014). The decrease in n-3 and n-6 LCPUFA observed in the three tissues studied may be a consequence of the oxidative stress induced by the HFD, which has an impact on the reduction in the activity of desaturase enzymes (Δ-5 and Δ-6 desaturases), as previously shown (Valenzuela et al, 2015). In this way, the antioxidant components of EVOO would protect the effect of a HFD on the activity of desaturase enzymes in the liver, on the tissue levels of n-3 and n-6 LCPUFA, on lipoperoxidation as measured through F2-isoprostanes and TBARS (Table 3), and on the negative correlation of lipoperoxidation parameters and liver levels of FIGURE 2.…”
Section: Discussionsupporting
confidence: 60%
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“…Another interesting aspect of EVOO is its high content of 18:1 n-9, which, although it is more stable to lipo-oxidation compared to PUFAs, can be also oxidized in low quantity, which could generate a protective response as an increase in cellular antioxidant defenses (Haeiwa et al, 2014). The decrease in n-3 and n-6 LCPUFA observed in the three tissues studied may be a consequence of the oxidative stress induced by the HFD, which has an impact on the reduction in the activity of desaturase enzymes (Δ-5 and Δ-6 desaturases), as previously shown (Valenzuela et al, 2015). In this way, the antioxidant components of EVOO would protect the effect of a HFD on the activity of desaturase enzymes in the liver, on the tissue levels of n-3 and n-6 LCPUFA, on lipoperoxidation as measured through F2-isoprostanes and TBARS (Table 3), and on the negative correlation of lipoperoxidation parameters and liver levels of FIGURE 2.…”
Section: Discussionsupporting
confidence: 60%
“…The HFD also produced an increase in reticular stress in mice which can cause alterations in the folding of hepatic proteins (Lu et al, 2015), potentially modifying many enzymatic functions . 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). It has been described that the accumulation of fat in the liver (from over load of saturated fat and refined carbohydrates of nutritional origin) generates a decrease in the activity of the nuclear peroxisome proliferator-activated receptor transcription factor alpha (PPAR-α) as a direct consequence of the reduction in tissue levels of n-3 LCPUFA and, in addition, an increase in the activity of the sterol regulatory element binding protein transcription factor -1 c (SREBP-1 c) (Pawlak et al, 2015), thus promoting a pro-lipogenic state, particularly expressed as greater synthesis of 16:0, as shown in tables 4, 5 and 6, and a reduction in the oxidation of fatty acids as a source of energy (Cheng et al, 2015).…”
Section: Discussionmentioning
confidence: 82%
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