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Calvo et al. Omega-3 fatty acids in cardiovascular health

These TAG-lowering mechanisms are accompanied factors for CVD has been widely recognized along with
by a secondary decrease of VLDL-C: in vitro studies the role of n-3 PUFAs on its management. However,
[7]
have described PUFA-mediated activation of non- recent findings have shown that maintaining normal
proteosomal degradation of apolipoprotein B (Apo B). blood pressure (BP) levels even in non-hypertensive
This protein, found in the membrane of chylomicrons, individuals significantly lowers the incidence of CVD,
LDL-C and VLDL-C, allows the transport of lipids representing important evidence for the use of n-3
towards peripheral tissues. [80] Activation of this pathway PUFAs as a powerful preventive intervention. [93]
results in the selective degradation of the Apo B which A recent study by Huang et al. [94] on 1,154 Chinese
would have been integrated into naïve VLDL, thus adults found hypertensive subjects to have lower
reducing liver secretion of this lipoprotein. [81,82] plasma PUFA concentrations when compared to
healthy counterparts. This echoes the results of a
Several randomized studies have shown that PUFAs previous study on 447 Eskimo people, where both
also contribute to a slight increase of high density high dietary intake and elevated plasma levels of n-3
lipoprotein (HDL-C), ranging between 2.3-7.9% for PUFAs were associated with lower levels of diastolic
EPA, and 2.9-18.3% for DHA. [83,84] PUFA-mediated blood pressure. [95]
reduction of cholesteryl ester transfer protein (CETP)
activity may be accountable for this effect, as it would PUFAs may regulate BP through various mechanisms,
lead to a decrease in the net flow of cholesterol esters most powerfully through conversion into vasodilator
from HDL-C to LDL-C and VLDL-C. Recent in vitro PG and promotion of renin release from the kidney. [96]
studies also suggest PUFAs to be regulators of CETP Moreover, it has been demonstrated that a diet
and apolipoprotein A1 gene expression. [85,86] rich in n3-PUFAs suppresses the activity of the
angiotensin-converting enzyme, reduces the
On the other hand, the effects that PUFAs exert on formation of angiotensin II, improves the generation
LDL-C are yet to be defined. A study on adult women of eNO (endothelial nitric oxide) and suppresses the
by Ooi et al. [87] where the effects of diets with high expression of TGF-β. [97] Recently, in murine models
and low fish intake (1.23 g/day and 0.27 g/day of with angiotensin II-dependent HTN, the combination of
EPA and DHA, respectively) were assessed showed a soluble epoxide hydrolase inhibitor along with a diet
a non-significant decrease in serum LDL-C levels for rich in n3-PUFAs was tested, showing higher levels of
both diets. However, significantly lower Apo-B100 EPA and DHA epoxides and a reduction of inflammatory
concentration, greater LDL-C Apo-B100 production markers in the kidney (PGs and MCP-1), contributing
rate and higher conversion percentage of TAG-rich to a decrease in systolic BP and inflammation. [98]
lipoproteins (TRL) into LDL-C were reported in high fish
intake diets. Other studies have reported that EPA and Various cytochrome P450 (CYP) isoforms have also
DHA supplement intake considerably increases LDL-C been identified in the physiological production of
levels when compared to placebo and EPA-exclusive active metabolites of AA, EPA and DHA as alternative
intake. [88] However, recent evidence suggest that EPA substrates. [99] In this context, Agbor et al. [100]
as opposed to DHA has more prominent effects on demonstrated the contribution of isoform CYP1A1
LDL in patients with hyper-TG due to its antioxidant tothe metabolism of n3-PUFAs, and the activation
properties in various Apo B-containing proteins, [89] of endothelial nitric oxide synthase and consequent
improving secondarily endothelial function and increase innitric oxide (NO) bioavailability associated
inflammatory profile. [90] Studies in animals suggest that with a diet rich in n3-PUFAs [Figure 5].
very high intake of PUFAs of marine origin increases
the union of the TRL to the endothelial LPL, prolonging Furthermore, a study by Hoshi et al. [101] exposed the
the interaction period and thus resulting in a boost activation of large conductance Ca -activated K
+
2+
of LDL-C formation. Furthermore, very high intake of channels by DHA, through a fast and reversible stimulus
n-3 PUFAs has been found to boost the production of independent of Ca concentration. However, the exact
2+
smaller TRL with less amount of Apo-E, which show a bonding site remains to be identified. The activation of
tendency to convert into LDL-C; [91] as well as increase these channels in smooth muscle cells allows passive
the expression of hepatic LDL-C receptors, amplifying K efflux, which translates into the hyperpolarization of
+
its catabolism. [92] Indeed, the effects of PUFAs on the cell membrane and thus its hypotensive effect. [102]
LDL-C levels appear to significantly vary across
specific PUFA types and quantity. [88,89] On the other hand, modifications in fatty acid
composition in the lipid matrix of the cell membrane
Hypertension play an important role in the pathogenesis of
The role of HTN as one of the main independent risk hypertension. [103] A decrease of PUFAs in the cell
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