**3. Fatty acid oxidation**

Fatty acids are usually oxidized by most of the cells of tissues in the body, except the RBCs. The cells of the central nervous system also do not use fatty acids for their energy requirements, using instead carbohydrates or ketone bodies. Heart cell fully depends on energy derived from fatty acid oxidation. Fatty acids constitute the principal source of energy for cells between meals, during hypoglycemia, and/or in diabetes. Beta-oxidation of fatty acids takes place in the mitochondria and, to some extent, in the peroxisomes, particularly the very long chain fatty acids [28]. Unlike in the mitochondria, beta-oxidation of fatty acid in the peroxisomes is not coupled to ATP; the high-potential electrons are rather transferred to O2, yielding hydrogen peroxide (H2O2) and generating heat. The enzyme catalase, found exclusively in peroxisomes, converts H2O2 into water and oxygen. H2O2 is also used intracellularly to digest unwanted wastes like proteins and/or to defend against intracellular foreign particles including toxins or microorganisms. All fatty acids are not oxidized at the same rates, which implicates that the purposes of cellular accumulation of fatty acids are not the same for all cells. Some fatty acids might have been exploited for energy purposes, some of them might be exploited for the structural purposes, and some of them (or their derivatives) might help the cell for the signal transductions. For example, 30–40% of all esterified fatty acids in the neural plasma membrane phospholipids consist of DHA [29], while EPA constitutes only a tiny percent of the brain total fatty acid. Among the saturated fatty acids, lauric acid (12:0) is oxidized

**17**

*Fatty Acids: From Membrane Ingredients to Signaling Molecules*

at the fastest rate and is the most efficient energy substrate[30]. Oleic acid (18:1) is also oxidized at a remarkably faster rate, similar to that of lauric acid. Of the ω-6 essential fatty acids studied, linoleic acid (18:2, ω-6) is oxidized at a faster rate, with arachidonic acid (20:4, ω -6) being oxidized at the slowest rate. DHA and EPA possess different oxidizing properties [31, 32]. DHA is a poor substrate for both mitochondrial and peroxisomal beta-oxidation [33], while EPA can be oxidized and to a much greater extent than DHA [33, 34]. The mechanisms of these properties are not fully elucidated, although intensive investigations are continuously going on. Furthermore, ω-3 fatty acids are incorporated into cell membranes in a highly selective manner where they act as structural components influencing fluidity of the membrane [35]. The ω-3 fatty acids also compromise themselves for enzymatic biotransformations into eicosanoids/docosanoids that act as intracellular signaling molecules and, finally, they get involved in the activity of membrane-bound enzymes, ion channels, and receptors [36]. When EPA is administered to rats, both the EPA and DHA accumulate in different organs, including brain [37], indicating EPA is elongated to DHA. DHA administration also leads to an accumulation of EPA both in the plasma and brains, however, only a tiny percent [37]. As DHA seems difficult to metabolize, we thus speculate that DHA is retroconverted to EPA for further metabolism. Therefore, EPA and DHA imply different metabolic properties

Platelets are derived from megakaryocytes and cause aggregation and play important roles in physiological conditions and pathological conditions as well. Fatty acids are enriched in the plasma membranes of platelets and thus may contribute to the physiology and pathology of platelets. Oral administration of ω-3 PUFAs to rats decreases the degree of platelet aggregation both in rats and humans [38, 39]; hence, it is evident that fatty acids may affect the platelet physiology and atherosclerosis. The mechanisms through which PUFA affects the platelet aggregation is unclear; however, it is assumed that ω-3 PUFA deceases the levels of atherogenic ω-6 PUFA particularly platelet membrane-AA, which acts as a proaggregatory fatty acid. Therefore, ω-3 prevents platelet aggregation by inhibiting PLA2 and interrupting the prostaglandin/thromboxane pathways [40, 41]. In addition, ω-3 PUFAs modulate the platelet membrane fluidity [42], specific lipid domains that hold the receptors for a variety of aggregation factors, such as ADP, thrombin,

The effect of fish oil on hypertension came into light when the Norwegian under Nazi invasion had to consume more fish rather than land-based food items during WWII [43]. The Norwegian had low blood pressure, low degree of platelet aggregation, and hypocholesterolemia as well. Afterwards, in studies on the Greenlandic Eskimos, Dyerberg and Bang [44] and Fischer et al. [45] reported that the Eskimos had also a low incidence hypertension and blood cholesterol levels. Then, oil components of marine animals and fish, in particular EPA and DHA, were attributed to lower incidence of cardiovascular risk factors, such as hypertension, hypercholesterolemia, and platelet hyperaggregation. We have previously reported that oral administration of EPA and DHA to rats

fibrin, etc. [37], and doing so, they decrease platelet aggregation.

**4.2 Effects of fatty acids on hypertension**

*DOI: http://dx.doi.org/10.5772/intechopen.80430*

in the cells of the brains.

**4.1 Platelet physiology**

**4. Roles of ω-6 and ω-3 PUFAs in physiology**

*Fatty Acids: From Membrane Ingredients to Signaling Molecules DOI: http://dx.doi.org/10.5772/intechopen.80430*

at the fastest rate and is the most efficient energy substrate[30]. Oleic acid (18:1) is also oxidized at a remarkably faster rate, similar to that of lauric acid. Of the ω-6 essential fatty acids studied, linoleic acid (18:2, ω-6) is oxidized at a faster rate, with arachidonic acid (20:4, ω -6) being oxidized at the slowest rate. DHA and EPA possess different oxidizing properties [31, 32]. DHA is a poor substrate for both mitochondrial and peroxisomal beta-oxidation [33], while EPA can be oxidized and to a much greater extent than DHA [33, 34]. The mechanisms of these properties are not fully elucidated, although intensive investigations are continuously going on. Furthermore, ω-3 fatty acids are incorporated into cell membranes in a highly selective manner where they act as structural components influencing fluidity of the membrane [35]. The ω-3 fatty acids also compromise themselves for enzymatic biotransformations into eicosanoids/docosanoids that act as intracellular signaling molecules and, finally, they get involved in the activity of membrane-bound enzymes, ion channels, and receptors [36]. When EPA is administered to rats, both the EPA and DHA accumulate in different organs, including brain [37], indicating EPA is elongated to DHA. DHA administration also leads to an accumulation of EPA both in the plasma and brains, however, only a tiny percent [37]. As DHA seems difficult to metabolize, we thus speculate that DHA is retroconverted to EPA for further metabolism. Therefore, EPA and DHA imply different metabolic properties in the cells of the brains.
