Oleic acid metabolism

Chloroacetamides induce an accumulation of 18 1 in 5. acutus and inhibit 18 1 desaturation in vitro. Furthermore, they dramatically reduce the incorporation of 18 1 into a non-extractable fraction after lipid or fatty acid extraction. This inhibition is specific to 18 1, requires metabolically active cells, and does not occur in a metazachlor tolerant line [6]. Oleic acid metabolism could thus play a central role in the mode of action of chloroacetamides. The NEF is currently under further investigation and its analysis might lead to the primary target of the herbicides. 

Certain long-chain unsaturated fatty acids of metabolic significance in mammals are shown in Figure 23-1. Other C20, C22, and C24 polyenoic fatty acids may be derived from oleic, linoleic, and a-flnolenic acids by chain elongation. Palmitoleic and oleic acids are not essential in the diet because the tissues can introduce a double bond at the position of a saturated fatty acid. 

Under physiologic conditions, the balance of membrane lipid metabolism, particularly that of arachidonoyl and docosahexaenoyl chains, favors a very small and tightly controlled cellular pool of free arachidonic acid (AA, 20 4n-3) and docosahexaenoic acid (DHA, 22 6n-3), but levels increase very rapidly upon cell activation, cerebral ischemia, seizures and other types of brain trauma [1, 2], Other free fatty acids (FFAs) in addition to AA, released during cell activation and the initial stages of focal and global cerebral ischemia, are stearic acid (18 0), palmitic acid (16 0) and oleic acid (18 1). 

This finding has been replicated several times in clinical studies. Let me cite one example. In a careful metabolic study carried out in 1990, Mensink and Katan determined the plasma LDL/HDL ratio when 10% of the energy from oleic acid was replaced in the diet by either the corresponding trans fat or the corresponding saturated fatty acid, stearic acid. The resulting LDL/HDL ratios were 2.02 on the oleic acid diet, 2.34 on the stearic acid diet, and 2.58 on the trans fatty acid diet. This is one more example of the impact of small structural changes in molecules on their biological properties. 

A simple transposition of a C=C bond occurs during metabolism of the common fatty acid oleic acid (see Fig. 17-9), and you will encounter some spectacular examples of double-bond repositioning in the synthesis of cholesterol (see Fig. 21-35). 

Unsaturated fatty acids. Mitochondrial P oxidation of such unsaturated acids as the A9-oleic acid begins with removal of two molecules of acetyl-CoA to form a A5-acyl-CoA. However, further metabolism is slow. Two pathways have been identified (Eq. 17-l).26 29b The first step for both is a normal dehydrogenation to a 2-fraus-5-czs-dienoyl-CoA. In pathway I this intermediate reacts slowly by the normal p oxidation sequence to form a 3-czs-enoyl-CoA intermediate which must then be acted upon by an auxiliary enzyme, a ds-AMra s-A2-enoyl-CoA isomerase (Eq. 17-1, step c), before P oxidation can continue. 

Wang, S. and Koo, S.I. 1993a. Evidence for distinct metabolic utilization of stearic acid in comparison with palmitic and oleic acids in rats. J. Nutr. Biochem. 4, 594—601. 

Three major families of unsaturated fatty acids are seen in warm-blooded animals, that is, the n-9, monounsaturated fatty acids (e.g. oleic acid, OA), and the n-6 and n-3, both polyunsaturated fatty acids (PUFAs). However, only the n-6 and n-3 families, derived from LA and ALA, respectively, are EFA. These must be obtained from the diet since mammals lack the desaturase enzymes necessary for the insertion of a double bond in the n-6 and n-3 positions of the fatty acid carbon chain. Fatty acid nomenclature is as follows The first number denotes the number of carbon atoms in the acyl chain and the second refers to the number of unsaturated (double) bonds. This is followed by a symbol n or co and a number that denotes the number of carbon atoms from the methyl terminal of the molecule to the first double bond. Hence, LA is 18 2(n-6), while the more unsaturated ALA is denoted as 18 3(n-3) (Figure 26.1). These fatty acids must be metabolized to their longer chain derivatives before carrying out many of their activities. 

Physically, the membrane may exist in two states the "solid" gel crystalline and the "liquid" fluid crystalline states. For each type of membrane, there is a specific temperature at which one changes into the other. This is the transition temperature (Tc). The Tc is relatively high for membranes containing saturated fatty acids and low for those with unsaturated fatty acids. Thus, bilayers of phosphatidylcholine with two palmitate residues have a Tc = 41°C but that with two oleic acid residues has a Tc = -20°C. The hybrid has a Tc = -5°C. Sphingomyelin bilayer, on the other hand, may have a Tc of close to body temperature. In the gel crystalline state, the hydrophobic tails of phospholipids are ordered, whereas in the fluid crystalline state they are disordered. At body temperature, all eukaryotic membranes appear to be in the liquid crystalline state, and this is caused, in part, by the presence of unsaturated fatty acids and in part by cholesterol. The latter maintains the fatty acid side chains in the disordered state, even below the normal Tc. There is thus no evidence that membranes regulate cellular metabolic activity by changing their physical status from the gel to the fluid state,... 

Enjalbert, F., Nicot, M.-C., Bayourthe, C., Moncoulon, R. 1998. Duodenal infusions of palmitic, stearic or oleic acids differently affect mammary gland metabolism of fatty acids in lactating dairy cows. J. Nutr. 128, 1525-1532. 

Palmitic acid may be converted to stearic acid (C1K 0) by elongation of the carbon chain. Desaturation of stearic acid produces oleic acid (C18 1 A9). Linoleic acid (Ci8 2A9,12), however, cannot be synthesized in mammalian tissues. Therefore, it is an essential fatty acid for animals and must be obtained from the diet it has two important metabolic roles. One is to maintain the fluid state of membrane lipids, lipoproteins, and storage lipids. The other role is as a precursor of arachidonic acid, which has a specialized role in the formation of prostaglandins (Sec. 13.9). 

Based on the postulated common metabolic pathway involved in DOD and TOD formation by PR3, it was assumed that palmitoleic acid containing a singular C9 cis double bond (a common structural property shared by oleic and ricinoleic acids), could be utilized by PR3 to produce hydroxy fatty acid. Bae et al. (2007) reported that palmitoleic acid could be utilized as a substrate for the production of hydroxy fatty acid by PR3. Structural analysis of the major product produced from palmitoleic acid by PR3 confirmed that strain PR3 could introduce two hydroxyl groups on carbon 7 and 9 with shifted migration of 9-cis double bond into 8-tram configuration, resulting in the formation of 7,10-dihydroxy-8( )-hexadecenoic acid (DHD) (Fig. 31.3).The time course study of DHD production showed that DHD formation was time-dependently increased, and peaked at 72 h after the addition of palmitoleic acid as substrate. However, production yield of DHD (23%) from palmitoleic acid was relatively low when compared to that of DOD (70%) from oleic acid (Hou and Bagby, 1991). 

Laboratory investigations conducted shortly after the spill confirmed earlier studies that showed that N and P were limiting, and that almost all of the alkanes in the Alaskan oil and an appreciable amount of the PAHs had been metabolized in 6 weeks with the addition of inorganic salts or an oleophilic fertilizer containing N and P. Field tests confirmed the abundance of hydrocarbon-degrading bacteria. Specific N and P fertilizers were supplemented to the beaches because they would remain associated with the oil. The oleophilic fertilizer was a liquid containing urea in oleic acid as the N source and tri(aureth-4)-phosphate as the P source. Within 2 weeks, differences in the quantities of oil were visually evident between fertilizer-treated and untreated beaches, and subsequent quantitative measurements revealed that 60-70% of the oil had been degraded within 16 months. 

Dietary LA and ALA are metabohzed by the same set of A and desaturases and elongases to their respective metabolites (see Fig. 2), and, hence, these two fatty acids compete with one another for the same set of enzymes. A and A desaturases prefer i -3 to co-6. Oleic acid (OA, to-9) that is not an EFA also is metabolized by the same A and A desaturases. But in view of the preference of these enzymes to LA and ALA under normal physiologic conditions, the metabolites of co-9... 

The stigma of the emcic acid (C22 ln - 9) in rapeseed oil has lingered despite firm evidence that this fatty acid was more of a threat to rats than to humans. It is sufficient to say that the discovery of chain shortening of emcic acid to oleic acid by peroxisomes was one of the most fundamental breakthroughs in understanding fatty acid metabolism in the last few decades. Once in the oleic acid form, the emcic acid residue is as readily catabolized by mitochondria, as are palmitic and other fatty acids (4). The reduction of emcic acid in rapeseed oil resulted in a marked increase in octadecanoic acids, and their contribution in canola oil is around 95% of all fatty acids present (Table 2). 

Fig. 13.12 Polyunsaturated fatty acids required for eicosanoid synthesis. Oleic acid is the only fatty acid synthesized by mammals de novo. Linoleic (co-3) and a-linolenic acid (9 or greater fatty acids. Ingested o>3 fatty acids are metabolized to other co-3 fatty acids with o>9 double bonds. The same applies to co-6 fatty acids. The major dietary sources of polyunsaturated fatty acids are fish and plants oils...

Oleic acid solubilizes 61 mg of testosterone undecanoate in Restandol 40 mg soft gelatin capsules. Testosterone undecanoate is an ester prodrug of testosterone intended for oral administration in hormone replacement therapy. Free testosterone is inactive following oral administration due to virtually complete hepatic first-pass extraction. However, the undecanoate ester prodrug is transported via the intestinal lymphatic system, thereby circumventing the hepatic portal circulation and the associated presystemic first-pass metabolism. The oral dose of testosterone undecanoate is 40-160 mg equivalents of testosterone (one to four capsules) once daily. Restandol 40 mg soft... 

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