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8 Dietary Fats: Total Fat and Fatty Acids SUMMARY Fat is a major source of fuel energy for the body and aids in the absorption of fat-soluble vitamins and carotenoids. Neither an Adequate Intake (AI) nor Recommended Dietary Allowance (RDA) is set for total fat because there are insufficient data to determine a defined level of fat intake at which risk of inadequacy or prevention of chronic disease occurs. An Acceptable Macronutrient Distribu- tion Range (AMDR), however, has been estimated for total fat—it is 20 to 35 percent of energy (see Chapter 11). A Tolerable Upper Intake Level (UL) is not set for total fat because there is no defined intake level of fat at which an adverse effect occurs. Saturated fatty acids are synthesized by the body to provide an adequate level needed for their physiological and structural func- tions; they have no known role in preventing chronic diseases. Therefore, neither an AI nor RDA is set for saturated fatty acids. There is a positive linear trend between total saturated fatty acid intake and total and low density lipoprotein (LDL) cholesterol concentration and increased risk of coronary heart disease (CHD). A UL is not set for saturated fatty acids because any incremental increase in saturated fatty acid intake increases CHD risk. It is neither possible nor advisable to achieve 0 percent of energy from saturated fatty acids in typical whole-food diets. This is because all fat and oil sources are mixtures of fatty acids, and consuming 0 percent of energy would require extraordinary changes in pat- terns of dietary intake. Such extraordinary adjustments may intro- duce undesirable effects (e.g., inadequate intakes of protein and 422
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423 D IETARY FATS: TOTAL FAT AND FATTY ACIDS certain micronutrients) and unknown and unquantifiable health risks. The AMDR for total fat is set at 20 to 35 percent of energy. It is possible to have a diet low in saturated fatty acids by following the dietary guidance provided in Chapter 11. n-9 cis Monounsaturated fatty acids are synthesized by the body and have no known independent beneficial role in human health and are not required in the diet. Therefore, neither an AI nor an RDA is set. There is insufficient evidence to set a UL for n-9 cis monounsaturated fatty acids. Linoleic acid is the only n-6 polyunsaturated fatty acid that is an essential fatty acid; it serves as a precursor to eicosanoids. A lack of dietary n-6 polyunsaturated fatty acids is characterized by rough and scaly skin, dermatitis, and an elevated eicosatrienoic acid:arachidonic acid (triene:tetraene) ratio. The AI for linoleic acid is based on the median intake in the United States where an n-6 fatty acid deficiency is nonexistent in healthy individuals. The AI is 17 g/d for young men and 12 g/d for young women. While intake levels much lower than the AI occur in the United States without the presence of a deficiency, the AI can provide the ben- eficial health effects associated with the consumption of linoleic acid (see Chapter 11). There is insufficient evidence to set a UL for n-6 polyunsaturated fatty acids. n-3 Polyunsaturated fatty acids play an important role as structural membrane lipids, particularly in nerve tissue and the retina, and are precursors to eicosanoids. A lack of α-linolenic acid in the diet can result in clinical symptoms of a deficiency (e.g., scaly dermatitis). An AI is set for α-linolenic acid based on median intakes in the United States where an n-3 fatty acid deficiency is nonexistent in healthy individuals. The AI is 1.6 and 1.1 g/d for men and women, respectively. While intake levels much lower than the AI occur in the United States without the presence of a deficiency, the AI can provide the beneficial health effects associated with the consumption of n-3 fatty acids (see Chapter 11). There is insufficient evidence to set a UL for n-3 fatty acids. Trans fatty acids are not essential and provide no known benefit to human health. Therefore, no AI or RDA is set. As with saturated fatty acids, there is a positive linear trend between trans fatty acid intake and LDL cholesterol concentration, and therefore increased risk of CHD. A UL is not set for trans fatty acids because any incre- mental increase in trans fatty acid intake increases CHD risk. Because trans fatty acids are unavoidable in ordinary, nonvegan diets, consuming 0 percent of energy would require significant changes in patterns of dietary intake. As with saturated fatty acids, such adjustments may introduce undesirable effects (e.g., elimina-
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424 DIETARY REFERENCE INTAKES tion of commercially prepared foods, dairy products, and meats that contain trans fatty acids may result in inadequate intakes of protein and certain micronutrients) and unknown and unquanti- fiable health risks. Nevertheless, it is recommended that trans fatty acid consumption be as low as possible while consuming a nutri- tionally adequate diet. Dietary guidance in minimizing trans fatty acid intake is provided in Chapter 11. BACKGROUND INFORMATION Total Fat Fat is a major source of fuel energy for the body. It also aids in the absorption of the fat-soluble vitamins A, D, E, and K and carotenoids. Dietary fat consists primarily (98 percent) of triacylglycerol, which is com- posed of one glycerol molecule esterified with three fatty acid molecules, and smaller amounts of phospholipids and sterols. Fatty acids are hydro- carbon chains that contain a methyl (CH3-) and a carboxyl (-COOH) end. The fatty acids vary in carbon chain length and degree of unsaturation (number of double bonds in the carbon chain). The fatty acids can be classified into the following categories: • Saturated fatty acids • Cis monounsaturated fatty acids • Cis polyunsaturated fatty acids — n-6 fatty acids — n-3 fatty acids • Trans fatty acids Dietary fat derives from both animal and plant products. In general, animal fats have higher melting points and are solid at room temperature, which is a reflection of their high content of saturated fatty acids. Plant fats (oils) tend to have lower melting points and are liquid at room tem- perature (oils); this is explained by their high content of unsaturated fatty acids. Exceptions to this rule are the seed oils (e.g., coconut oil and palm kernel oil), which are high in saturated fat and solid at room temperature. Trans fatty acids have physical properties generally resembling saturated fatty acids and their presence tends to harden fats. In the discussion below, total fat intake refers to the intake of all forms of triacylglycerol, regardless of fatty acid composition, in terms of percentage of total energy intake. In addition to the functions of fat and fatty acids described above, fatty acids also function in cell signaling and alter expression of specific genes
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425 D IETARY FATS: TOTAL FAT AND FATTY ACIDS involved in lipid and carbohydrate metabolism (Jump and Clarke, 1999; Sessler and Ntambi, 1998). Fatty acids may themselves be ligands for, or serve as precursors for, the synthesis of unknown endogenous ligands for nuclear peroxisome proliferator activating receptors (Kliewer et al., 1997; Latruffe and Vamecq, 1997). These receptors are important regulators of adipogenesis, inflammation, insulin action, and neurological function. Phospholipids Phospholipids are a form of fat that contains one glycerol molecule that is esterified with two fatty acids and either inositol, choline, serine, or ethanolamine. Phospholipids are primarily located in the membranes of cells in the body and the globule membranes in milk. A very small amount of dietary fat occurs as phospholipid. The metabolism of phospholipids is described below for total fat. The various fatty acids that are contained in phospholipids are the same as those present in triglycerides. Saturated Fatty Acids The majority of dietary saturated fatty acids come from animal products such as meat and dairy products (USDA, 1996). The remaining comes from plant sources. These sources provide a series of saturated fatty acids for which the major dietary fatty acids range in chain length from 8 to 18 carbon atoms. These are: • 8:0 Caprylic acid • 10:0 Caproic acid • 12:0 Lauric acid • 14:0 Myristic acid • 16:0 Palmitic acid • 18:0 Stearic acid The saturated fatty acids are not only a source of body fuel, but are also structural components of cell membranes. Various saturated fatty acids are also associated with proteins and are necessary for their normal function. Saturated fatty acids can be synthesized by the body. Fats in general, including saturated fatty acids, play a role in providing desirable texture and palatability to foods used in the diet. Palmitic acid is particularly useful for enhancing the organoleptic properties of fats used in commercial products. Stearic acid, in contrast, has physical properties that limit the amount that can be incorporated into dietary fat.
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426 DIETARY REFERENCE INTAKES Cis Monounsaturated Fatty Acids Cis monounsaturated fatty acids are characterized by having one double bond with the hydrogen atoms present on the same side of the double bond. Typically, plant sources rich in cis monounsaturated fatty acids (e.g., canola oil, olive oil, and the high oleic safflower and sunflower oils) are liquid at room temperature. Monounsaturated fatty acids are present in foods with a double bond located at 7 (n-7) or 9 (n-9) carbon atoms from the methyl end. Monounsaturated fatty acids that are present in the diet include: • 18:1n-9 Oleic acid • 14:1n-7 Myristoleic acid • 16:1n-7 Palmitoleic acid • 18:1n-7 Vaccenic acid • 20:1n-9 Eicosenoic acid • 22:1n-9 Erucic acid Oleic acid accounts for about 92 percent of dietary monounsaturated fatty acids. Monounsaturated fatty acids, including oleic acid and nervonic acid (24:1n-9), are important in membrane structural lipids, particularly nervous tissue myelin. Other monounsaturated fatty acids, such as palmitoleic acid, are present in minor amounts in the diet. n-6 Polyunsaturated Fatty Acids The primary n-6 polyunsaturated fatty acids are: • 18:2 Linoleic acid γ-Linolenic acid • 18:3 Dihomo-γ-linolenic acid • 20:3 • 20:4 Arachidonic acid • 22:4 Adrenic acid • 22:5 Docosapentaenoic acid Linoleic acid cannot be synthesized by humans and a lack of it results in adverse clinical symptoms, including a scaly rash and reduced growth. Therefore, linoleic acid is essential in the diet. Linoleic acid is the precursor to arachidonic acid, which is the substrate for eicosanoid production in tissues, is a component of membrane structural lipids, and is also impor- tant in cell signaling pathways. Dihomo-γ-linolenic acid, also formed from linoleic acid, is also an eicosanoid precursor. n-6 Polyunsaturated fatty acids also play critical roles in normal epithelial cell function (Jones and
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427 D IETARY FATS: TOTAL FAT AND FATTY ACIDS Kubow, 1999). Arachidonic acid and other unsaturated fatty acids are involved with regulation of gene expression resulting in decreased expres- sion of proteins that regulate the enzymes involved with fatty acid synthesis (Ou et al., 2001). This may partly explain the ability of unsaturated fatty acids to influence the hepatic synthesis of fatty acids. n-3 Polyunsaturated Fatty Acids n-3 Polyunsaturated fatty acids tend to be highly unsaturated with one of the double bonds located at 3 carbon atoms from the methyl end. This group includes: α-Linolenic acid • 18:3 • 20:5 Eicosapentaenoic acid • 22:5 Docosapentaenoic acid • 22:6 Docosahexaenoic acid α-Linolenic acid is not synthesized by humans and a lack of it results in adverse clinical symptoms, including neurological abnormalities and poor growth. Therefore, α-linolenic acid is essential in the diet. It is the precursor for synthesis of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), which are formed in varying amounts in animal tissues, espe- cially fatty fish, but not in plant cells. EPA is the precursor of n-3 eicosanoids, which have been shown to have beneficial effects in preventing coronary heart disease, arrhythmias, and thrombosis (Kinsella et al., 1990). Trans Fatty Acids Trans fatty acids are unsaturated fatty acids that contain at least one double bond in the trans configuration. The trans double-bond configura- tion results in a larger bond angle than the cis configuration, which in turn results in a more extended fatty acid carbon chain more similar to that of saturated fatty acids rather than that of cis unsaturated, double-bond– containing fatty acids. The conformation of the double bond impacts on the physical properties of the fatty acid. Those fatty acids containing a trans double bond have the potential for closer packing or aligning of acyl chains, resulting in decreased mobility; hence fluidity is reduced when compared to fatty acids containing a cis double bond. Partial hydrogena- tion of polyunsaturated oils causes isomerization of some of the remaining double bonds and migration of others, resulting in an increase in the trans fatty acid content and the hardening of fat. Hydrogenation of oils, such as corn oil, can result in both cis and trans double bonds anywhere between carbon 4 and carbon 16. A major trans fatty acid is elaidic acid (9-trans 18:1).
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428 DIETARY REFERENCE INTAKES During hydrogenation of polyunsaturated fatty acids, small amounts of several other trans fatty acids (9-trans,12-cis 18:2; 9-cis,12-trans 18:2) are produced. In addition to these isomers, dairy fat and meats contain 9-trans 16:1 and conjugated dienes (9-cis,11-trans 18:2). The trans fatty acid content in foods tends to be higher in foods containing hydrogenated oils (Emken, 1995). Conjugated Linoleic Acid Conjugated linoleic acid (CLA) is a collective term for a group of geometric and positional isomers of linoleic acid in which the trans/cis double bonds are conjugated; that is, the double bonds occur without an intervening carbon atom not part of a double bond. At least nine different isomers of CLA have been reported as minor constituents of food (Ha et al., 1989), but only two of the isomers, cis-9,trans-11 and trans-10,cis-12, possess biological activity (Pariza et al., 2001). There is limited evidence to suggest that the trans-10,cis-12 isomer reduces the uptake of lipids by the adipocyte, and that the cis-9,trans-11 isomer is active in inhibiting carcino- genesis. Similarly, there are limited data to show that cis-9,trans-11 and trans-10,cis-12 isomers inhibit atherogenesis (Kritchevsky et al., 2000). CLA is naturally present in dairy products and ruminant meats as a consequence of biohydrogenation in the rumen. Butyrivibrio fibrisolvens, a ruminant microorganism, is responsible for the production of the cis-9, trans -11 CLA isomer that is synthesized as a result of the bio- hydrogenation of linoleic acid (Noble et al., 1974). The cis-9,trans-11 CLA isomer may be directly absorbed or further metabolized to trans-11 octadecenoic acid (vaccenic acid) (Pariza et al., 2001). After absorption, vaccenic acid can then be converted back to cis-9,trans-11 CLA within mammalian cells by ∆9 desaturase (Adlof et al., 2000; Chin et al., 1994; Griinari et al., 2000; Santora et al., 2000). Additionally, the biohydrogenation of several other polyunsaturated fatty acids has been shown to produce vaccenic acid as an intermediate (Griinari and Bauman, 1999), thus pro- viding additional substrate for the endogenous production of cis-9,trans-11 CLA. Griinari and coworkers (2000) estimate that approximately 64 per- cent of the CLA in cow’s milk is of endogenous origin. Verhulst and coworkers (1987) isolated a microorganism, Propioni- bacterium acnes, that appears to have the ability to convert linoleic acid to trans-10,cis-12 CLA, an isomer of CLA that is found in rumen digesta (Fellner et al., 1999). Trans-10 octadecenoic acid is formed in the rumen via biohydrogenation of trans-10,cis-12 CLA, and both have been reported to be found in cow’s milk (Griinari and Bauman, 1999). However, endogenous production of trans-10,cis-12 CLA from trans-10 octadecenoic acid does not occur because mammalian cells do not possess the ∆12 desaturase enzyme (Adlof et al., 2000; Pariza et al., 2001). Therefore, any trans-10,cis-12 CLA
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429 D IETARY FATS: TOTAL FAT AND FATTY ACIDS isomer that is reported in mammalian tissue or sera would likely originate from gastrointestinal absorption. Physiology of Absorption, Metabolism, and Excretion Total Fat Absorption. Dietary fat undergoes lipolysis by lipases in the gastro- intestinal tract prior to absorption. Although there are lipases in the saliva and gastric secretion, most lipolysis occurs in the small intestine. The hydrolysis of triacylglycerol is achieved through the action of pancreatic lipase, which requires colipase, also secreted by the pancreas, for activity. In the intestine, fat is emulsified with bile salts and phospholipids secreted into the intestine in bile, hydrolyzed by pancreatic enzymes, and almost completely absorbed. Pancreatic lipase has high specificity for the sn-1 and sn-3 positions of dietary triacylglycerols, resulting in the release of free fatty acids from the sn-1 and sn-3 positions and 2-monoacylglycerol. These products of digestion are absorbed into the enterocyte, and the triacyl- glycerols are reassembled, largely via the 2-monoacylglycerol pathway. This pathway conserves the fatty acid at the sn-2 position. The triacylglycerols are then assembled together with cholesterol, phospholipid, and apoproteins into chylomicrons. Following absorption, fatty acids of carbon chain length 12 or less may be transported as unesterified fatty acids bound to albumin directly to the liver via the portal vein, rather than acylated into triacylglycerols. Dietary phospholipids are hydrolyzed by pancreatic phospholipase A2 and cholesterol esters by pancreatic cholesterol ester hydrolase. The lyso- phospholipids are re-esterified and packaged together with cholesterol and triacylglycerols in intestinal lipoproteins or transported as lysophospholipid via the portal system to the liver. Chylomicrons enter the circulation through the thoracic duct. These particles enter the circulation and within the capillaries of muscle and adipose tissue. Chylomicrons come into contact with the enzyme lipo- protein lipase, which is located on the surface of capillaries. Activation of lipoprotein lipase apolipoprotein CII, an apoprotein present on chylo- microns, results in the hydrolysis of the chylomicron triacylglycerol fatty acids. Most of the fatty acids released in this process are taken up by adipose tissue and re-esterified into triacylglycerol for storage. Triacylglycerol fatty acids also are taken up by muscle and oxidized for energy or are released into the systemic circulation and returned to the liver.
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430 DIETARY REFERENCE INTAKES Metabolism. Most newly absorbed fatty acids enter adipose tissue for storage as triacylglycerol. However, in the postabsorptive state or during exercise when fat is needed for fuel, adipose tissue triacylglycerol under- goes lipolysis and free fatty acids are released into the circulation. Hydrolysis occurs via the action of the adipose tissue enzyme hormone-sensitive lipase. The activity of this lipase is suppressed by insulin. When plasma insulin concentrations fall in the postabsorptive state, hormone-sensitive lipase is activated to release more free fatty acids into the circulation. Thus, in the postabsorptive state, free fatty acid concentrations in plasma are high; conversely, in the postprandial state, hormone-sensitive lipase activity is suppressed and free fatty acid concentrations in plasma are low. Free fatty acids circulate in the blood bound to albumin. The major site of fatty acid oxidation is skeletal muscle. When free fatty acid concen- trations are relatively high, muscle uptake of fatty acids is also high. As in liver, fatty acids in the muscle are transported via a carnitine-dependent pathway into mitochondria where they undergo β-oxidation, which involves removal of two carbon fragments. These two carbon units enter the citric acid cycle as acetyl coenzyme A (CoA), through which they are completely oxidized to carbon dioxide with the generation of large quantities of high- energy phosphate bonds, or they condense to form ketone bodies. Muscle can oxidize both fatty acids and glucose for energy. However, the uptake of fatty acids in excess of the needs for oxidation for energy by muscle does result in temporary storage as triacylglycerol (Bessesen et al., 1995). High uptake of fatty acids by skeletal muscle also reduces glucose uptake by muscle and glucose oxidation (Pan et al., 1997; Roden et al., 1996). Fatty acids released from adipose tissue or to a lesser extent during hydrolysis of chylomicron and very low density lipoprotein (VLDL) triacylglycerols are also taken up and oxidized by the liver. Oxidation of fatty acids containing up to 18 carbon atoms occurs mainly in the mito- chondria. Oxidation of excess fatty acids in the liver, which occurs in pro- longed fasting and with high intakes of medium-chain fatty acids, results in formation of large amounts of acetyl CoA that exceed the capacity for entry to the citric acid cycle. These 2-carbon acetyl CoA units condense to form ketone bodies (e.g., acetoacetate and β-hydroxybutyrate) that are released into the circulation. During starvation or prolonged low carbohy- drate intake, ketone bodies can become an important alternate energy substrate to glucose for the brain and muscle. High dietary intakes of medium-chain fatty acids also result in the generation of ketone bodies. This is explained by the carnitine-independent influx of medium-chain fatty acids into the mitochondria, thus by-passing this regulatory step of fatty acid entry into β-oxidation. Fatty acids of greater than 18 carbon atoms require chain shortening in peroxisomes prior to mitochondrial β-oxidation.
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431 D IETARY FATS: TOTAL FAT AND FATTY ACIDS Fatty acids that do not enter into oxidative pathways can be re-esterified into triacylglycerols or other lipids. The major pathway for triacylglycerol synthesis in liver is the 3-glycerophosphate pathway, which shows a high degree of specificity for saturated fatty acids at the sn-1(3) position and for unsaturated fatty acids at the sn-2 position. In the liver, triacylglycerols can either be stored temporarily or incorporated into triacylglycerol-rich VLDL and released into the plasma. The triacylglycerol fatty acids of VLDL have the same fate as chylomicron triacylglycerol fatty acids. When VLDL triacylglycerols undergo lipolysis, the remaining triacylglycerol-depleted particle is called a VLDL remnant. These remnants are either removed directly by the liver or they are further metabolized in the vascular com- partment to form low density lipoproteins (LDL). Excretion. Fatty acids are generally catabolized entirely by oxidative processes from which the only excretion products are carbon dioxide and water. Small amounts of ketone bodies produced by fatty acid oxidation are excreted in urine. Fatty acids are present in the cells of the skin and intestine, thus small quantities are lost when these cells are sloughed. Saturated Fatty Acids Absorption. When saturated fatty acids are ingested along with fats con- taining appreciable amounts of unsaturated fatty acids, they are absorbed almost completely by the small intestine. In general, the longer the chain length of the fatty acid, the lower will be the efficiency of absorption. However, unsaturated fatty acids are well absorbed regardless of chain length. Studies with human infants have shown the absorption to be 75, 62, 92, and 94 percent of palmitic acid, stearic acid, oleic acid, and linoleic acid, respectively, from vegetable oils (Jensen et al., 1986). The absorption of palmitic acid and stearic acid from human milk is higher than from cow milk and vegetable oils (which are commonly used in infant formulas) because of the specific positioning of these long-chain saturated fatty acids at the sn-2 position of milk triacylglycerols (Carnielli et al., 1996a; Jensen, 1999). The intestinal absorption of palmitic acid and stearic acid from vegetable oils was 75 to 78 percent compared with 91 to 97 percent from fats with these fatty acids in the sn-2 position (Carnielli et al., 1996a). Still, absorption of stearic acid was over 90 percent complete in healthy adults when contained in triacylglycerols of mixed fatty acids (Bonanome and Grundy, 1989). Long-chain saturated fatty acids released into the lumen through the action of pancreatic lipase are less readily solubilized into mixed micelles than are unsaturated fatty acids; in the alkaline pH of the intestine they can form insoluble soaps with calcium and other divalent
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432 DIETARY REFERENCE INTAKES cations and can be excreted (Carnielli et al., 1996a; Lucas et al., 1997; Tomarelli et al., 1968). Following absorption, long-chain saturated fatty acids are re-esterified along with other fatty acids into triacylglycerols and released in chylomicrons. Medium-chain saturated fatty acids (C8:0 and C10:0) are absorbed and transported bound to albumin as free fatty acids in the portal circulation and cleared by the liver. About two-thirds of lauric acid (C12:0) is transported with chylomicron triacylglycerols, whereas the remaining one-third enters the portal circulation as free fatty acids. Metabolism. Pathways of oxidation of saturated fatty acids are similar to those for other types of fatty acids (see earlier section, “Total Fat”). Unoxidized stearic acid (9 to 14 percent) is rapidly desaturated and con- verted to the monounsaturated fatty acid, oleic acid (Emken, 1994; Rhee et al., 1997). For this reason, dietary stearic acid has metabolic effects that are closer to those of oleic acid rather than those of other long-chain saturated fatty acids. The saturated fatty acids, in contrast to cis mono- or polyunsaturated fatty acids, have a unique property in that they suppress the expression of LDL receptors (Spady et al., 1993). Through this action, dietary saturated fatty acids raise serum LDL cholesterol concentrations (Mustad et al., 1997). Excretion. Saturated fatty acids, like other fatty acids, are generally com- pletely oxidized to carbon dioxide and water. cis-Monounsaturated Fatty Acids Absorption. The absorption of cis-monounsaturated fatty acids (based on oleic acid data) is in excess of 90 percent in adults and infants (Jensen et al., 1986; Jones et al., 1985). The pathways of cis-monounsaturated fat digestion and absorption are similar to those of other fatty acids (see earlier section, “Total Fat”). Metabolism. Oleic acid, the major monounsaturated fatty acid in the body, is derived mainly from the diet. Small amounts also come from desaturation of stearic acid. Stable isotope tracer methods have shown that approximately 9 to 14 percent of dietary stearic acid is converted to oleic acid in vivo (Emken, 1994; Rhee et al., 1997). Based on the amount of stearic acid in the average diet (approximately 3 percent of energy), desaturation of dietary stearic acid is not a main source of oleic acid in the body. Oleic acid is oxidized, as are all other fatty acids, by β-oxidation. However, there is some evidence that oxidation of chylomicron-derived oleic acid is significantly greater than for palmitic acid (Schmidt et al.,
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