Why are mammals unable to produce Essential Fatty Acids?

Why are mammals unable to produce Essential Fatty Acids?

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Why do we have to get them from our diet, and if they aren't taken in our diet we will face disease? Then why we don't have the enzymes which are require for EFA synthesis?

Well, the essential fatty acids that humans fail to produce are not the same ones that other species fail to produce. For example, while cats produce their own Vitamin C and will therefore never develop scurvy, they can't produce their own taurine and will become sick if they don't consume enough of it.

To answer why a species might lose the ability to produce an essential amino acid, you have to consider what that species is eating most of the time. If its diet is rich in the amino acid anyway, individuals who lose the ability to synthesize it either feel no cost or--possibly more likely--even benefit by not wasting resources synthesizing compounds that may be abundant already in the diet and must be excreted if unused.

Turns out that this loss of ability to synthesize your own fatty acids is a particularly common consequence of evolving parasitic lifestyles, which makes sense: if you're just stealing someone else's acids, why bother to produce your own? Even outside of parasites, there's some interesting discussion on why the nine amino acids essential to all animals might have evolved from a genomics paper here, discussing which amino acids you really do have to make on your own and which you can get away with consuming depending on your species' lifestyle and dietary habits.

Omega-3 fatty acid

Omega−3 fatty acids, also called Omega-3 oils, ω−3 fatty acids or n−3 fatty acids, [1] are polyunsaturated fatty acids (PUFAs) characterized by the presence of a double bond, three atoms away from the terminal methyl group in their chemical structure. [2] They are widely distributed in nature, being important constituents of animal lipid metabolism, and they play an important role in the human diet and in human physiology. [3] [4] The three types of omega−3 fatty acids involved in human physiology are α-linolenic acid (ALA), found in plant oils, and eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), both commonly found in marine oils. [3] Marine algae and phytoplankton are primary sources of omega−3 fatty acids (which also accumulate in fish). Common sources of plant oils containing ALA include walnut, edible seeds, clary sage seed oil, algal oil, flaxseed oil, Sacha Inchi oil, Echium oil, and hemp oil, while sources of animal omega−3 fatty acids EPA and DHA include fish, fish oils, eggs from chickens, squid oils and krill oil.

Mammals are unable to synthesize the essential omega−3 fatty acid ALA and can only obtain it through diet. However, they can use ALA, when available, to form EPA and DHA, by creating additional double bonds along its carbon chain (desaturation) and extending it (elongation). Namely, ALA (18 carbons and 3 double bonds) is used to make EPA (20 carbons and 5 double bonds), which is then used to make DHA (22 carbons and 6 double bonds). [1] [2] The ability to make the longer-chain omega−3 fatty acids from ALA may be impaired in aging. [5] In foods exposed to air, unsaturated fatty acids are vulnerable to oxidation and rancidity. [2] [6]

Dietary supplementation with omega−3 fatty acids does not appear to affect the risk of cancer or heart disease. [7] Furthermore, fish oil supplement studies have failed to support claims of preventing heart attacks or strokes or any vascular disease outcomes. [8] [9]

Food Requirements

What are the fundamental requirements of the animal diet? The animal diet should be well balanced and provide nutrients required for bodily function and the minerals and vitamins required for maintaining structure and regulation necessary for good health and reproductive capability. These requirements for a human are illustrated graphically in Figure

For humans, a balanced diet includes fruits, vegetables, grains, and protein. (credit: USDA)

Brain lipids and ageing

12.6.1 Desaturases and the relationship between omega-3 fatty acids and antioxidants

ALA is desaturated and elongated in the liver. Although ageing is accompanied by a gradual decline in cell function, the liver appears to retain its function relatively well unless it is affected by some disease ( Anantharaju et al., 2002 ). But its activity is far from enough to provide sufficient DHA to other organs, including to the brain. Thus DHA must be supplied by the diet, and the advancing age can lead to changes in fat digestion. It is not clear whether the age-related reduction in apparent fat digestion is a general phenomenon affecting all fats ( Peachey et al., 1999 ), or if it involves particular fatty acids.

The activities of desatorases, particularly delta-6-desaturase (the first enzyme in the synthesis of long-chain, more unsaturated fatty acids (it acts on ALA and LA) are still to be evaluated, but they are very much less active immediately after birth, and essentially zero in the brains of animals. Their activities in the liver are greatly reduced with age ( Hrelia et al., 1989 Bourre and Piciotti, 1992 ). As a result, DHA comes either from the hepatic transformation of dietary ALA, or directly from the diet. But the capacities of astrocytes should not be neglected ( Williard et al., 2001 ). Little DHA is synthesised at the blood-brain barrier, but some may be produced at the choroid plexus as it has a high delta-6-desaturase activity ( Bourre et al., 1997a ).

The rationale for expecting a benefit from dietary ALA is that it is the metabolic precursor of EPA and DHA. However, the extent of its conversion is actually controversial, even among investigators using similar tracer technologies. Emken et al. (1994) reported that as much as 15% of ALA is converted to EPA+DHA, while Pawlosky et al. (2001) found that only 0.2% was converted. The rate of conversion may also vary according sex, age and pathophysiological conditions ( Williams and Burdge, 2006 Goyens et al., 2006 ). The delta-6 desaturase activity is reduced in old rats fed a diet containing ALA, but is not in rats fed an ALA-deficient diet ( Dinh et al., 1993 ). Delta-desaturase activity does not only change with age, it is also influenced by the polyunsaturated fatty acid content of the diet and to the omega-6/omega-3 balance. R rats given an ALA-deficient diet and then refed a normal sufficient diet recovered only partially ( Dinh et al., 1995 ).

Hence, DHA is also considered to be an essential nutrient ( Muskiet et al., 2004 ). This is in agreement with the fact that omega-3 (and omega-6) fatty acids are essential for the brain, as initially shown in studies on foetal brain cells. These cells multiply, and take up and release neurotransmitters only if there is ARA or DHA in the medium, and not if the medium contains only LA or ALA ( Bourre et al., 1983 Tixier-Vidal et al., 1986 ). Vegetarians need much more ALA than the general population because of their restricted dietary intake of DHA. ALA is converted to DHA relatively poorly and there is active competition for the enzyme involved with omega-6 fatty acids ( Davis and Kris-Etherton, 2003 ). Further work is clearly needed to determine how much ALA is converted to EPA and DHA (if any), especially in the brains of elderly humans.

Fatty Acid Degradation by Mitochondria in Neural Cells as Compared with Other Tissues

Apart from certain hypothalamic neurons, fatty acid oxidation predominantly takes place in astrocytes. 21, 22, 23, 39, 40 After cellular uptake, NEFA are enzymatically activated to acyl-CoA derivatives. In the activated form, fatty acids can be either esterified to membrane lipids or degraded by the mitochondrial β-oxidation to provide cellular energy ( Figure1 ). In both homogenates of neural cells and mitochondria obtained from the brain tissue from rodents, a poor oxidative degradation of long-chain fatty acids (C12 to C18) has been detected. In these studies, any restrictions by the BBB are excluded. Rates of the liberation of 14 CO2 from 14 C-labeled fatty acids or the oxygen consumption measured with isolated cells or brain mitochondria reveal poor fatty acid oxidation. 41 For illustration, using palmitoyl-carnitine as a substrate, the oxygen consumption by isolated rat brain mitochondria during ADP phosphorylation was estimated to be 20 nanoatoms of oxygen per min per milligram of protein at 25ଌ, which is eightfold lower than that of heart mitochondria under comparable conditions. 41 In contrast to long-chain fatty acids, the medium-chain octanoic acid is rapidly oxidized in the brain. 15 However, cerebral octanoate oxidation seems to be a special case for two reasons: First, octanoate oxidation mostly takes place in astrocytes, and, in contrast to long-chain fatty acids, its oxidation by mitochondria is not under the control of the acylcarnitine/carnitine antiporter.

A large number of studies have demonstrated that brain mitochondria have high oxygen consumption with pyruvate or glutamate as hydrogen donors, as compared with heart and skeletal muscle mitochondria. Therefore, it was a surprising observation that brain mitochondria do not use long-chain fatty acids as hydrogen source, in contrast to the mitochondria from heart muscle or kidney, two tissues that exhibit high ATP turnover.

Low-level oxidation of long-chain fatty acids by isolated brain mitochondria has been attributed to (i) the low translocation rate of long-chain fatty acid-CoA esters across inner mitochondrial membrane and (ii) the low enzymatic capacity of the β-oxidation pathway. The first suggestion is supported by the discovery that the brain-specific isoenzyme of the carnitine palmitoyltransferase 1 has a low activity. 42 Moreover, the enzymatic capacity of the β-oxidation in brain mitochondria is remarkably lower than in mitochondria from the other high-energy turnover tissues. 41 Particularly, the 3-ketoacyl-coenzyme A thiolase activity, the terminal enzyme of the four steps of the β-oxidation pathway, is very low. The activity of this enzyme in the brain has only 0.7% of that in the rat heart mitochondria. The other enzymes of the β-oxidation pathway, such as the acyl-CoA dehydrogenase or the enoyl-CoA-dehydrogenase have �% and 19% of that of the heart mitochondria. 41

In contrast to the low activity of the mitochondrial 3-ketoacyl-coenzyme A thiolase, neurons have a particularly high activity of the cytoplasmic long-chain acyl-CoA thioesterase 7. 43 Acyl-CoA thioesterase 7 is considered to be a regulatory point in the fatty acid metabolism for keeping the acyl-CoA concentration in neurons low, which is beneficial because of the low lipid-storage capacity and the low β-oxidation of fatty acids. It has been suggested that acyl-CoA thioesterase 7 guarantees fatty acid homeostasis in neurons, particularly in fasting-induced alterations of the fatty acid metabolism in neurons. 43 Finally, acyl-CoA thioesterase has been proposed to exert a protective function against detrimental effects caused by excess of fatty acids.

In summary, the slow rate of β-oxidation of fatty acids seems to be a unique intrinsic feature of the brain tissue, particularly of the mitochondria of neurons. For comparison, in the heart and kidney tissue, 60% to 80% of the energy need is provided by fatty acid oxidation.


Generation of mammary gland-specific fasn KO mice.

Mice with mammary epithelial cell-specific Fasn KO were developed by crossing mice homozygous for the floxed Fasn alleles (5) with transgenic mice bearing a Cre recombinase transgene controlled by the WAP promoter (Jackson Laboratory). Knockout of Fasn in this model occurs only in the mammary epithelial cells, not in mammary adipose tissue, and only upon pregnancy and lactation. To determine whether multiple pregnancies increased the effect of Fasn KO, female mice were subjected to one, two, or three pregnancies. By lactation day L15 of the first pregnancy (L15P1), FASN staining was observed in a large number of epithelial cells during lactation, suggesting incomplete knockout. However, staining was largely absent by L17 of the second pregnancy (L17P2) and decreased further by L16 of the third pregnancy (L16P3). In contrast, very strong FASN staining was observed in WT mice during all three pregnancies. Virgin mice also showed positive FASN staining (Fig. 1A).

Fig. 1.Epithelial cell-specific deletion of the fatty acid synthase gene (Fasn) in the mammary gland. Right inguinal mammary glands were harvested, sectioned, and stained by IHC for FASN. A: FASN knockout (KO) mothers showed only partial deletion of FASN following the first pregnancy, and further deletion in late lactation of the second and third pregnancies. Age-matched virgin glands showed very strong FASN staining in adipocytes and positive staining in the epithelium. Wild-type (WT) mothers showed strongly positive staining during all three pregnancies. B: deletion of FASN was heterogeneous and occurred gradually over the course of lactation. FASN-positive epithelial cells were present on lactation day L2 and L10 of the third pregnancy. By L16, nearly all epithelial cells were negative for FASN, and only adipocytes showed positive staining. All images are shown at ×20 resolution. LXPZ, lactation day X of pregnancy Z. Virgin glands are age-matched.

Despite an obviously gradual deletion of Fasn over the course of multiple pregnancies, time-dependent deletion was also observed over the course of the lactation period. On L2 of pregnancy 3 (L2P3) approximately one-half of the epithelial cells stained strongly positive for FASN. This number decreased to less than 25% by L10P3, and FASN was nearly completely absent in all epithelial cells by L16P3 (Fig. 1B).

Fasn KO in lactating mammary gland decreases pup growth and survival.

Because FASN is responsible for producing short- and medium-chain fatty acids in milk (30) and fatty acids are important nutritional components of milk for the mother's growing pups, we sought to determine how FASN KO affects the growth of pups nursed by KO mothers for each pregnancy. No significant differences in the average litter size or the mother's age at parturition were observed between WT and KO mothers for all three pregnancies (Table 1). In the first pregnancy, all pups showed similar growth rates regardless of the mother's genotype (Fig. 2A). Interestingly, although the growth curves were similar, we observed a significantly greater preweanling death rate for pups from KO mothers than for pups nursed by WT mothers. While 75% of pups from WT mothers survived to weaning age (L25), only 61% of pups from KO mothers survived to weaning age during the first pregnancy (P = 0.01 Fig. 2B). In the second pregnancy, there was a significant decrease in the growth rate of pups from KO mothers compared with pups from WT mothers (Fig. 2C). No pups from KO mothers survived beyond L19, whereas 75% of pups from WT mothers survived to weaning age (P < 0.0001 Fig. 2D). In the third pregnancy, pups from KO mothers displayed a similar trend in the growth of pups compared with the second pregnancy (Fig. 2E). Also, no pups from the third pregnancy of KO mothers survived beyond L9, whereas all pups from WT mothers survived to weaning age (P < 0.0001 Fig. 2F). In all, the growth and survival trends of pups from KO mothers over the course of three pregnancies correlates with the progressive deletion of FASN.

Table 1. Litter statistics for growth and survival curves

Values represent means ± SE. WT, wild type KO, Fasn (fatty acid synthase) knockout.

Fig. 2.Deletion of FASN hinders growth and survival of nursing pups. Average weight of pups and their survival were monitored from L2 through L25 following the first (A), second (B), and third (C) pregnancies. Error bars represent SE. *P < 0.05, **P < 0.01, ***P < 0.001. P values for survival curves are indicated in the panel.

It has been previously reported that both homozygous and heterozygous KO of FASN leads to developmental complications (7). To further demonstrate the specificity of the FASN KO phenotype, pups from the second pregnancy of KO mothers were genotyped to determine whether growth complications might have possibly been due to unexpected expression of the WAP-Cre recombinase and premature KO of FASN. As expected, pups demonstrated 50% Mendelian inheritance of the Cre recombinase transgene (data not shown), providing evidence that the premature death of KO pups was not a result of erroneous expression of WAP-Cre in pups.

Deletion of FASN induces premature involution and cell death.

Litters from KO mothers typically perished all together in a time frame of 2–3 days (Fig. 3), and mammary glands of KO mothers were immediately harvested following the deaths of all their pups. We harvested mammary glands from lactating, age-matched, WT mothers from the same pregnancy and on the same lactation day as KO mothers to analyze any changes that had occurred in KO mammary glands during the lactation period. Although the difference in pregnancy 1 appeared less dramatic, whole mount mammary gland analysis showed a consistent and marked difference in the density of glands in KO mothers compared with WT mothers for all three pregnancies. All age-matched virgin mice showed normal tree-like branching (Fig. 4A). Closer examination with H&E staining further demonstrated a marked difference in the alveolar density between KO and WT mammary glands. Adequate formation of actively secreting alveoli was evident in KO mice on L15P1. However, compared with WT mice, KO mice had fewer alveoli and showed a larger proportion of adipocytes.

Fig. 3.Preweanling death occurs as a whole litter. Survival of pups was monitored for each litter following the second (A) and third (B) pregnancies of KO mothers. Each line represents the survival of pups in a single litter from a KO mother. Typically, litters perished over the course of 2–3 days.

Fig. 4.KO mammary glands are sparse in alveolar structures. A: left inguinal mammary glands were harvested and whole mounted at the indicated lactation day of each pregnancy. B: right inguinal mammary glands were harvested and stained with H&E at the indicated lactation day of each pregnancy. Virgin glands are age-matched.

In contrast to the first pregnancy, mammary glands from KO mice in the second and third pregnancies appeared to be undergoing involution at day L16–17, whereas age-matched, WT mice of the same lactation day and pregnancy displayed large and actively secreting alveoli (Fig. 4B).

To verify that KO glands were experiencing early involution, we compared WT and KO mammary glands at various time points during each lactation period and performed a TUNEL assay to analyze cell death. As expected, glands from both WT and KO mice had experienced involution by L25P1. KO glands, in accordance with having fewer alveoli at L15, also showed fewer epithelial cells at L25 compared with WT mice (Fig. 5A). In the second pregnancy, WT glands had developed mature alveoli and were abundantly secreting at L12 and L17, whereas KO glands showed a decreased number of alveoli at L12 and showed histological signs of involution at L17 (Fig. 5B). In the third pregnancy, we analyzed glands at L2, L10, L16, and L19 to gain a more comprehensive understanding of the histological progression during the lactation phase in KO mice. At L2, both WT and KO mice showed comparable development of actively secreting alveoli. However, by L10, a discrepancy in the number and size of alveoli was apparent, and by L16 and L19, glands were clearly undergoing involution (Fig. 5C), as they appeared very similar to glands of L25P1. TUNEL staining showed no difference in cell death at L15P1 (Fig. 5D), nor L2 and L10 of the third pregnancy (Fig. 5F). However, in accord with their marked histological changes, there was a statistically significant increase in TUNEL-positive cells at L17P2 and L6P3, validating cell death and involution at these time points (Fig. 5, D–G). A positive and negative TUNEL control using DNase I digestion and no rTdT enzyme, respectively, confirmed the results of the TUNEL staining (Fig. 5H).

Fig. 5.FASN deletion induces early involution and cell death. Right inguinal mammary glands were harvested, sectioned, and stained for histology with H&E (A–C) or for cell death via TUNEL assay (D–F). Red arrows point to TUNEL-positive cells. G: TUNEL stains were quantified by counting the number of TUNEL-positive cells per mm 2 of tissue. H: DNase I digestion was used as a positive TUNEL control, and no rTdT enzyme was used for a negative control. Error bars represent SE. ***P < 0.001.

FASN KO hinders mammary gland maturation but not secretory activation during lactation.

As we previously mentioned, the deletion of FASN gradually increased over the course of lactation and multiple pregnancies. Therefore, we questioned whether KO glands were strictly involuting early, as a consequence of increased FASN deletion, or if they also experienced developmental deficits during lactation. Glands experiencing involution, whether WT or KO, had a much smaller lumen size than actively lactating glands. However, analysis of lumen measurements at earlier time points during lactation demonstrated a statistically significant difference (P < 0.001) between WT and KO glands at days L12 and L10, but not at L2 (Fig. 6A). Interestingly, a comparison of FASN-positive vs. FASN-negative lumens showed no difference in lumen size at either L2 or L10 in KO glands with mosaic deletion of FASN (Fig. 6B). Despite the differences observed in lumen size, KO glands still showed adequate formation of lipid droplets on the luminal side of epithelial cells at all stages of lactation (Fig. 6, C–E). This was true even in lumens where FASN had been deleted, as shown by immunofluorescent double staining for adipophilin and FASN on L10P3 (Fig. 6F).

Fig. 6.Deletion of FASN hinders alveola. A: luminal measurements from WT and KO mice were averaged and compared for the respective lactation days of each pregnancy. B: measurements of FASN-positive lumens and FASN-negative lumens in KO mice were averaged and compared for L2P3 and L10P3. C–E: mammary gland sections from the first, second, and third pregnancies were stained for adipophilin as a marker of secretory activation, respectively. F: mammary glands from L10P3 were stained for adipophilin (red), FASN (green), and DAPI (blue). Error bars represent SE. ***P < 0.001.

Fasn KO in the lactating mammary gland alters the lipid profile in milk.

FASN is responsible for the production of short- and medium-chain fatty acids (<16 carbons), as well as a substantial portion of long-chain fatty acids (16–20 carbons), whereas dietary sources are the major supply for very long-chain fatty acids (>20 carbons) (28). Because we identified a deficit in the growth and survival of pups nursed by KO mothers, we hypothesized that FASN KO in the mother's mammary gland was affecting the fatty acid profile of the milk, and thereby, pups were succumbing to premature death, in part, by malnutrition. To test this hypothesis, we performed FAME analysis on milk collected from lactating mothers on days L2, L10, and L18 during each pregnancy and quantified the presence of each fatty acid.

Milk analysis from the first pregnancy showed significant decreases in 14:0 (P < 0.001), 14:1 (P = 0.03), 16:0 (P < 0.01), 18:0 (P < 0.05), 18:2 (P < 0.01), and total fatty acid (P < 0.01) in milk from KO mothers compared with WT (Fig. 7A). Milk analysis from the second pregnancy showed significant decreases in 14:0 (P < 0.001), 14:1 (P < 0.001), 16:0 (P < 0.001), and 22:0 (P = 0.03), and a similarly decreasing trend in the total fatty acid (P = 0.09) (Fig. 7B). Finally, milk analysis from the third pregnancy showed significant decreases in 14:0 (P < 0.001), 16:0 (P < 0.001), 18:0 (P < 0.001), 20:0 (P = 0.02), and total fatty acid (P = 0.03) (Fig. 7C).

Fig. 7.FASN deletion changes the fatty acid profile of mammary gland milk. Milk was collected during the lactation period of each pregnancy. Milk was pooled from all 10 glands. Graphs represent fatty acid methyl ester analysis of the first (A), second (B), and third (C) pregnancies. All fatty acid values were normalized to total protein content. Error bars represent SE. *P < 0.05, **P < 0.01, ***P < 0.001.

Growth and survival deficiencies of pups are rescued by nursing from a WT mother.

To clearly demonstrate that the functional differences in lactation from impaired mammary gland development and the consequential growth and survival trends in pups were in fact due to the Fasn KO in the mammary gland of lactating mothers, we swapped the litters of age-matched KO and WT mothers between day L1 and day L3 and monitored the growth of pups being nursed by the surrogate mother. Again, there were no significant differences in litter size or the age of all mothers at parturition between KO and WT mothers for all three pregnancies (Table 2). Similarly to our previous results (Fig. 2), pups born to a WT mother but nursed by a KO mother showed a significant decrease in growth and survival. When mothers were swapped after their first pregnancy, we observed a significant decrease in the growth and survival (P = 0.0003) of pups born to a WT mother and nursed by a KO mother (Fig. 8A). During the second and third pregnancies, WT pups nursed by a KO mother showed significantly decreased growth and survival (P < 0.0001 Fig. 8, B and C). Importantly, pups born to a KO mother and nursed by a WT mother were phenotypically rescued, showing significantly greater growth and survival (Fig. 8).

Table 2. Litter statistics for cross-fostering growth and survival curves

Values represent means ± SE.

Fig. 8.Phenotypic rescue of offspring by cross-fostering mothers at birth. Litters from KO mothers were swapped with litters from WT mothers between L 1 and L3 for the first (A), second (B), and third (C) pregnancies. Average pup weight and survival were monitored every day beginning on the day after swapping mothers. Error bars represent SE. *P < 0.05, **P < 0.01, ***P < 0.001. P values for survival curves are indicated in the panel.

Global warming may threaten availability of essential brain-building fatty acid

By 2100, 96% of the global population may not have sufficient access to a naturally occurring essential brain-building omega-3 fatty acid, according to a study in the journal Ambio.

Global warming may reduce the availability of Docosahexaenoic acid (DHA), the most abundant fatty acid found in mammalian brains, which has a crucial role in processes such as neuroprotection, cell survival, and inflammation. Despite its requirement for neural development and health, humans are unable to produce enough of their own DHA. They rely on obtaining the nutrient through a diet of fish and seafood, and/or by taking supplements.

Stefanie Colombo at Dalhousie University, Canada Tim Rodgers at University of Toronto and colleagues at Ryerson University and University of Toronto developed a mathematical model to investigate the potential decrease in available DHA with varying global warming scenarios. In the aquatic food chain, DHA is produced primarily by algae and the biochemical reactions involved in the process are sensitive to slight changes in temperature.

The authors found that if global warming continues unabated, declines in DHA production combined with population growth could lead to 96% of the global population not having sufficient access to DHA from domestic fish production. People living in countries with large fish production and relatively low populations, such as Greenland, Norway, Chile, and New Zealand would still be able to consume the recommended dose of 100 mg per day. By contrast, the largest countries in East and South-East Asia (such as China, Japan and Indonesia), along with most of the countries in Africa could shift from producing an excess of DHA to falling below the threshold for the recommended dose by 2100.

Dr. Colombo, Mr. Rodgers and colleagues said: "According to our model, global warming could result in a 10 to 58% loss of globally-available DHA in the next 80 years. A decrease in levels will have the greatest effect on vulnerable populations and periods of human development, such as foetuses and infants, and may also affect predatory mammals, especially those in Polar Regions."

To predict global annual production of DHA in each of the United Nations fishing zones, the authors used data from the Sea Around Us project database, an initiative that provides reconstructed fisheries data to support impact assessments of fishing on marine ecosystems. The authors also used data from the United Nations for global inland fisheries catch and aquaculture production data. Temperature increases were predicted using the global warming scenarios outlined in the Fifth Assessment Report (AR5) of the United Nations Intergovernmental Panel on Climate Change (IPCC).

Dr. Colombo, Mr. Rodgers and colleagues said: "It is also interesting to see that freshwater fishing zones showed greater declines in DHA than marine zones, due to larger projected temperature increases in freshwater than the oceans. Changes in availability of DHA may therefore have a greater impact on populations in certain areas of the world, especially inland Africa."


Figure 7. Waxy coverings on some leaves are made of lipids. (credit: Roger Griffith)

Wax covers the feathers of some aquatic birds and the leaf surfaces of some plants. Because of the hydrophobic nature of waxes, they prevent water from sticking on the surface (Figure 7). Waxes are made up of long fatty acid chains esterified to long-chain alcohols.

Why are mammals unable to produce Essential Fatty Acids? - Biology

The bulk of dietary lipid is neutral fat or triglyceride, composed of a glycerol backbone with each carbon linked to a fatty acid. Foodstuffs typically also contain phospholipids, sterols like cholesterol and many minor lipids, including fat-soluble vitamins. Finally, small intestinal contents contain lipids from sloughed epithelial cells and considerable cholesterol delivered in bile.

In order for the triglyceride to be absorbed, two processes must occur:

  • Large aggregates of dietary triglyceride, which are virtually insoluble in an aqueous environment, must be broken down physically and held in suspension - a process called emulsification.
  • Triglyceride molecules must be enzymatically digested to yield monoglyceride and fatty acids, both of which can efficiently diffuse or be transported into the enterocyte

The key players in these two transformations are bile acids and pancreatic lipase , both of which are mixed with chyme and act in the lumen of the small intestine. Bile acids are also necessary to solubilize other lipids, including cholesterol.

Emulsification, Hydrolysis and Micelle Formation

Bile acids play their first critical role in lipid assimilation by promoting emulsification. As derivatives of cholesterol, bile acids have both hydrophilic and hydrophobic domains (i.e. they are amphipathic). On exposure to a large aggregate of triglyceride, the hydrophobic portions of bile acids intercalate into the lipid, with the hydrophilic domains remaining at the surface. Such coating with bile acids aids in breakdown of large aggregates or droplets into smaller and smaller droplets.

Hydrolysis of triglyceride into monoglyceride and free fatty acids is accomplished predominantly by pancreatic lipase. The activity of this enzyme is to clip the fatty acids at positions 1 and 3 of the triglyceride, leaving two free fatty acids and a 2-monoglyceride. The drug orlistat (Xenical) that is promoted for treatment of obesity works by inhibiting pancreatic lipase, thereby reducing the digestion and absorption of fat in the small intestine.

Lipase is a water-soluble enzyme, and with a little imagination, it's easy to understand why emulsification is a necessary prelude to its efficient activity. Shortly after a meal, lipase is present within the small intestine in rather huge quantities, but can act only on the surface of triglyeride droplets. For a given volume of lipid, the smaller the droplet size, the greater the surface area, which means more lipase molecules can get to work.

As monoglycerides and fatty acids are liberated through the action of lipase, they retain their association with bile acids and complex with other lipids to form structures called micelles . Micelles are essentially small aggregates (4-8 nm in diameter) of mixed lipids and bile acids suspended within the ingesta. As the ingesta is mixed, micelles bump into the brush border of small intestinal enterocytes, and the lipids, including monoglyceride and fatty acids, are taken up into the epithelial cells.

Absorption and Transport into Blood

The major products of lipid digestion - fatty acids and 2-monoglycerides - enter the enterocyte by simple diffusion across the plasma membrane. A considerable fraction of the fatty acids also enter the enterocyte via a specific fatty acid transporter protein in the membrane.

Lipids are transported from the enterocyte into blood by a mechanism distinctly different from what we've seen for monosaccharides and amino acids.

Once inside the enterocyte, fatty acids and monoglyceride are transported into the endoplasmic reticulum, where they are used to synthesize triglyeride. Beginning in the endoplasmic reticulum and continuing in the Golgi, triglyceride is packaged with cholesterol, lipoproteins and other lipids into particles called chylomicrons . Remember where this is occurring - in the absorptive enterocyte of the small intestine.

Chylomicrons are extruded from the Golgi into exocytotic vesicles, which are transported to the basolateral aspect of the enterocyte. The vesicles fuse with the plasma membrane and undergo exocytosis, dumping the chylomicrons into the space outside the cells.

Because chylomicrons are particles, virtually all steps in this pathway can be visualized using an electron microscope, as the montage of images below demonstrates.

Transport of lipids into the circulation is also different from what occurs with sugars and amino acids. Instead of being absorbed directly into capillary blood, chylomicrons are transported first into the lymphatic vessel that penetrates into each villus called the central lacteal. Until recently, it was not understood how the large chylomicrons are taken up into the lacteals. As it turns out, there are patches of the lacteal in which endothelial cells are held together through specialized "button junctions" that are much more permeable to chylomicrons than normal cellular junctions. Chylomicron-rich lymph then drains into the system lymphatic system, which rapidly flows into blood. Blood-borne chylomicrons are rapidly disassembled and their constitutent lipids utilized throughout the body.

When large numbers of chylomicrons are being absorbed, the lymph draining from the small intestine appears milky and the lymphatics are easy to see. In the image below, of abdominal contents from a coyote, the fine white lines (arrows) are intestinal lymphatics packed with chylomicrons. That lymph passes through mesenteric lymph nodes (LN) and then into larger lymphatics.

Another lipid of importance that is absorbed in the small intestine is cholesterol. Cholesterol homeostatis results from a balance of cholestrol synthesis, absorption of dietary cholesterol, and elimination of cholesterol by excretion in bile. Years ago it was shown that cholesterol, but not plant sterols, is readily absorbed in the intestine. More recently, a specific transport protein (NPC1L1) has been identified that ferries cholesterol from the intestinal lumen into the enterocyte. From there, a bulk of the cholesterol is esterified, incorporated into chylomicrons and shuttled into blood by the mechanisms described above.

If you are interested in confirming for yourself at least some of the processes described above, you should perform the following experiment:

  • Consume a cup of rich cream or a sack of fast-food French fries.
  • Do something productive like studying for about 30 minutes.
  • Draw a blood sample from yourself (a capillary tube is enough) - use an anticoagulant to prevent clotting.
  • Centrifuge the blood sample to separate cells and plasma.

When you examine your plasma it will look distinctly milky due to the presence of billions of light-reflecting chylomicrons (the condition is called lipemia ). If you want extra credit, continue the blood sampling every 15 minutes until your plasma clears, then plot your results on graph paper. Alternatively, you can simply examine the image to the right to see what dog serum looks like after several hours of fasting in comparison to lipemic serum collected shortly after a meal of puppy chow.

Absorption of Amino Acids and Peptides

Why are mammals unable to produce Essential Fatty Acids? - Biology

Lipids are the generic names assigned to a group of fat soluble compounds found in the tissues of plants and animals,: and are broadly classified as: a) fats, b) phospholipids, c) sphingomyelins, d) waxes, and e) sterols.

Fats are the fatty acid esters of glycerol and are the primary energy depots of animals. These are used for long-term energy requirements during periods of extensive exercise or during periods of inadequate food and energy intake. Fish have the unique capability of metabolizing these compounds readily and, as a result, can exist for long periods of time under conditions of food deprivation. A typical example is the many weeks of migration by salmon in their return upstream to spawn stored lipid deposits are burned for fuel to enable body processes to continue during the strenuous journey.

Phospholipids are the esters of fatty acids and phosphatidic acid. These are the main constituent lipids of cellular membranes allowing the membrane surfaces to be hydrophobic or hydrophylic depending on the orientation of the lipid compounds into the intra or extracellular spaces.

Sphingomyelins are the fatty acid esters of sphingosine and are present in brain and nerve tissue compounds.

Waxes are fatty acid esters of long-chain alcohols. These compounds can be metabolized for energy and to impart physical and chemical characteristics through the stored lipids of some plant and several animal compounds.

Sterols are polycyclic, long-chain alcohols and function as components of several hormone systems, especially in sexual maturation and sex-related physiological functions.

Fatty acids can exist as straight chain or branch chain components many of the fish fats contain numerous unsaturated double bonds in the fatty acid structures. A short bond designation for. fatty acids will be used throughout where the w number identifies the position of the first double bond counting from the methyl end. Linolenic acid would be written 18:3 w 3. The first number identifies the number of carbons the second number, the number of double bonds and the last number, the position of the double bonds.

Many reviews of fish nutrition have been published which contain information on lipid requirements. Most work on lipid requirements of fish has been with salmonids. Rainbow trout have an essential fatty acid (EFA) requirement for the linolenic of w 3 1 series rather than for linolenic or w 6 as required by most mammals. The main emphasis on lipid requirements has been on EFA and on the energy value of lipids.

The difference between fatty acid compositions of marine and freshwater fish has been noted by several authors. Some examples of fatty acid patterns are given in Table 1. Although these fish lipids are higher in w 3 fatty acids, it is clear that freshwater fish have higher levels of w 6 fatty acids than marine species. The average w 6/ w 3 ratios are 0.37 and 0.16 for freshwater and marine fish, respectively. Fish in general contain more w 3 than w 6 polyunsaturated fatty acids (PUFA) and should have a higher dietary requirement for w 3 PUFA thus the dietary EFA requirement of marine fish for w 3 PUFA may be higher than that of freshwater fish.

The same type of difference in the w 6/ w 3 ratio between freshwater and seawater is seen when some species of fish migrate from oceans to streams or vice versa. The PUFA ratio of sweet smelt ( Plecoglosus altivelis ) changes drastically in only one month as they migrate from the sea to a freshwater river. A similar but reverse change occurs in the masu salmon ( Oncorhynchus masu ) as they migrate from freshwater to seawater. Even within the same species of fish, the salinity of the water seems to cause a dramatic change in the fatty acid pattern.

The difference between marine and freshwater fish may be due simply to differences in the fatty acid content in the diet or it may be related to a specific requirement in fish related to physiological adaptations to the environments. The phospholipids are generally considered to be structural or functional lipid, being incorporated to a large extent in the membrane structure of cell and subcellular particles. The triglycerides are more often storage lipids and reflect the fatty acid composition of the diet to a greater extent than do the phospholipids. In Table 2, the fatty acid compositions of the triglyceride and phospholipid fractions of fish lipids are presented. It can be seen that the effect of changing environment on the fatty acid composition of the phospholipid is as great in the case of salmon, and considerably greater in the case of the sweet smelt, than it is on the triglyceride composition. Rainbow trout on diets containing either corn oil, which is high in w 6 but low in w 6 PUFA, showed a higher mortality and growth reduction in seawater than in freshwater over the twelve-week feeding period.

There are several other factors besides the salinity of the water which affect the fatty acid composition and especially the PUFA of fish. In Tables 1 and 2 it can be seen that the salmonids, even in freshwater, tend to have a higher total PUFA of the 20 and 22 carbon chain length, and a lower w 6/ w 3 ratio than the other fish. The salmonids are mostly cold-water fish. The fatty acids from a number of marine animals from temperate and arctic waters show some significant differences in the general pattern unfortunately analysis included fatty acids longer than 20:1. There are a number of other experiments demonstrating the effect of environmental temperature on fatty acid composition of aquatic animals. The general trend toward higher content of long chain PUFA at lower temperatures is quite clear. The w 6/ w 3 ratio decreases with a decrease in temperature (Table 3). If the trends in fatty acid composition can be taken as clues to the EFA requirements of fish, the w 3 requirement would be greater for fish raised at lower temperatures. Fish raised in warmer waters, such as common carp, channel catfish, and tilapia may do better with a mixture of w 6 and w 3 fatty acids.

Some of the fatty acid compositions listed in Table 3 may be seriously affected by the dietary lipids. The mosquito fish and guppies were fed trout pellets which had an w 6/ w 3 ratio of 2.75. The catfish were fed diets supplemented with either beef tallow or menhaden oil, with w 6/ w 3 ratios of 18.13 and 0.15, respectively. These fish were able to alter the dietary w 6/ w 3 ratio in favour of w 3 fatty acid incorporation into the flesh lipids even at the highest temperature. Commercially available trout pellets are often low in w 3 PUFA and high in w 6 fatty acids. It is important not to ignore the effect of dietary lipid composition on fatty acid composition of fish fed artificial diets. It is clear from the data in Table 3 that the w 6/ w 3 ratio of the fish lipids is greatly affected by the w 6/ w 3 ratio of the dietary lipids. When the dietary ratio is very high in w 6 fatty acids supplied by animal lard or vegetable oils, there is a tendency for fish to alter the ratio of PUFA incorporated in favour of w 3 fatty acids. When the dietary oil is a fish oil high in to3 fatty acids, there is little change in the w 6/ w 3 ratio of lipids incorporated into the fish. This is further suggestive evidence of an EFA requirement of fish for w 3 PUFA.

Seasonal variations in the fatty acid composition of fish species have often been reported. Seasonal changes have been observed in total lipid and iodine values of herring oils. The iodine value or degree of unsaturation of the oil was minimal in April and maximal in June. The great increase in unsaturation corresponded to the onset of feeding in spring. The absence of a gas liquid chromatograph (GLC) at the time precluded identification of changes in individual fatty acids.

Flesh and viscera lipid content of the sardine Sardinops melanosticta vary from 3.9 to 10.77 percent and from 10.9 to 38.3 percent, respectively. The fatty acids of principal interest with respect to EFA metabolism are 20:4 w 6, 20:5 w 3, and 22:6 w 3. There was considerable variation in all of these fatty acids in both neutral and polar lipid from both tissues. In the flesh, the 20:4 w 6 was consistently higher in the neutral lipid than in the polar lipid. The total 20:5 w 3 plus 22:6 w 3 was consistently higher in polar lipid than in the neutral lipid. Thus, in spite of the major fluctuations in fatty acids caused by changes in diet and temperature throughout the seasons, there was a consistent preferential incorporation of PUFA of the w 3 series into the polar or phospholipid fraction of the lipids.

One of the best clues to the EFA requirements of a species can be gained from the fatty acid composition of the lipids incorporated into the offspring or egg. The act of reproduction or spawning also has a significant effect on the seasonal fluctuation of lipids in fish. Fatty acid composition of fish egg lipids is probably distinctive for each species and contains increased levels of 16:0, 20:4 w 6, 20:5 w 3 and 22:6 w 3 compared to the liver lipids of the same female fish (Ackman, 1967).

Elevated levels of 16:0, 20:5 w 3, and 22:6 w 3 and reduced 18:1 in the ovary occurred compared to mesenteric fat of Pacific sardine fed a natural copepod diet. The blood fatty acids of the sardine fed the natural diet were similar to those of the ovary. When the sardines were fed trout food, both the blood and mesenteric fat responded to the diet with elevated 18:2 w 6 and reduced 20:5 w 3 arid 22:6 w 3. The effect of the diet on ovary fatty acid content was considerably less, as relatively high levels of 20:5 w 3 and 22:6 w 3 were retained.

The ovary lipids of the sweet smelt show an increase in 16:0, and a reduction in the PUFA, especially in the phospholipids, compared to the lipids from the flesh of fish caught at the same time of year. The w 6/ w 3 ratio of the ovary was lower than that of the flesh lipids, 0.21 and 0.17 for the ovary compared to 0.31 and 0.20 for the triglycerids and phospholipids of the flesh, respectively.

The hatchability of eggs from common carp fed several different formulated feeds is greatly reduced when the 22:6 w 3 of the egg lipids is less than 10 percent. Further, the muscle, plasma, and erythrocyte fatty acid compositions are more affected by dietary lipid than those of the eggs.

The EFA requirements of a number of species of fish have been investigated in nutritional studies. The fish themselves have given ample evidence for EFA preference by the types of fatty acids they incorporate into their lipids. Fish, in general, tend to utilize w 3 over w 6. This is especially observed when the dietary lipids are high in w 6, as the fish tend to alter the w 6/ w 3 ratio toward the w 3 fatty acids in the tissue lipids. The lipids of the egg must satisfy the EFA requirement of the embryo until it is able to feed. The fatty acid composition data suggest that the w 3 requirement is greater in seawater than in freshwater and higher in cold water than in warm water.

Detailed information is still lacking on the dietary lipid requirements of many species of fish, but there is an abundance of information on the fatty acid composition of fish oils. Information on the lipid composition of fish can be used to make some guesses about dietary lipid requirements. Linolenic acid (18:3 w 3) resulted in some sparing action and growth promotion in rats, and fatty acids of the w 6 EFA prevented all of the EFA-deficiency symptoms. Research with homeothermic land-dwelling animals showed that the w 6 series of fatty acids are the "essential fatty acids", while the w 3 series are considered to be non-essential or only have a partial sparing action on EFA-deficiency. The w 6 series of fatty acids have been shown to be essential to enough species that it began to become accepted that these are the essential fatty acids for all animals.

It was assumed by many that fish also required w 6 fatty acids. Many researchers began by supplementing fish diets with vegetable oils, such as corn, peanut, or sunflower oil, which were rich in linoleic acid. The main sympton observed during the development of EFA deficiency in chinook salmon fed fat-free diets was a marked depigmentation that can be prevented by addition of 1 percent trilinolein, but not by 0.1 percent linolenic acid.

Although the w 6 fatty acids are considered to be essential, one of the general characteristics of fish oils is the low levels of w 6 series fatty acids and the higher levels of w 3 type fatty acids. There is evidence that polyunsaturated fatty acids (PUPA) of the w 3 series, which are present in relatively large concentrations in fish oil, play the role of essential fatty acid for fish.

When a test diet containing 13 percent corn oil and 2 percent cod-liver oil was fed to rainbow trout, subsequent deletion of the cod-liver oil from the diet depressed growth and produced some kidney degeneration which might be attributed to a lack of sufficient w 3 PUFA present in significant quantities in cod-liver oil (McLaren et al ., 1947). Dietary fish oil is superior to corn oil in promoting growth of rainbow trout (Salmo gairdneri) and the yellow-tail ( Seriola guingueradiata ). Dietary linolenic acid or ethyl linolenate (18:3 w 3) gives a positive growth response for rainbow trout which may be attributed to a dietary requirement for w 3 fatty acids.

One of the most widely accepted theories explaining the presence of such high levels of 20:5 w 3 and 22:6 w 3 fatty acids in fish oils is related to the effect of unsaturation on the melting point of a lipid. The greater degree of unsaturation of fatty acids in the fish phospholipids allows for flexibility of cell membrane at lower temperatures. The w 3 structure allows a greater degree of unsaturation than the w 6 or w 9. This theory is consistent with the fact that cold water fish have a greater nutritional requirement for w 3 fatty acids, while the EFA requirement of some warm water fish can be satisfied by a mixture of w 6 plus w 3.

Rainbow trout, a cold water fish, requires w 3 fatty acids as EFA in the diet. The EFA requirement can be met by 1 percent 18:3 w 3 in the diet. Inclusion of 18:2 w 6 in the diet may result in some improvement in growth and feed conversion compared to EFA deficient diets however, the w 6 fatty acids will not prevent some EFA deficiency symptoms such as the "shock syndrome". Although it is clear that rainbow trout require w 3 fatty acids, it remains to be shown conclusively whether some dietary level of w 6 fatty acid is essential.

In all the above studies with rainbow trout, dietary 18:2 w 6 or 18:3 w 3 were readily converted to C-20 and C-22 PUFA of the same series, and 18:3 w 3 or 22:6 w 3 had similar EFA value for rainbow trout. Either 20:5 w 3 or 22:6 w 3 is superior to 18:3 w 3 in an EFA value for rainbow trout, and the former two fatty acids in combination are superior to either alone. This is consistent with data for mammals, where 20:4 w 6 has higher EFA value than 18:2 w 6. The superior nutritional value of C-20 and C-22 carbon w 3-PUFA is further supported by the excellent growth promoting effects of dietary fish oils such as pollock liver oil and salmon oil for rainbow trout.

One of the most important warm water fish in North America is the channel catfish (Ictalurus punctatus) . The quantitative EFA requirement of the catfish has not yet been determined. However, the evidence is convincing that the w 3 requirement is not as great as that of rainbow trout. Analysis of fatty acids of lipids from catfish purchased at five processing plants showed very low levels of 20:4 w 6, 20:5 w 3, and 22:6 w 3 0.8 - 5.5, 0.2 - 1.3, and 0.6 - 6.1 percent of the total fatty acids, respectively. It was shown that corn oil added to a semipurified casein based diet initially resulted in a positive growth response and protein sparing, but later growth inhibition was observed. The apparent repressive effects of corn oil may be due to its 18:2 w 6 content since 20:5 w 3 and 22:6 w 3 present in menhaden oil had no apparent detrimental effects. The growth suppressing effects of 18:2 w 6 were also noted when 3 percent corn oil was added to 3 percent beef tallow and 3 percent menhaden oil. The growth suppression caused by unsaturated fatty acids does not appear to be limited to w 6 fatty acids. Linseed oil (high in 18:3 w 3) in the diet of catfish resulted in growth suppression similar to that caused by corn oil compared with dietary beef tallow, olive oil and menhaden oil.

The picture for another warm water fish, the common carp (Cyprinus carpio) is much clearer than that for the channel catfish. This fish has an EFA requirement for both w 3 and w 6 fatty acids. The best weight gains and feed conversions are obtained in fish receiving a diet containing both 1 percent 18:2 w 6 and 1 percent 18:3 w 3. With the carp, 20:5 w 3 and 22:6 w 3 at 0.5 percent of the diet are superior to 1 percent of 18:3u3. Carp fed a fat-free, or EFA deficient, diet incorporated high levels of 20:3 w 9 in their lipids, especially in the phospholipids.

The eel ( Anguilla japonica ), another warm water fish, has a requirement for both w 3 and w 6 fatty acids. Corn oil (high in w 6) and cod liver oil (high in w 3)in a 2:1 mixture are most favourable for the growth of eels. The eel requires w 6 and w 3 in the same proportion as the carp, but at a lower level in the diet namely, 0.5 percent of each, rather than 1.0 percent of each PUFA.

The plaice becomes depleted of both w 3 and w 6 PUFA when fed a fat-free diet. The addition of 12:0 and 14:0 to the diet result in the synthesis of saturated and monoenoic fatty acids of chain lengths up to C18 however, increased levels of 20:3 w 9 noted in trout and mammals have not been reported in plaice. Plaice fed dietary 18:2 w 6 and 18:3 w 3 will not produce significant amounts of 20:4 w 6, 20:5 w 3, or 22:6 w 3.

The growth of turbot (Scophthalmus matimus) is much better with w 3 PUFA than with w 6 or saturated fat (hydrogenated coconut oil) in the diet. The turbot also appears to be unable to convert dietary 18:2 w 6 to 20:4 w 6 when fed corn oil, or to convert endogenous 18:1 w 9 to 20:3 w 9 when fed the EFA deficient diet. Although it appears to have an EFA requirement for w 3 fatty acids such as are present in cod liver oil, this requirement is not satisfied by 18:3 w 3. The chain elongation and desaturation of 18:l w 9, 18:2 w 6, or 18:3 w 3 has been found to be very limited (3-15 percent) in turbot compared to the rainbow trout where 70 percent of the 18:3 w 3 was converted to 22:6 w 3. The required level of long-chain w 3 fatty acids for turbot is at least 0.8 percent of the diet.

The red sea bream (Chrysophyrys major) grows better when the dietary lipid is of marine origin (pollock residual oil) rather than a vegetable oil (such as corn oil). The EFA requirement of the red sea bream is not satisfied by either linoleic acid of corn oil or supplemented linolenate. A mixture of 20:5 w 3 and 22:6 w 3 supplemented to the corn oil diet has been shown to be effective in improving growth and condition of these fish. Thus, even in warm water, marine fish seem to require not just w 3 fatty acids but 0)3 fatty acids of 20 to 22 carbon-chain length. A direct correlation between feed efficiency and the 18:1 level in the lipids of the red sea bream has been postulated.

Among warm water marine fish, mullet and fundulus possess the ability to chain, elongate, and desaturate 18:2 w 6 or 18:3 w 3 PUFAs. The process is, however, inhibited in fundulus by high levels (about 5 percent) of these PUFAs of 18:2 w 6 or 18:3 w 3 in the diet.

It appears that high levels of 18-carbon w 6 or w 3 fatty acids inhibit the synthesis and metabolism of 18:l w 9. It is interesting to note that the channel catfish, which also exhibits negative growth response to dietary 18:2 w 6 or 18:3 w 3, incorporates very high levels of 18:1 into its body lipids. The inclusion of either 18:2 w 6 or 18:3 w 3 in the diet reduces the levels of 18:1 fatty acids in body lipids. A similar reduction has also been observed in red sea bream liver phospholipid when either of the PUFAs is added to the diet.

The competitive inhibition of chain elongation and desaturation of members from one series of fatty acids for members of another series is well established, with w 3 > w 6 > w 9 being the usual order of potency for inhibition.

The pathways of fatty acid metabolism have been reviewed by Mead and Kayama (1967). Fish are able to synthesize, de novo from acetate, the even-chain, saturated fatty acids, as shown in Figure 1. Radio tracer studies have shown that fish can convert 16:0 to the w 7 monoene and 18:0 to the w 9 monoene. The w 5, w 11 and w 3 monoenes are proposed based on the identification of these isomers in the monoenes of herring oil.

Fish are unable to synthesize any fatty acids of the w 6 and u3 series unless a precursor with this w structure is present in the diet. Fish are able to desaturate and elongate fatty acids of the w 9, w 6, or w 3 series as outlined in Figure 1. There is competitive inhibition of the elongation desaturation of fatty acids of one series by members of the other series. The w 3 fatty acids are the most potent inhibitors, the w 9 are the least. The ability to elongate and desaturate fatty acids is not the same in all species of fish, as was noted earlier. The turbot was able to desaturate and elongate only 3-15 percent of 18:1 w 9, 18:2 w 6, or 18:3 w 3, when given the C 14 labelled fatty acid in the rainbow trout, 70 percent of the label from 18:3 w 3 (C 14 ) was found in 22:6 w 3.

The essential fatty acids are not unique in their ability to supply energy. The b -oxidation of fatty acids in fish is basically the same as in mammals. The EFA and saturated and monoenoic fatty acids are all equally utilized by fish for energy production.

Fig. 1 Flow diagram for fatty acid synthesis mechanisms in fish - Saturated and monoenoic fatty acids (Adapted from Castell, 1979)

Fig. 1 Flow diagram for fatty acid synthesis mechanisms in fish - Polyunsaturated fatty acids (Adapted from Castell, 1979)

Increased swelling rates of liver mitochondria occur in rainbow trout fed diets deficient in w 3 fatty acids. It is possible that EFA plays an important role in the permeability as well as the plasticity of membranes. The role of w 3 fatty acids in membrane permeability may be one of the factors accounting for differences in content of this family of fatty acids between freshwater and marine fish.

Fish mitochondria with high levels of the w 3 PUFA and very low levels of w 6 fatty acids are very similar to mammalian mitochondria with respect to cytochrome content, b -oxidation of fatty acids, operation of the tricarboxylic acid cycle, electron transport, and oxidative phosphorylation. The w 3 PUFA may play the same role in fish that the w 6 fatty acids play in rats. The EFA play another role in the mitochondria. In addition to their importance in membrane structure, the EFA are important in some enzyme systems.

Unsaturated fatty acids play an important role in the transportation of other lipids. It has been repeatedly shown that feeding PUFA will lower the cholesterol levels in animals with above-normal blood lipid and cholesterol levels. Fish oils are more effective in lowering cholesterol levels than are most dietary lipids. The major portion of the fatty acids absorbed across the intestinal mucosa are transported as protein-lipid complexes stabilized by phospholipids. The low body temperature in fish probably results in a greater importance for unsaturation in transport of lipids than in homeothermic animals.

The requirement by fish for PUFA of the w 3 series creates problems with respect to feed storage. These types of fatty acids are very labile on oxidation. The products of lipid oxidation may react with other nutrients such as proteins, vitamins, etc., and reducing the available dietary levels or the oxidation products may be toxic. The effect of oxidized lipids on dietary proteins, enzymes and amino acids have been demonstrated.

The use of oxidized menhaden oil in the diets of swine and rats caused decreased appetite, reduced growth, yellowish-brown pigmentation of depot fat, and decreased haemoglobin and haematocrit levels. The negative effects of the oxidized fish oils were reversed by the addition of alpha-tocopherol acetate or ethoxyoquin to the diet.

Much of the use of vegetable oils in fish diets in the 1950s and 1960s might, in part, have been based on their greater stability in prepared diets. It has been demonstrated that rancid herring and hake meals in fish feeds caused dark colouration, anaemia, lethargy, brown-yellow pigmented liver, abnormal kidneys, and small gill clubbing in chinook salmon. The symptons can be alleviated by addition of alpha-tocopherol to the diets containing rancid fish meals. The addition of vitamin E would prevent the toxic or negative effects of adding 5 percent highly oxidized salmon oil to the diet of rainbow trout. This same sparing effect of alpha-tocopherol can also apply to rancid carp feed.

The positive nutritional value of w 3 fatty acids in fish lipids for fish feeds can become a negative factor if adequate care is not taken in the preparation and storage of feeds. Only fresh oils with low peroxide values should be used in feeds. Fish feed ingredients such as fish meals should be protected against oxidation. The level of vitamin E added to the diet should be increased as the PUFA level is increased. The finished feed, if possible, should be stored in air tight containers at reduced temperatures with minimum exposure to UV radiation and other factors accelerating the rate of lipid oxidation. The problems of rancidity or antioxidation of lipids in fish feeds should not be ignored.


  1. Cymbelline

    Clearly, many thanks for the information.

  2. Shunnar

    cool .... beautiful ... and not only

  3. Aldous

    Please explain the details

  4. Honza

    Yeah, I thought so too.

  5. Daren

    don't read books ...

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