Essential fatty acids as determinants of lipid requirements in infants, children and adults

Uauy, Ricardo; Mena, Patrícia; Valenzuela, Alfonso

doi:10.1038/sj.ejcn.1600745

Cited by 73 publications

(64 citation statements)

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“…Although the mechanism(s) by which these beneficial effects occurs is unknown, a potentially important anti-atherogenic and antiinflammatory mechanism of -3 PUFAs is their interference with the arachidonic acid cascade that generates pro-inflammatory eicosanoids (12,33). EPA not only can replace arachidonic acid in phospholipid bilayers but is also a competitive inhibitor of cyclooxygenase, reducing the production of 2-series PGs and thromboxane, in addition to the 4-series leukotrienes.…”

Section: Discussionmentioning

confidence: 99%

Formation of F-ring Isoprostane-like Compounds (F3-Isoprostanes) in Vivo from Eicosapentaenoic Acid

Gao¹,

Yin²,

Milne³

et al. 2006

Journal of Biological Chemistry

118

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Eicosapentaenoic acid (EPA, C20:5, -3) is the most abundant polyunsaturated fatty acid (PUFA) in fish oil. Recent studies suggest that the beneficial effects of fish oil are due, in part, to the generation of various free radical-generated non-enzymatic bioactive oxidation products from -3 PUFAs, although the specific molecular species responsible for these effects have not been identified. Our research group has previously reported that pro-inflammatory prostaglandin F 2 -like compounds, termed F 2 -isoprostanes (IsoPs), are produced in vivo by the free radical-catalyzed peroxidation of arachidonic acid and represent one of the major products resulting from the oxidation of this PUFA. Based on these observations, we questioned whether F 2 -IsoP-like compounds (F 3 -IsoPs) are formed from the oxidation of EPA in vivo. Oxidation of EPA in vitro yielded a series of compounds that were structurally established to be F 3 -IsoPs using a number of chemical and mass spectrometric approaches. The amounts formed were extremely large (up to 8.7 ؉ 1.0 g/mg EPA) and greater than levels of F 2 -IsoPs generated from arachidonic acid. We then examined the formation of F 3 -IsoPs in vivo in mice. Levels of F 3 -IsoPs in tissues such as heart are virtually undetectable at baseline, but supplementation of animals with EPA markedly increases quantities up to 27.4 ؉ 5.6 ng/g of heart. Interestingly, EPA supplementation also markedly reduced levels of pro-inflammatory arachidonate-derived F 2 -IsoPs by up to 64% ( p < 0.05). Our studies provide the first evidence that identify F 3 -IsoPs as novel oxidation products of EPA that are generated in vivo. Further understanding of the biological consequences of F 3 -IsoP formation may provide valuable insights into the cardioprotective mechanism of EPA.

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Section: Discussionmentioning

confidence: 99%

Formation of F-ring Isoprostane-like Compounds (F3-Isoprostanes) in Vivo from Eicosapentaenoic Acid

Gao¹,

Yin²,

Milne³

et al. 2006

Journal of Biological Chemistry

118

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“…Although the mechanism(s) by which the -3 fatty acids exert their biological activity is unknown, an important anti-atherogenic and anti-inflammatory mechanism of EPA action is its interference with the arachidonic acid cascade that generates pro-inflammatory eicosanoids via the cyclooxygenases and lipoxygenases (1,37). A recent Japanese study examining the effects of EPA on major coronary events in hypercholesterolemia (JELIS) demonstrated a 19% reduction in coronary events after 4.6 years of EPA intervention in hypercholesterolemic patients (33).…”

Section: Discussionmentioning

confidence: 99%

Formation of Highly Reactive Cyclopentenone Isoprostane Compounds (A3/J3-Isoprostanes) in Vivo from Eicosapentaenoic Acid

Brooks

Milne

Yin

et al. 2008

Journal of Biological Chemistry

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Omega-3 (-3) polyunsaturated fatty acids (PUFAs) found in marine fish oils are known to suppress inflammation associated with a wide variety of diseases. Eicosapentaenoic acid (EPA) is one of the most abundant -3 fatty acids in fish oil, but the mechanism(s) by which EPA exerts its beneficial effects is unknown. Recent studies, however, have demonstrated that oxidized EPA, rather than native EPA, possesses anti-atherosclerotic, anti-inflammatory, and anti-proliferative effects. Very few studies to date have investigated which EPA oxidation products are responsible for this bioactivity. Our research group has previously reported that anti-inflammatory prostaglandin A 2 -like and prostaglandin J 2 -like compounds, termed A 2 /J 2 -isoprostanes (IsoPs), are produced in vivo by the free radical-catalyzed peroxidation of arachidonic acid and represent one of the major products resulting from the oxidation of this PUFA. Based on these observations, we questioned whether cyclopentenoneIsoP compounds are formed from the oxidation of EPA in vivo. Herein, we report the formation of cyclopentenone-IsoP molecules, termed A 3 /J 3 -IsoPs, formed in abundance in vitro and in vivo from EPA peroxidation. Chemical approaches coupled with gas chromatography/mass spectrometry (GC/MS) and liquid chromatography/mass spectrometry (LC/MS) were used to structurally characterize these compounds as A 3 /J 3 -IsoPs. We found that levels of these molecules increase ϳ200-fold with oxidation of EPA in vitro from a basal level of 0.8 ؎ 0.4 ng/mg EPA to 196 ؎ 23 ng/mg EPA after 36 h. We also detected these compounds in significant amounts in fresh liver tissue from EPA-fed rats at basal levels of 19 ؎ 2 ng/g tissue. Amounts increased to 102 ؎ 15 ng/g tissue in vivo in settings of oxidative stress. These studies have, for the first time, definitively characterized novel, highly reactive A/J-ring IsoP compounds that form in abundance from the oxidation of EPA in vivo.

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“…Je Âquier reminds us that the requirement for linoleic acid is usually accepted to be in the range 3 ± 5%, and for linolenic acid 0.5 ± 1.0%, of dietary energy (FAOaWHO, 1994). Uauy has reviewed these EFA requirements for adults elsewhere in these proceedings, and emphasises that it is most unlikely that the need for EFAs will constitute the limiting criteria governing minimum fat requirements (Uauy, 1999). It was only in 1971 that the ®rst unequivocal case of adult EFA de®ciency was described in a patient with only 60 cm of bowel who had received 100 d fat-free intravenous feeding (Collins et al, 1971).…”

Section: S88mentioning

confidence: 99%

Response to and range of acceptable fat intake in adults

Jéquier

1999

Eur J Clin Nutr

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Cellular energy metabolism depends on two main energy substrates: glucose and fatty acids. The major determinants of the fuel mix oxidized are glucose availability and insulin secretion that both promote glucose oxidation. Fatty acid oxidation occurs mainly when glucose availability is reduced, for instance during the postabsorptive period, or when energy expenditure is increased, for instance during exercise of long duration. When eucaloric diets with high carbohydrate and low fat content are ingested, de novo lipogenesis is stimulated in adults, but the rate of conversion of glucose to fatty acids is low, which means that carbohydrate intake does not have much in¯uence on fat requirements. The lower limit of fat intake depends on three factors: the fat requirement to meet energy needs, the need for essential fatty acids, and the amount of fat in the diet that is necessary to absorb fat-soluble vitamins. The lower limit of fat intake to meet the energy needs of adults is assumed to be between 10 and 15% of dietary energy, provided that enough carbohydrates are available. For adults, the requirement for essential fatty acids is in the range of 3 ± 5% of dietary energy for linoleic acid, and 0.5 ± 1.0% of dietary energy for linolenic acid. Fat energy should not be below 10% of total energy intake in order to ensure an unrestricted absorption of fat-soluble vitamins, particularly vitamins A and E. The recommendations on upper limits of fat intake for adults must take into account the degree of physical activity. International recommendations indicate that active individuals in energy balance may consume up to 35% of their total energy intake as dietary fat, whereas sedentary individuals should not consume more than 30% of their energy from fat. Saturated fatty acids should not exceed 10% of the energy intake. IntroductionWhile protein and energy requirements have been studied extensively in humans (Scrimshaw et al, 1972), the relative contribution of carbohydrates and fats to cover energy needs has received less attention. In many rural communities of developing countries, carbohydrates contribute between 70 and 75% to total energy intake, while fat intake contributes only 12 ± 15% (FAOUN, 1970). By contrast, the traditional adult Eskimo diet in the last century contained about 7% carbohydrate and 50% fat energy (Bang et al, 1980). A range of fat intake between 12 and 50% of total energy intake appears to be compatible with a normal body composition and the maintenance of good health in individuals who are adapted to these types of diets and to their environment. This does not imply, however, that these extreme values of fat and carbohydrate intakes can be recommended for adults of developed countries with a sedentary lifestyle. Lower limit of fat intake in adultsThe lower limit of fat intake depends on three factors: the fat requirement to meet energy needs, the need for essential fatty acids, and the amount of fat in the diet that is necessary to absorb the fat soluble vitamins.Fat requirement to meet energy nee...

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Essential fatty acids as determinants of lipid requirements in infants, children and adults

Cited by 73 publications

References 100 publications

Formation of F-ring Isoprostane-like Compounds (F3-Isoprostanes) in Vivo from Eicosapentaenoic Acid

Formation of F-ring Isoprostane-like Compounds (F3-Isoprostanes) in Vivo from Eicosapentaenoic Acid

Formation of Highly Reactive Cyclopentenone Isoprostane Compounds (A3/J3-Isoprostanes) in Vivo from Eicosapentaenoic Acid

Response to and range of acceptable fat intake in adults

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