Lead exposure and (n-3) fatty acid deficiency during rat neonatal development alter liver, plasma, and brain polyunsaturated fatty acid composition

Lead (Pb) exposure has been reported to increase arachidonic (AA) and docosahexaenoic (DHA) acids. To determine whether Pb effects on fatty acid composition are influenced by dietary (n-3) fatty acid restriction, weanling female rats were fed either an (n-3)-adequate or -deficient diet to maturity and mated. At parturition, dams in each group were subdivided to receive either 0.2% Pb or Na-acetate in their drinking water during lactation only. Pups were analyzed for fatty acid content in liver, plasma, and brain at either 3 or 11 wk. The (n-3)-deficient diets markedly decreased total (n-3) fatty acids, and increased total (n-6) fatty acids including both AA and docosapentaenoic (n-6) in each compartment (P < 0.05). The main effects of Pb were in the livers of weanling rats where there was a 56% loss in total fatty acid concentration concurrent with increased relative percentages of AA and DHA. Thus, because there was a greater percentage of liver nonessential fatty acid lost relative to the essential fatty acids (EFA), there was no net change in AA concentration. There was a diet x Pb interaction for a decrease in liver DHA concentration evident only in the (n-3)-adequate group. There were also diet x Pb interactions in plasma at 11 wk and in brain at 3 wk. These data are consistent with the hypothesis of a Pb-induced increase in fatty acid catabolism, perhaps as a source of energy.     

Dietary ratio of (n-6)/(n-3) polyunsaturated fatty acids alters the fatty acid composition of bone compartments and biomarkers of bone formation in rats

The effects of dietary polyunsaturated fatty acids (PUFA) on ex vivo bone prostaglandin E(2) (PGE(2)) production and bone formation rate were evaluated in rats. Weanling male Sprague-Dawley rats were fed AIN-93G diet containing 70 g/kg of added fat for 42 d. The dietary lipid treatments were formulated with safflower oil and menhaden oil to provide the following ratios of (n-6)/(n-3) fatty acids: 23.8 (SMI), 9.8 (SMII), 2.6 (SMIII), and 1.2 (SMIV). Ex vivo PGE(2) production in liver homogenates and bone organ cultures (right femur and tibia) were significantly lower in rats fed diets with a lower dietary ratio of (n-6)/(n-3) fatty acids than in those fed diets with a higher dietary ratio. Regression analysis revealed a significant positive correlation between bone PGE(2) and the ratio of arachidonic acid (AA)/eicosapentaenoic acid (EPA), but significant negative correlations between bone formation rate and either the ratio of AA/EPA or PGE(2) in bone. Activities of serum alkaline phosphatase isoenzymes, including the bone-specific isoenzyme (BALP), were greater in rats fed a diet high in (n-3) or a low ratio of (n-6)/(n-3), further supporting the positive action of (n-3) fatty acids on bone formation. These results demonstrated that the dietary ratio of (n-6)/(n-3) modulates bone PGE(2) production and the activity of serum BALP in growing rats.     

Comparison of n-3 polyunsaturated fatty acid contents of wild and cultured Australian abalone

The fatty acid contents of wild and cultured Australian adult blacklip abalone, Haliotis rubra, were analysed by gas liquid chromatography. Wild abalone contained significantly higher levels of total n-3 polyunsaturated fatty acids (PUFA), eicosapentaenoic acid (20:5n-3), docosapentaenoic acid (22:5n-3) and alpha-linolenic acid (18:3n-3) than cultured abalone (P<0.05). The predominant n-3 PUFA was docosapentaenoic acid in wild abalone, while in cultured abalone a high level of eicosapentaenoic acid was found. The concentration of docosahexaenoic acid (22:6n-3) was low in both wild and cultured abalone, and cultured abalone had a significantly higher percentage composition of this fatty acid than wild abalone (P<0.01). Significantly higher levels of arachidonic acid (20:4n-6), 22:2n-6, 22:4n-6 and total n-6 PUFA were also found in wild abalone than in cultured animals (P<0.05). The ratio of n-3 PUFA to n-6 PUFA was the same in wild and cultured abalone. Manipulation of nutrient sources of cultured abalone may influence their lipid composition. Consumption of either wild or cultured abalone will contribute to dietary n-3 PUFA intake, with benefits to human health.     

Modulation of lipid chylomicron-synthesizing enzymes in rats by the dietary (n-6):(n-3) fatty acid ratio

The effect of diets with various (n-6):(n-3) polyunsaturated fatty acid (PUFA) ratios and a constant polyunsaturated: saturated fatty acid ratio on the basal activity of chylomicron lipid synthesizing enzymes was investigated in rat intestinal microsomes. Enzymes studied were: acyl-CoA:cholesterol acyltransferase (ACAT); acyl-CoA:lysophosphatidylcholine acyltransferase (MGAT) and acyl-CoA:1,2-diacylglycerol acyltransferase (DGAT). Results showed that after a 4-wk feeding period, ACAT, ACLAT and DGAT basal activities were significantly enhanced by the dietary fatty acids of the (n-3) series, whereas MGAT activity was not affected. When the highest (n-6):(n-3) ratio (51.0) was compared with the lowest (0.8), the increase attained was about 58, 76 and 73% for ACAT, ACLAT and DGAT, respectively. Fatty acid composition of microsomal lipids was drastically altered by the diets because (n-3) PUFA replaced the (n-6) series as the dietary (n-6):(n-3) ratio was lowered. These compositional changes could explain the observed modification in the membrane-bound enzyme activities. We suggest that (n-3) PUFA ingestion leads to an enhanced velocity of chylomicron synthesis in rats.     

Comparison of n-3 polyunsaturated fatty acid contents of wild and cultured Australian abalone

The fatty acid contents of wild and cultured Australian adult blacklip abalone, Haliotis rubra, were analysed by gas liquid chromatography. Wild abalone contained significantly higher levels of total n-3 polyunsaturated fatty acids (PUFA), eicosapentaenoic acid (20:5n-3), docosapentaenoic acid (22:5n-3) and α-linolenic acid (18:3n-3) than cultured abalone (P<0.05). The predominant n-3 PUFA was docosapentaenoic acid in wild abalone, while in cultured abalone a high level of eicosapentaenoic acid was found. The concentration of docosahexaenoic acid (22:6n-3) was low in both wild and cultured abalone, and cultured abalone had a significantly higher percentage composition of this fatty acid than wild abalone (P<0.01). Significantly higher levels of arachidonic acid (20:4n-6), 22:2n-6, 22:4n-6 and total n-6 PUFA were also found in wild abalone than in cultured animals (P<0.05). The ratio of n-3 PUFA to n-6 PUFA was the same in wild and cultured abalone. Manipulation of nutrient sources of cultured abalone may influence their lipid composition. Consumption of either wild or cultured abalone will contribute to dietary n-3 PUFA intake, with benefits to human health.     

Modulation of essential (n-6):(n-3) fatty acid ratios alters fatty acid status but not bone mass in piglets

Dietary (n-6) and (n-3) fatty acids have been implicated as important regulators of bone metabolism. The main objective of this research was to define the response of whole-body growth, fatty acid status and bone mass to a reduced dietary (n-6):(n-3) fatty acid ratio. A secondary objective was to determine whether there is an amount of fat x fatty acid ratio interaction for these outcomes. Piglets (n = 32) were randomized to 1 of 4 diets: group 1: [30 g fat/L + (n-6):(n-3) ratio 4.5:1]; group 2: [30 g fat/L + (n-6):(n-3) ratio 9.0:1]; group 3: [60 g fat/L + (n-6):(n-3) ratio 4.5:1]; and group 4: [60 g fat/L + (n-6):(n-3) ratio 9.0:1]. After 21 d, outcomes assessed included growth, fatty acid status and bone mass and metabolism. Growth and bone mass did not differ among the four groups nor did arachidonic acid (AA as g/100 g fatty acids) in plasma, adipose and brain. Piglets fed diets 1 and 3 with the lower (n-6):(n-3) ratio had lower liver AA (P < 0.001). Those fed diets 1 and 2 containing 30 g fat/L had lower docosahexaenoic acid (DHA as g/100 g fatty acids) in liver (P < 0.001), plasma (P = 0.019) and adipose tissue (P = 0.045). However, piglets fed diets 1 and 3 had higher (P < 0.001) brain DHA than those fed diets with a higher (n-6):(n-3) ratio. Higher plasma DHA was associated with less bone resorption (r = -0.44, P = 0.01). Therefore, elevation of dietary (n-3) fatty acids supports growth and fatty acid status while not compromising bone mass. The results may be of relevance to the nutritional management of preterm infants whose DHA status is often too low and bone resorption too high.     

Dietary (n-3) fatty acids alter fatty acid composition and prostaglandin synthesis in rat testis

The objective of this study was to determine the efficacy of linolenic acid [18:3(n-3)], compared with the long-chain (n-3) fatty acids in fish oil, in suppressing arachidonic acid [20:4(n-6)] metabolism in rat testis. Six groups of rats were fed three levels of 18:3(n-3) or fish oil, and the fatty acid composition of testis parenchyma lipids and prostaglandin (PG) I2 synthesis by tunica were determined after 12 wk. Levels of docosapentaenoic acid [22:5(n-6)], the major 22-carbon fatty acid in rat testis lipids, were significantly depressed compared with the control by both linolenic acid and fish oil; however, testis weights were not affected significantly. Arachidonic acid levels also were depressed significantly in testis lipids by dietary (n-3) fatty acids, but the decreases were not as pronounced as those observed in other tissues. The synthesis of PGI2 was significantly reduced compared with the control by (n-3) fatty acid feeding, but there were no differences among the experimental groups. Both 18:3(n-3) and the longer-chain (n-3) fatty acids from fish oil reduce levels of 20:4(n-6) and 22:5(n-6) in testis lipids and the capacity of the tunica to synthesize PGI2, but these fatty acids seem to cause no defect in testicular development as indicated by weight.     

Dietary (n-3) polyunsaturated fatty acids exert antihypertensive effects by modulating calcium signaling in T cells of rats

After 10 wk of feeding an experimental diet enriched with (n-3) polyunsaturated fatty acids (PUFA), i.e., eicosapentaenoic acid [EPA, 20:5(n-3)] and [DHA, 22:6(n-3)] (EPAX), blood pressure in spontaneously hypertensive rats (SHR), but not in normotensive Wistar-Kyoto (WKY) rats was reduced relative to rats fed an unsupplemented control diet. Concanavalin A-stimulated T-cell proliferation was diminished in both strains of rats fed the PUFA/EPAX diet. The experimental diet lowered secretion of interleukin-2 in SHR, but not in WKY rats compared with rats fed the control diet. To determine whether there was a defect in calcium homeostasis in T cells during hypertension, we employed the following agents: caffeine, which recruits calcium from the cytosolic Ca(2+)-induced Ca(2+)-release pool; ionomycin, which at low concentrations opens calcium channels; and thapsigargin (TG), which mobilizes [Ca(2+)]i from the endoplasmic reticulum (ER) pool. Caffeine-induced increases in [Ca(2+)]i were not modified by the PUFA/EPAX diet. The ionomycin-induced increases in [Ca(2+)]i in T cells from SHR were greater than in those from WKY rats; consumption of the PUFA/EPAX diet did not modify Ca(2+) influx in cells of either strain. The TG-induced increases in [Ca(2+)]i in T cells from SHR were greater than those in cells from WKY rats. Interestingly, consumption of the experimental diet reduced TG-evoked increases in [Ca(2+)]i in T cells from SHR and increased those in T cells from WKY rats, indicating that the PUFA/EPAX diet could reverse the calcium mobilization from the ER pool in T cells. These results suggest that (n-3) PUFA exert antihypertensive effects and modulate T-cell calcium signaling during hypertension in rats.     

Long-term intake of trans (n-3) polyunsaturated fatty acids reduces the b-wave amplitude of electroretinograms in rats

Weanling rats were fed three diets differing in their concentrations of the cis- and trans-isomers of alpha-linolenic acid [18:3(n-3)] for 12 mo to study the long-term effects of these fatty acids on the electroretinogram (ERG). The diets contained 18:3(n-3) in its natural form at 2.0 g/100 g total fatty acids (C group), partially isomerized 18:3(n-3) [1.3 g/100 g cis 18:3(n-3) + 0.7 g/100 g trans 18:3(n-3); cT group] and the control level of cis 18:3(n-3) with trans 18:3(n-3) [2.0 g/100 g cis 18:3(n-3) + 0.7 g/100 g trans 18:3(n-3); CT group]. The ERG and the levels of trans-isomers of the polyunsaturated fatty acids (PUFA) of retinal and hepatic phospholipids were determined after 3, 6, 9 and 12 mo of feeding the experimental diets. Dietary trans alpha-linolenic acid altered the fatty acid composition of retinal and hepatic phospholipids by significantly increasing the Delta19trans-isomer of docosahexaenoic acid. Moreover, dietary trans-isomers of alpha-linolenic acid significantly decreased the b-wave amplitude of the ERG by 9 mo of feeding. We conclude that long-term intake of small amounts of trans-isomers of alpha-linolenic acid could disturb visual function. However, further studies are required to determine the mechanisms responsible for this phenomenon.     

Dietary n-3 and n-6 fatty acids alter avian metabolism: molecular-species composition of breast-muscle phospholipids

The effects of diets high in n-3 polyunsaturated fatty acids (PUFA; provided by fish oil), n-6 PUFA (sunflower oil) or in more-saturated fatty acids (tallow) on the distribution of subclasses of choline phospholipids (PC) and ethanolamine phospholipids (PE) from the breast muscle of broiler chickens were examined. Supplementation with the different fatty acids had no effect on the distribution of phospholipid subclasses. Feeding sunflower oil or tallow gave a molecular-species profile similar in both fatty acid subtype and proportion. In the diacyl PC phospholipids, 16 : 0-18 : 1n-9 and 16 : 0-18 : 2n-6 accounted for approximately 60 % of the total molecular species, whereas for the alkylenyl PC the predominant species were 16 : 0-18 : 1n-9 and 16 : 0-20 : 4n-6. Of the diacyl PE the dominant species was 18 : 0-20 : 4n-6 which accounted for 50 % of the molecular species, and of the alkylenyl PE the dominant species were 16 : 0-18 : 1n-9, 16 : 0-20 : 4n-6 and 18 : 0-20 : 4n-6. Supplementation with fish oil significantly increased levels of both eicosapentaenoic acid (20 : 5n-3) and docosahexaenoic acid (22 : 6n-3) in PC and PE when compared with either sunflower oil or tallow supplementation. The increase in the n-3 PUFA incorporation was associated with a corresponding decrease in the proportion of arachidonic acid (20 : 4n-6) in both PC and PE. Different dietary fats induce different patterns of fatty acid incorporation and substitution in the sn-2 position of the diacyl and alkylenyl PC and PE of avian breast muscle, and this finding is indicative of selective acyl remodelling in these two phospholipids.     

Increasing the dietary (n-3) to (n-6) polyunsaturated fatty acid ratio increases tumor necrosis factor production by murine resident peritoneal macrophages without an effect on elicited peritoneal macrophages.

Tumor necrosis factor (TNF), prostaglandin (PG) E2 and 6-keto-PGF1 alpha production by murine peritoneal macrophages was monitored following in vitro stimulation with lipopolysaccharide. Macrophages were obtained from mice fed diets containing increasing ratios of (n-3) to (n-6) fatty acids by addition of (n-3) polyunsaturated fatty acids (PUFA) to the (n-6) fatty acids in the diet, or by substituting (n-3) PUFA for the (n-6) fatty acids in the diet. Increasing the dietary (n-3) to (n-6) fatty acid ratio from 0 to 1 increased both cell-associated and secreted TNF production by resident peritoneal macrophages but did not affect TNF production by macrophages elicited with Complete Freund's Adjuvant (CFA). With increasing dietary (n-3): (n-6) ratio there was a decrease in the prostaglandin production by resident peritoneal macrophages, which may partly explain the increased TNF production. The CFA-elicited macrophages produced less prostaglandin than the resident macrophages, and the lower prostaglandin production may partly explain the lack of effect of dietary (n-3) PUFA on TNF production by CFA-elicited macrophages. Increasing the TNF production by resident macrophages with dietary (n-3) PUFA may be beneficial in enhancing antitumor actions and antipathogenicity; by not increasing the high TNF production of inflammatory macrophages, (n-3) PUFA may protect against undesirable systemic inflammatory effects of overproduction.     

Reduction in n-3 PUFA levels and EPA/AA ratio in serum after desert travels in China

OBJECTIVES: The effects of 3 months of desert travel in China on serum fatty acids and tocopherol were studied. METHODS: In project staff members (6 males, 3 females, aged 19-27 years), serum levels of fatty acids and alpha-tocopherol were analyzed before and after travel by gas liquid chromatography and high-performance liquid chromatography, respectively. RESULTS: Comparison of the levels before and after the trip showed no differences in serum total cholesterol, triglycerides, total protein or alpha-tocopherol. There were no changes in the levels of total fatty acids, while the percentage of polyunsaturated fatty acids increased (p < 0.05). Levels of n-3 PUFA lowered from 166 micrograms/ml to 103 micrograms/ml, and those of n-6 PUFA had increased from 988 micrograms/ml to 1140 micrograms/ml after the trip (p < 0.01 and p < 0.001, respectively). No change was observed in the serum levels of alpha-linolenic acid (C18:3n-3), but lowering of the levels of eicosapentaenoic acid (EPA, C20:5n-3) from 41.4 micrograms/ml to 16.3 micrograms/ml and docosahexaenoic acid (DHA, C22:6n-3) from 107.8 micrograms/ml to 71.7 micrograms/ml was found after the trip (p < 0.05 and p < 0.01, respectively). Serum levels of linoleic acid (LA, C18:2n-6) increased from 832 micrograms/ml to 598 micrograms/ml (p < 0.001), and arachidonic acid (AA, C20:4n-6) tended to increase. The ratios of n-3/n-6 PUFA and EPA/AA decreased from 0.171 to 0.091 and from 0.258 to 0.096 after the trip, respectively (p < 0.01 for both). CONCLUSIONS: Our findings indicated that 3 months of desert travel increased the serum levels of n-6 PUFA and LA and reduced the serum levels of n-3 PUFA and EPA and the ratios of n-3/n-6 PUFA and EPA/AA, possibly due to a relative essential fatty acid deficiency.     

Dietary polyunsaturated fat that is low in (n-3) and high in (n-6) fatty acids alters the SNARE protein complex and nitrosylation in rat hippocampus

Docosahexaenoic acid [DHA, 22:6(n-3)] is enriched in brain membrane phospholipids and is important to brain development and function through its influence on neurite outgrowth and neurotransmitter secretion. Fusion of intracellular vesicles with the plasma membrane involving SNARE [soluble N-ethylmaleimide-sensitive fusion (NSF) protein attachment protein receptor] protein assembly, membrane fusion, and then disassembly are events common in membrane extension and neurotransmitter release. We determined whether feeding an (n-3) fatty acid-deficient diet, known to reduce brain phospholipid DHA, alters SNARE protein and SNARE complex expression or protein nitrosylation in the hippocampus of rats. Female rats were fed diets with 1.3 or 0.02% energy (n-3) alpha-linolenic acid from 2 wk before gestation then throughout gestation and lactation (n = 8/diet), and the male offspring were weaned to the maternal diet. Hippocampus phospholipid fatty acids and SNARE proteins were determined in male offspring at 90 d of age. Hippocampus phospholipid DHA was lower and (n-6) docosapentaenoic acid [DPA, 22:5(n-6)] was higher in the (n-3) fatty acid-deficient rats compared with the control group (P < 0.05). Multiplex Western blots using antibodies to syntaxin, synaptosome-associated protein of 25kDa (SNAP-25), and complexin II, showed higher ternary SNARE complexes but no differences in syntaxin, SNAP-25, or complex II expression in hippocampus of the (n-3) fatty acid-deficient rats compared with the control group (P < 0.05). S-nitrosylation of syntaxin was also significantly lower in the (n-3) fatty acid-deficient rats than in the control group. These studies suggest that altered SNARE complex binding or disassembly could be important in explaining the diverse cellular events associated with altered tissue DHA.     

Mechanisms of action of (n-3) fatty acids

(n-3) PUFA are a family of biologically active fatty acids. The simplest member of this family, α-linolenic acid, can be converted to the more biologically active very long-chain (n-3) PUFA EPA and DHA; this process occurs by a series of desaturation and elongation reactions, with stearidonic acid being an intermediate in the pathway. Biological activity of α-linolenic and stearidonic acids most likely relates to their conversion to EPA. The very long-chain (n-3) PUFA have a range of physiological roles that relate to optimal cell membrane structure and optimal cell function and responses. Thus, (n-3) PUFA play a key role in preventing, and perhaps treating, many conditions of poor health and well-being. The multiple actions of (n-3) PUFA appear to involve multiple mechanisms that connect the cell membrane, the cytosol, and the nucleus. For some actions, (n-3) PUFA appear to act via receptors or sensors, so regulating signaling processes that influence patterns of gene expression. Some effects of (n-3) PUFA seem to involve changes in cell membrane fatty acid composition. Changing membrane composition can in turn affect membrane order, formation of lipid rafts, intracellular signaling processes, gene expression, and the production of both lipid and peptide mediators. Under typical Western dietary conditions, human cells tend to have a fairly high content of the (n-6) fatty acid arachidonic acid. Increased oral intake of EPA and DHA modifies the content of arachidonic acid as well as of EPA and DHA. Arachidonic acid is the substrate for eicosanoids involved in physiology and pathophysiology. The eicosanoids produced from EPA frequently have properties that are different from those that are produced from arachidonic acid. EPA and DHA are also substrates for production of resolvins and protectins, which seem to be biologically extremely potent. Increasing the contents of EPA and DHA in membranes modifies the pattern of production of these different lipid mediators.     

Associations of plasma n-3 polyunsaturated fatty acids with blood pressure and cardiovascular risk factors among Chinese

The relationship between plasma fatty acid (FA) levels and hypertension in Chinese is not fully understood. The aim of this study was to examine relationships between plasma phospholipid (PL) FAs and hypertension in Chinese subjects. One thousand one hundred and fifty-four subjects in Hangzhou, China, were recruited in this cross-sectional study. Two hundred and fourteen (160 males, 54 females) subjects with hypertension and 940 (664 males, 276 females) healthy subjects were identified. The prevalence of hypertension in females (19.6%) was significantly higher than that in males (16.4%). Compared with healthy subjects, hypertensive subjects showed significantly lower plasma PL 22:5n-3 (p?=?0.017), 22:6n-3 (p?=?0.008), PL polyunsaturated fatty acids (PUFAs; p?相似文献   

Diet (n-3) polyunsaturated fatty acid content and parity interact to alter maternal rat brain phospholipid fatty acid composition

Low tissue levels of (n-3) polyunsaturated fatty acids (PUFAs), particularly docosahexaenoic acid [DHA, 22:6(n-3)], are implicated in postpartum depression. The effects of 1-4 sequential reproductive cycles on maternal brain phospholipid fatty acid composition were determined in female rats fed diets containing alpha-linolenic acid (ALA), containing ALA and pre-formed DHA (ALA+DHA), or lacking ALA (low-ALA). Virgin females, fed the diets for commensurate durations served as a control for reproduction. Whole-brain total phospholipid composition was determined at weaning by TLC/GC. A single reproductive cycle on the low-ALA diet decreased brain DHA content by 18% compared to ALA primiparas (P < 0.05), accompanied by incorporation of docosapentaenoic acid ((n-6) DPA, 22:5(n-6)) to 280% of ALA primiparas (P < 0.05). DHA was not further decreased after subsequent cycles; however, there was an additional increase in (n-6) DPA after the second cycle (P < 0.05). Brain DHA of virgin females fed the low-ALA diet for 27 wk decreased 15% (P < 0.05), but was accompanied by a more modest increase in (n-6) DPA than in parous low-ALA dams (P < 0.05). Virgin females and parous dams fed the diet containing ALA+DHA exhibited only minor changes in brain fatty acid composition. These observations demonstrate that brain DHA content of adult animals is vulnerable to depletion under dietary conditions that supply inadequate (n-3) PUFAs, that this effect is augmented by the physiological demands of pregnancy and lactation, and that maternal diet and parity interact to affect maternal brain PUFA status.     

Association of n-3 and n-6 long-chain polyunsaturated fatty acids in plasma lipid classes with inflammatory bowel diseases

In order to establish the biochemical basis for dietary interventions, we investigated the fatty acid composition of plasma lipid classes in patients with inactive inflammatory bowel disease. In this cross-sectional study thirty patients with ulcerative colitis (UC), twenty-one with Crohn disease (CD) and twenty-four controls were investigated (mean age: UC, 40.8 (sd 12.1); CD, 37.6 (sd 11.0); control, 31.5 (sd 8.4) years). Fatty acid composition of plasma lipids was determined by high-resolution capillary GLC. In plasma phospholipids, significantly higher values of eicosapentaenoic (20 : 5n-3), docosapentaenoic (22 : 5n-3) and gamma-linolenic (18 : 3n-6) acids were found in control patients and patients with UC as compared to patients with CD [median % (weight by weight), control v. UC v. CD : 20 : 5n-3, 0.09 (interquartile range (IQR) 0.05) v. 0.14 (IQR 0.10) v. 0.16 (IQR 0.10), P < 0.05; 22 : 5n-3, 0.14 (IQR 0.10) v. 0.27 (IQR 0.16) v. 0.31 (IQR 0.10), P < 0.001; 18 : 3n-6, 0.02 (IQR 0.02) v. 0.03 (IQR 0.02) v. 0.05 (IQR 0.03), P < 0.05]. When compared to the control, values of the principal n-3 and n-6 long-chain PUFA, arachidonic acid (20 : 4n-6) and DHA (22 : 6n-3) were significantly higher in patients with UC but not in patients with CD [median % (w/w), UC v. control: 20 : 4n-6, 8.43 (IQR 3.23) v. 6.92 (IQR 2.96), P < 0.05; 22 : 6n-3, 1.22 (IQR 0.56) v. 0.73 (IQR 0.39), P < 0.05]. As seen there are considerable differences between the long-chain PUFA status of patients suffering from UC or CD. The data obtained in the present study do not support the concept of eicosapentaenoic acid or DHA deficiency in patients with either UC or CD.     

Genetic variants of the FADS1 FADS2 gene cluster are associated with altered (n-6) and (n-3) essential fatty acids in plasma and erythrocyte phospholipids in women during pregnancy and in breast milk during lactation

The enzymes encoded by fatty acid desaturase (FADS) 1 and FADS2 are rate-limiting enzymes in the desaturation of linoleic acid [LA; 18:2(n-6)] to arachidonic acid [ARA; 20:4(n-6)], and alpha-linolenic acid [ALA; 18:3(n-3)] to eicosapentaenoic acid [EPA; 20:5(n-3)] and docosahexaenoic acid [DHA; 22:6(n-3)]. ARA, EPA, and DHA play central roles in infant growth, neural development, and immune function. The maternal ARA, EPA, and DHA status in gestation influences maternal-to-infant transfer and breast milk provides fatty acids for infants after birth. We determined if single nucleotide polymorphisms in FADS1 and FADS2 influence plasma phospholipid and erythrocyte ethanolamine phosphoglyceride (EPG) (n-6) and (n-3) fatty acids of women in pregnancy or their breast milk during lactation. We genotyped rs174553, rs99780, rs174575, and rs174583 in the FADS1 FADS2 gene cluster and analyzed plasma and erythrocyte fatty acids and dietary intake for 69 pregnant women and breast milk for a subset of 54 women exclusively breast-feeding at 1 mo postpartum. Minor allele homozygotes of rs174553(GG), rs99780(TT), and rs174583(TT) had lower ARA but higher LA in plasma phospholipids and erythrocyte EPG and decreased (n-6) and (n-3) fatty acid product:precursor ratios at 16 and 36 wk of gestation. Breast milk fatty acids were influenced by genotype, with significantly lower 14:0, ARA, and EPA but higher 20:2(n-6) in the minor allele homozygotes of rs174553(GG), rs99780(TT), and rs174583(TT) and lower ARA, EPA, 22:5(n-3), and DHA in the minor allele homozygotes G/G of rs174575. We showed that genetic variants of FADS1 and FADS2 influence blood lipid and breast milk essential fatty acids in pregnancy and lactation.     

Incorporation of (n-3) fatty acids in foods: challenges and opportunities

The health benefits of long-chain (n-3) PUFA have been widely reported in the literature. Despite the potential benefits, consumption of these fatty acids continues to fall below recommendations from various health and regulatory agencies. Incorporation of long-chain PUFA in foods represents a considerable challenge due to the increased risk of lipid oxidation resulting in the development of off-flavors and reduced shelf life. As a result, new sources of (n-3) fatty acids are needed that are more efficiently converted to long-chain (n-3) fatty acids than α-linolenic acid (ALA) and can be more easily incorporated into food. Stearidonic acid [SDA, 18:4 (n-3)] is an intermediate in the desaturation of ALA to EPA. Soybeans have been modified to contain SDA. Clinical studies have demonstrated a significant increase in EPA levels when SDA is consumed. Being more stable, SDA has been added to a variety of foods and has demonstrated equal consumer acceptance compared to a regular soybean oil control. SDA-enhanced soybean oil can provide to food companies and consumers an option to increase (n-3) fatty acid consumption in foods consumers typically eat.