Type 1 diabetes compromises plasma arachidonic and docosahexaenoic acids in newborn babies

The activity of Δ6- and Δ5-desaturase, enzymes required for the synthesis of AA and DHA, are impaired in human and experimental diabetes. We have investigated whether neonates of type 1 diabetic women have compromised plasma AA and DHA at birth. Cord blood was obtained from healthy babies born to mothers with (n=31) and without (n=59) type 1 diabetes. FA composition of plasma choline phosphoglycerides (CPG), TG, and cholesterol esters (CE) was assayed. The neonates of the diabetics had lower levels of AA (20∶4n−6, P<0.0001), adrenic acid (22∶4n−6, P<0.01), Σn−6 metabolites (P<0.0001), docosapentaenoic acid (22∶5n−3, P<0.0001), DHA (22∶6n−3, P<0.0001), Σn−3 (P<0.0001), and Σn−3 metabolites (P<0.0001) in CPG compared with the corresponding babies of the nondiabetic mothers. Similarly, they had lower levels of AA (P<0.05), Σn−6 metabolites (P<0.05), DHA (P<0.0001), and Σn−3 metabolites (P<0.01) in plasma CE. There was also a nonsignificant reduction of AA and DHA in TG in the babies of the diabetic group. The current investigation indicates that healthy neonates born to mothers with type 1 diabetes have highly compromised levels of AA and DHA. These nutrients are of critical importance for neurovisual and vascular system development. In poorly controlled maternal diabetes, it is conceivable that the relative “insufficiency” of AA and DHA may exacerbate speech and reading impairments, behavioral disorders, suboptimal performance on developmental tests, and lower IQ, which have been reported in some children born to mothers with type 1 diabetes mellitus. Further studies are needed to understand the underlying mechanism for this biochemical abnormality and its implications for fetal and infant development.     

Retinal fatty acids of piglets fed docosahexaenoic and arachidonic acids from microbial sources

Docosahexaenoic acid (DHA, 22∶6n-3) and arachidonic acid (AA, 20∶4n-6) serve important roles in perinatal visual and neural development. A neonatal pig model was used to determine if dietary supplementation with DHA and AA at slightly greater concentrations than normally found in human milk would influence fatty acid accretion in retina. One-day-old piglets were assigned to one of four diets (n=5/group): (i) STD, standard diet containing fat similar to infant formula; (ii) STD+DHA, 0.7% of fatty acids as DHA; (iii) STD+AA, 0.9% as AA; and (iv) STD+BOTH, 0.8% as DHA plus 1.0% as AA. After 25 d, fatty acids in retina phosphatidylcholine (PC) and phosphatidylethanolamine (PE) were determined. Supplementation with DHA resulted in approximately twofold increases (P<0.05) in PC-DHA (4.88% in STD vs. 10.03% in STD+DHA and 9.47% in STD+BOTH). Similarly, AA supplementation increased PC-AA 1.3–1.4-fold (4.47% in STD vs. 6.19% in STD+AA and 5.70% in STD+BOTH). For PE, supplementation with either fatty acid or in combination resulted in no significant increases, except for a 1.2-fold increase in DHA for STD+BOTH (32.66%) vs. STD (28.38%). Thus, PC responded to dietary supplementation, with addition of DHA, AA, or BOTH, resulting in increases in respective fatty acids; PE was less responsive, with only STD+BOTH resulting in increased DHA. No significant competition between DHA and AA in incorporation into phospholipids was observed. In conclusion, consumption of a combination of DHA and AA by neonatal pigs supported accretion of DHA in retina phospholipids, while simultaneously supplying the AA necessary for membrane phospholipids and eicosanoid biosynthesis. Based on a presentation at the AOCS Annual Meeting & Expo in San Antonio, Texas, May 7–11, 1995.     

Effect of dietary α-linolenic acid intake on incorporation of docosahexaenoic and arachidonic acids into plasma phospholipids of term infants

The fractional conversion rates of plasma phospholipid α-linolenic acid (18:3n-3) and linoleic acid (18:2n-6) to docosahexaenoic acid (22:6n-3) and arachidonic acid (20:4n-6), respectively, and the fractional rates of incorporation of 22:6n-3 and 20:4n-6 into plasma phospholipids were determined in 27 healthy 3-wk-old term infants who had received formulas with ≈16% of fat as 18:2n-6 and 0.4% (n=6), 1.0% (n=11), or 3.2% (n=10) as 18:3n-3 from birth. The infants were given a single dose of both [U-¹³C] 18:2n-6 and [U-¹³C]18:3n-3 with a feeding, and blood samples were collected 8, 12, and 24 h afterward for determination of the isotopic enrichments of the [M+18] isotopomers of plasma phospholipid fatty acids by negative chemical ionization gas chromatography/mass spectrometry. A simple precursor/product compartmental model was used to estimate fractional rates of conversion and incorporation. All infants converted 18:3n-3 to 22:6n-3 and 18:2n-6 to 20:4n-6. Although the fractional rate of conversion of 18:3n-3 to 22:6n-3 did not differ among groups, the fractional rate of incorporation of 22:6n-3 into the plasma phospholipid fraction was greater in infants who received 3.2% vs. 0.4% or 1.0% 18:3n-3 (4.1±2.2 vs 1.6±1.5 or 2.0±1.0% of the plasma phospholipid 22:6n-3 pool daily). The fractional rate of conversion of 18:2n-6 to 20:4n-6 was less in infants who received the 3.2% 18:3n-3 intake (0.4±0.3% of the plasma phospholipid 18:2n-6 pool daily vs. 1.1±0.7% and 0.8±0.5% in those who received 0.4 and 1.0% 18:3n-3, respectively). The fractional rate of incorporation of 20:4n-6 into plasma phospholipid also was less in the 3.2% vs. the 0.4 and 1.0% 18:3n-3 groups (2.7±1.4% vs. 5.9±2.6 and 4.4±1.7%, respectively, of the plasma phospholipid 20:4n-6 pool daily).     

The relative incorporation of arachidonic and eicosapentaenoic acids into human platelet phospholipids

The incorporation of arachidonic acid (AA) as compared to eicosapentaenoic acid (EPA) into human platelet phospholipids was tested by incubating washed platelets with a known mixture of [³H]AA and [¹⁴C]EPA. Following incubation, the platelet lipids were extracted, the individual phospholipids—phosphatidylcholine (PC), phosphatidylserine (PS), phosphatidylinositol (PI) and phosphatidylethanolamine (PE)—were separated by thin layer chromatography, and their corresponding [³H]/[¹⁴C] ratios were determined. Based on a [³H]/[¹⁴C] ratio of unity for the substrate mixture, the PC, PS, PI and PE exhibited ratios of 0.55, 0.93, 1.12 and 0.74, respectively, which were significantly different from 1.00 in all instances except in the case of PS. These results indicate that PC and PE selectively incorporated EPA, while PI showed preference toward AA. These selectivities may account partly for the differing AA/EPA mass ratios that have been observed among the individual phospholipids of human subjects consuming fish oils.     

Dietary supplementation with arachidonic and docosahexaenoic acids has no effect on pulmonary surfactant in artificially reared infant rats

Despite the potential use of long-chain polyunsaturated fatty acid (LCPUFA) supplementation to promote growth and neural development of the infant, little is known about potential harmful effects of the supplementation. The present study determined whether supplementation with arachidonic acid (AA) and/or docosahexaenoic acid (DHA) in rat milk formula (RMF) affects saturation of pulmonary surfactant phospholipids (PL). Beginning at 7 d of age, infant rats were artificially fed for 10 d with RMF supplemented with AA at 0, 0.5, and 1.0% of total fatty acid, or supplemented with DHA at 0, 0.5, and 1.0%, or cosupplemented with AA and DHA at levels of 0∶0, 0.5∶0.3, and 1.0∶0.6% of the fat blend. Lung tissue PL contained 43 weight percent palmitate (16∶0) of total fatty acids in infant rats fed the unsupplemented RMF. The supplementation with AA at both 0.5 and 1.0% decreased the weight percentage of 16∶0 and stearate (18∶0), indicating a decrease in saturation of PL. The observed decreases were accompanied by increases in AA and linoleic acid (18∶2n−6). Surfactant phosphatidylcholine (PC) consisted of 71 weight percent 16∶0 in the unsupplemented group, and this highly saturated PC was not altered by the cosupplementation with AA and DHA although there was a slight increase in DHA. Similarly, the cosupplementation did not change fatty acid composition of surfactant PL when compared with the unsupplemented group. The cosupplementation slightly decreased the weight percentage of 16∶0 with a proportional increase in 18∶0 leading to an unchanged weight percentage of total saturated fatty acids. These results suggest that, unlike lung tissue PL, the composition of saturated fatty acids in surfactant PL, particularly PC, is resistant to change by dietary AA and DHA supplementation. This, together with the unchanged concentration of total fatty acids in surfactant PC, indicates that LCPUFA cosupplementation causes no effect on pulmonary surfactant.     

The potential role for arachidonic and docosahexaenoic acids in protection against some central nervous system injuries in preterm infants

The risk of central nervous, visual, and auditory damage increases from 2/1000 live births in the normal birthweight to >200/1000 as birthweight falls below 1500 g. Such babies are most likely to be born preterm. Advances in infant care have led to increasing numbers of very-low-birthweight, preterm infants surviving to school age with moderate to severe brain damage. Steroids are one of the current treatments, but they cause significant, long-term problems. The evidence reported here suggests an additional approach to protecting the very preterm infant by supporting neurovascular membrane integrity. The complications of preterm, very-low-birthweight babies include bronchopulmonary dysplasia, retinopathy of prematurity, intraventricular hemorrhage, periventricular leukomalacia, and necrotizing enterocolitis, all of which have a vascular component. Arachidonic acid (AA) and DHA are essential, structural, and functional constituents of cell membranes. They are especially required for the growth and function of the brain and vascular systems, which are the primary biofocus of human fetal growth. Molecular dynamics and experimental evidence suggest that DHA could be the ligand for the retinoid X receptor (RXR) in neural tissue. RXR activation is an obligatory step in signaling to the nucleus and in the regulation of gene expression. Very preterm babies are born with minimal fat stores and suboptimal circulating levels of these nutrients. Postanatally, they lose the biomagnification of the proportions of AA and DHA by the placenta for the fetus. No current nutritional management repairs these deficits. The placental biomagnification profile highlights AA rather than DHA. The resultant fetal FA profile closely resembles that of the vascular endothelium and not the brain. Without this nourishment, cell membrane abnormalities would be predicted. We present a scientific rationale for a common pathogenic process in the complications of prematurity.     

Mechanism of decreased arachidonic acid in the renal cortex of rats with diabetes mellitus

The purpose of this study was to investigate the roles of decreased synthesis and increased consumption in the depression of arachidonic acid levels in renal cortex and glomeruli of rats with streptozotocin-induced diabetes mellitus. In diabetic rats, arachidonic acid was depressed 33.2% in renal cortex, 47.4% in liver and 66.1% in heart compared to values of control rats. Δ6 Desaturase activity was depressed in renal cortex, liver and heart of diabetic rats to 53.3, 55.5 and 63.7%, respectively, of control values. Δ5 Desaturase activity was also depressed 43.7, 55.5 and 47.6% in renal cortex, liver and heart of diabetic rats, respectively. In other rats the activities of five enzymes involved in the synthesis and esterification of arachidonic acid were measured in renal cortex and in isolated glomeruli. Both tissues from diabetic rats showed depressed activities of Δ5 and Δ6 desaturases, increased activities of long-chain acyl-CoA synthetase and 1-acyl-sn-glycero-3-phosphocholine acyltransferase and no change in the activity of elongase as compared to those in control tissues. Malondialdehyde, an end product of lipid peroxidation, was lower in the renal cortex of diabetic rats than in control rats, whereas β-oxidation of linoleic acid and arachidonic acid were similar in diabetic and in control rats. Basal and stimulated prostaglandin E² synthesis were significantly higher in isolated glomeruli from diabetic rats compared to those in control rats. In isolated tubules, prostaglandin E₂ synthesis was similarly low in both groups. From these data we conclude that the reduced level of arachidonic acid esterified in lipids of the kidney cortex is caused principally by depressed synthesis of arachidonic acid secondary to decreased activity of Δ5 and Δ6 desaturases. Increased consumption of arachidonic acid to support prostaglandin synthesis may have contributed to the depression of arachidonic acid in glomeruli but not in tubules.     

Effects of omega-3 fatty acids on vascular smooth muscle cells: Reduction in arachidonic acid incorporation into inositol phospholipids

A rapid increase in arachidonic acid incorporation into phosphatidylinositol (PI) occurred following exposure of cultured porcine pulmonary artery smooth muscle cells to calcium ionophore A23187. This response was specific for PI and phosphatidic acid; none of the other phosphoglycerides showed any increase in arachidonic acid incorporation. The incorporation of [³H]inositol also was increased, indicating that complete synthesis of PI rather than only fatty acylation occurred in response to the ionophore. The presence of omega-3 fatty acids, especially eicosapentaenoic acid (EPA), reduced arachidonic acid but not inositol incorporation into PI. Stimulated incorporation of EPA also occurred under these conditions, suggesting that EPA replaces arachidonic acid in the newly synthesized pool of PI. Although much less arachidonic acid was incorporated into the polyphosphoinositides following exposure to the ionophore, arachidonic acid incorporation into these phosphorylated derivatives also decreased when EPA was present. These findings suggest that when omega-3 fatty acids are available, less arachidonic acid is channeled into the inositol phospholipids of activated smooth muscle cells because of replacement by EPA. This may represent a mechanism whereby omega-3 fatty acids, especially EPA, can accumulate in the metabolically active pools of inositol phospholipids and thereby possibly influence the properties or responsiveness of vascular smooth muscle.     

Blood lipid docosahexaenoic and arachidonic acid in term gestation infants fed formulas with high docosahexaenoic acid,low eicosapentaenoic acid fish oil

The effect of fish oil high in docosahexaenoic acid (22∶6n−3) and low in eicosapentaenoic acid (20∶5n−3) in formula on blood lipids and growth of full-term infants was studied. Infants were fed formula with about 15% oleic acid (18∶1), 32% linoleic acid (18∶2n−6), 4.9% linolenic acid (18∶3n−3) and 0, 0.10 or 0.22% 22∶6n−3, or 35% 18∶1, 20% 18∶2n−6, 2.1% 18∶3n−3 and 0, 0.11 or 0.24% 22∶6n−3 from 3 d to 16 wk of age (n=16, 18, 17, 21, 17, 16, respectively). The formulae had <0.1% 20∶5n−3 and no arachidonic acid (20∶4n−6). Breast-fed infants (n=26) were also studied. Plasma phospholipid and red blood cell (RBC) phosphatidylcholine (PC) and phosphatidylethanolamine (PE) fatty acids were determined at 3 d and 4, 8, and 16 wk of age. These longitudinal analyses showed differences in blood lipid 22∶6n−3 between breast-fed and formula-fed infants depending on the feeding duration. At 16 wk, infants fed formula with 0.10, 0.11% 22∶6n−3, or 0.22% 22∶6n−3 had similar 22∶6n−3 levels in the plasma phospholipid and RBC PC and PE compared with breast-fed infants and higher 22∶6n−3 than infants fed formula without 22∶6n−3. Formula with 0.24% 22∶6n−3, however, resulted in higher plasma phospholipid 22∶6n−3 than in breast-fed infants at 16, but not 4 or 8 wk of age. Plasma and RBC phospholipid 20∶4n−6 was lower in formula-fed than breast-fed infants, but no differences in growth were found. Higher blood lipid C₂₀ and C₂₂ n−6 and n−3 fatty acids in infants fed formula with 20% 18∶2n−6 and 2.4% 18∶3n−3 compared with 32% 18∶2n−6 and 4.9% 18∶3n−3 show the increase in blood lipid 22∶6n−3 in response to dietary 22∶6n−3 depending on other fatty acids in the formula.     

Chemoenzymatic synthesis of structured triacylglycerols containing eicosapentaenoic and docosahexaenoic acids

There are indications in the recent literature that the location of polyunsaturated fatty acids, such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), in triacylglycerols (TAG) may influence their oxidative stability. To address that question, two types of structured lipids were designed and synthesized: firstly, a TAG molecule possessing pure EPA or DHA at the mid-position with stearic acid at the outer positions; and secondly, a TAG molecule possessing pure EPA or DHA located at one of the outer positions with stearic acid at the mid-position and the remaining end position. The former adduct was synthesized in two steps by a chemoenzymatic approach. In the first step 1,3-distearolyglycerol was afforded in good yield (74%) by esterifying glycerol with two equivalents of stearic acid in ether in the presence of silica gel using Lipozyme^TM as a biocatalyst. This was followed by a subsequent chemical esterification with pure EPA or DHA using 1-(3-dimethylaminopropyl)-3-ethylcarbodiimide as a coupling agent in the presence of 4-dimethylaminopyridine in dichloromethane in excellent yields (94 and 91, respectively). The latter adduct was synthesized in two enzymatic steps. In the first step tristearoylglycerol was prepared in very high yield (88%) by esterifying glycerol with a stoichiometric amount of stearic acid under vacuum at 70–75°C using an immobilized Candida antarctica lipase without a solvent. That adduct was subsequently treated in an acidolysis reaction with two equivalents of EPA or DHA without solvent at 70–75°C or in toluene at 40°C in the presence of Lipozyme to afford the desired product in moderate yields (44 and 29%, respectively). This work was presented at the Biocatalysis Symposium in April 2000, held at the 91st Annual Meeting and Expo of the American Oil Chemists’ Society, San Diego, CA.     

The metabolism of linoleic and arachidonic acids in rat testis

Linoleic and arachidonic acids, labeled with¹⁴C and injected intratesticularly, were used to study with time the interconversion of polyunsaturated fatty acids in rat testis and their incorporation into the major lipid classes. With both substrates¹⁴C activity was readily incorporated into longer chain, more highly unsaturated fatty acids. After the injection of 1-¹⁴C-linoleic acid the major portion of the¹⁴C was found in palmitic, linoleic, 8,11,14-eicosatrienoic, 5,8,11,14-eicosatetraenoic, 7,10,13,16-docosatetraenoic and 4,7,10,13,16-docosapentaenoic acids. Hydrogenation of the total fatty acids isolated from rat testes after intratesticular injection of 1-¹⁴C-linoleate revealed that the polyenoic acids hydrogenating to lignoceric acid (previously characterized as 9,12,15,18-tetracosatetraenoate and 6,9,12,15,18-tetracosapentaenoate) had a relatively high specific activity. After the injection of 1-¹⁴C-arachidonate significant¹⁴C activity was found in palmitate, 7,10,13,16-docosatetraenoate, 4,7,10,13,16-docosapentaenoate, 9,12,15,18-tetracosatetraenoate and 6,9,12,15,18-tetracosapentaenoate. The biosynthesis of the ω⁶ polyunsaturated fatty acids in rat testis is discussed in relation to these data. Investigation of the distribution of label in the complex lipid fractions demonstrated the majority of the¹⁴C activity to be present in phosphatides and triglycerides after injection of either of these¹⁴C substrates with only small quantities being present as nonesterified acids. At the time periods studied the polyenoic acids of triglycerides had a higher specific activity than the corresponding acids of phosphatides with the exception of linoleate. Presented in part at the Meeting of the American Institute of Nutrition, Atlantic City, April 1968 and at the AOCS Meeting in New York, April 1969. These data were taken from a thesis submitted by R. B. Bridges in partial fulfillment of the requirements for the Ph.D. degree, Vanderbilt University.     

Incorporation of arachidonic acid and eicosapentaenoic acid into phospholipids by polymorphonuclear leukocytes in vitro

The present study demonstrated that the patterns of the incorporation of [1-¹⁴C] arachidonic acid and [1-¹⁴C] eicosapentaenoic acid into individual phospholipids by polymorphonuclear leukocytes were similar. However, human leukocytes exhibited higher activity than guinea pig periotoneal leukocytes in the formation of arachidonoyl- and eicosapentaenoyl-phosphatidic acid. Cells from both origins showed a decrease of label in phosphatidylcholine accompanied by an increase of label in phosphatidylethanolamine after a longer period (30–120 min) of incubation, suggesting that part of the arachidonoyl or eicosapentaenoyl moiety in phosphatidylethanolamine may be derived from that of phosphatidylcholine. The observed difference between human cells and elicited cells in the time-course of the incorporation of both fatty acids into phosphatidylcholine and phosphatidylethanolamine appears to be due to different contents of the diacyl and ether-linked class compositions of these phospholipids in cells from different origins. Both labeled fatty acids were incorporated more rapidly into the diacyl-linked class, but were retained to a greater extent in alkylacyl-phosphatidyl-choline and alkenylacyl-phosphatidylethanolamine. The data suggest that, in addition to alkylacyl-phosphatidylcholine and phosphatidylinositol, alkenylacyl-phosphatidylethanolamine may be an important endogenous source of arachidonic acid and eicosapentaenoic acid in stimulated human leukocytes.     

Relative incorporation of linoleic and arachidonic acid in phospholipids and triglycerides of different rat tissues

Fat-deficient rats were fed different amounts of methyl linoleate for increasing periods of time. The fatty acid composition of triglycerides and phospholipids of epididymal fat pad, epirenal fat depot, intestinal fat depot, liver, and the pool of heart, kidney, lungs and pancreas was determined. The distribution of the total amount of linoleic and arachidonic acid incorporated into phospholipids and triglycerides per rat was calculated. Phospholipids and triglycerides of depot tissues presented different fatty acid compositions. Although the phospholipids of liver and the pool of heart, kidney, lung and pancreas specifically incorporated linoleic acid at the beginning they very rapidly attained a rather steady composition, whereas triglycerides went on incorporating the acid. The amount of linoleic acid incorporated into the phospholipids of depot tissues was rather small. The triglycerides undoubtedly contributed in the highest proportion to the total pool of linoleic acid. However, the highest proportion of arachidonic acid was found in the total pool of phospholipids. The total amount of linoleic acid incorporated into the phospholipids was an approximately lineal function of the amount of phospholipids independent of period of administration and doses of methyl linoleate. Besides presenting two lineal functions of the amount of phospholipids, arachidonic acid showed a vertical increase coincident with a vertical decrease of the amount of eicosa-5,8,11-trienoic acid. At this period no change in the amount of the phospholipid was shown. This phenomenon is explaioned as a possible direct replacement of eicosatrienoic acid by arachidonic acid.     

Comparative bioavailability of dietary alpha-linolenic and docosahexaenoic acids in the growing rat

Animal and human studies have indicated that developing mammals fed only α-linolenic acid (18∶3n−3) have lower docosahexaenoic acid (22∶6n−3) content in brain and tissue phospholipids when compared with mammals fed 18∶3n−3 plus 22∶6n−3. The aim of this study was to test the hypothesis that low bioavailability of dietary 18∶−3 to be converted to 22∶6n−3 could partly explain this difference in fatty acid accretion. For that purpose, we determined the partitioning of dietary 18∶3n−3 and 22∶6n−3 between total n−3 fatty acid body accumulation, excretion, and disappearance (difference between the intake and the sum of total n−3 fatty acids accumulated and excreted). This was assessed using the quantitative method of whole-body fatty acid balance in growing rats fed the same amount of a 5% fat diet supplying either 18∶3n−3 or 22∶6n−3 at a level of 0.45% of dietary energy (i.e., 200 mg/100 g diet). We found that 58.9% of the total amount of 18∶3n−3 ingested disappeared, 0.4% was excreted in feces, 21.2% accumulated as 18∶3n−3 (50% in total fats and 46% in the carcass-skin compartment), and 17.2% accumulated as long-chain derivatives (14% as 22∶6n−3 and 3.2% as 20∶5n−3+22∶5n−3). Similar results were obtained from the docosahexaenoate balance (as % of the total amount ingested): disappearance, 64.5%; excretion, 0.5%; total accumulation, 35% with 30.1% as 22∶6n−3. Thus, rats fed docosahexaenoate accumulated a twofold higher amount of 22∶6n−3, which was mainly deposited in the carcass-skin compartment (68%). Similar proportions of disappearance of dietary 18∶−3 and 22∶6n−3 lead us to speculate that these two n−3 polyunsaturated fatty acids were β-oxidized in the same amount.     

Availability of arachidonic acid in major phospholipids of mucosa and the stomach wall of rats

The purpose of this study was to examine the availability of arachidonic acid in phosphatdidylcholine (PC) and phosphatidylethanolamine (PE) of mucosa and the stomach wall of adult male Wistar rats fed a standard diet. There were significant differences in the fatty acid composition of PC and PE between various parts of the stomach. The mucosa had the lowest level of arachidonic acid (20:4n-6) in PC, followed by the corresponding stomach wall or glandular part, whereas the forestomach or the upper part had the highest level of 20:4n-6. The level of 20:4n-6 in PE was identical in gastric mucosa and the stomach wall of both the lower and upper parts. The levels of 18:1n-9 and 18:2n-6 were significantly higher in both PC and PE of mucosa than in the stomach wall. The levels of 16:0 and 18:0 in PC were lower in mucosa than in either forestomach or the glandular part. In mucosal PE, the levels of 18:0 and 22:6n-3 were lower than in forestomach and glandular part. The glandular part had significantly higher level of 16:0 and lower level of 20:4n-6 in PC compared to the forestomach. Conclusions: The arachidonic acid level of PC was significantly different in various parts of the rat stomach, with the lowest level in mucosa, whereas the level of 20:4n-6 in PE was identical in mucosa and stomach wall. These phospholipids had higher levels of saturated fatty acids in the stomach wall than in gastric mucosa.     

Fetal erythrocyte phospholipid polyunsaturated fatty acids are altered in pregnancy complicated with gestational diabetes mellitus

Insulin resistance and altered maternal metabolism in gestational diabetes mellitus (GDM) may impair fetal arachidonic acid (AA) and docosahexaenoic acid (DHA) status. The objectives were to test the hypothesis that fetal polyunsaturated fatty acids would be altered with GDM and identify factors related to fetal phospholipid (PL) AA and DHA. Maternal and cord vein erythrocyte PL fatty acids were determined in GDM (n=13) and healthy pregnant women (controls, n=12). Cord vein erythrocyte PL AA and DHA concentrations were significantly lower in GDM vs. controls. Maternal blood hemoglobin A₁C was inversely correlated to fetal erythrocyte PL DHA and AA in controls and GDM (n=25). Pregravid body mass index was negatively associated with fetal PL DHA. The data support the hypothesis that there is impairment in fetal accretion of DHA and AA in GDM.     

Essential fatty acids in maternal diet and in rat milk phospholipids

The administrations of semisynthetic diets supplemented with oils and fats containing different levels of linoleic acids to lactating rats result in corresponding changes in the polyunsaturated fatty acids of triglycerides in the collected milk. Milk phospholipids show a quite different trend, polyunsaturated acids of the linoleic acid family being highest with low dietary linoleic acid supply, and vice versa, suggesting a control in the secretion of polyunsaturated fatty acids in milk.     

Human placental lipid metabolism. III. Synthesis and hydrolysis of phospholipids

Both diacyl GPC (glycerylphosphorylcholine) and diacyl GPE (glycerylphosphorylethanolamine) are synthesized in human placental tissue from their respective monoacyl precursors. The origin of the monacyl phosphatides is apparently not the result of placental phosphatide acyl-hydrolase activity. The most likely source is maternal serum. The declining level of 1-acyl GPC in maternal serum is not attributable to lysophosphatide acylhydrolase activity and is probably explained by placental utilization for the synthesis of diacyl GPC.