Susan B. Johnson

A comparison of pyrrolidide and picolinyl ester derivatives for the identification of fatty acids in natural samples by gas chromatography-mass spectrometry.

The pyrrolidide and picolinyl ester derivatives of the fatty acids in two natural lipid samples rich in unsaturated fatty acids, pig testis lipids and cod liver oil were satisfactorily resolved on capillary columns of fused silica coated with stationary phases of varying polarity. The picolinyl esters, in particular, when subjected to gas chromatography-mass spectrometry on a column containing a cross-linked methyl silicone, gave distinctive mass spectra, which could be interpreted in terms of both the numbers and positions of the double bonds.

The effect of isomerictrans-18∶1 acids on the desaturation of palmitic, linoleic and eicosa-8,11,14-trienoic acids by rat liver microsomes

The inhibitory effects of the positional isomers oftrans-18∶1 acids on the desaturation of palmitic acid to palmitoleic (Δ9-desaturase), linoleic to γ-linolenic (Δ6-desaturase) and eicosa-8,11,14-trienoic to arachidonic acid (Δ5-desaturase) were investigated. Thesetrans-18∶1 acids were found to be inhibitory for the microsomal Δ6-, Δ9- and Δ5-desaturases of rat liver. The position of the double bond in thetrans-18∶1 acids seems to be important in determining the degree of inhibition. At inhibitor/substrate ratio of 3∶1, the Δ6-desaturase was most strongly inhibited bytrans-Δ3,-Δ4,-Δ7 and-Δ15-18∶1 isomers, whereas the Δ9-desaturase was most strongly inhibited bytrans-Δ3,-Δ5,-Δ7,-Δ10,-Δ12,-Δ13 and-Δ16 isomers. At inhibitor/substrate ratio of 6∶1, the Δ5-desaturase was most strongly inhibited by Δ3-, Δ9-, Δ13- and Δ15-isomers. When 18∶0 was added to the incubations of 16∶0, 18∶2 and 20∶3 at the same I/S ratios used for thetrans-18∶1 acids, weak inhibition for Δ9-desaturase and no inhibition for Δ5-and Δ6-desaturases was observed.

Serum arachidonic acid levels in normal and preeclamptic pregnancies

Fifteen serum samples from 11 women with preeclampsia and 19 samples from 10 normal third-trimester pregnancies were analyzed for total nonesterified fatty acids and total nonesterified arachidonic acid. The percentages of arachidonic acid in nonesterified fatty acids, in phospholipids, in triglycerides, and in cholesterol esters were also measured in each sample. The same analyses were done on serum from six samples of cord blood from each group. Cord blood sera from preeclamptic and normal pregnancies had much less total nonesterified fatty acids than the corresponding maternal sera but had much higher percentages of arachidonic acid in each of the major lipid categories. The maternal phospholipids and cholesterol esters had higher proportions of arachidonic acid in preeclampsia than in normal pregnancy. Samples from placentas of preeclamptic pregnancies had significantly lower proportions of arachidonic acid in the nonesterified fatty acids and triglycerides than normal placentas. These findings suggest a decreased availability of arachidonic acid in the fetal circulation which may result in decreased production of prostacyclin in preeclampsia.

Reduced adipose 18∶3ω3 with weight loss by very low calorie dieting

The human undergoing rapid and sustained weight loss by very low calorie dieting (VLCD) derives the majority of daily energy needs from adipose fatty acids. To evaluate the rates of metabolic utilization of individual fatty acids in humans, two groups of adult women outpatients were studied during major weight loss by VLCD. The diets used were either food or formula, providing the recommended dietary allowance for minerals and vitamins, with fat contents of 2–20 g/d. Group 1 consisted of 10 subjects [initial body mass index (BMI) 32.7, 157% of ideal body weight (IBW)] with a mean loss of 17.7 kg in 3–5 months. Group 2 consisted of 14 subjects (initial BMI 36.7, 167% of IBW) with a mean loss of 25.6 kg in 4–5 months. Adipose tissue biopsies were obtained by needle aspiration from Group 1 before and after weight loss and from Group 2 before, at the midpoint, and after weight loss. With weight loss in Group 1, the adipose tissue content of 18∶1ω9, 18∶2ω6, and 20∶4ω6 did not change, but 18∶3ω3 fell (0.67 to 0.56 wt%, p<0.0001) as did 20∶5ω3 (0.08 to 0.05, p<0.01). Adipose tissue 22∶6ω3 rose from 0.03 to 0.07 (p<0.01). In Group 2, only 18∶3ω3 showed a change, falling from 0.71 to 0.69 to 0.59 wt% across weight loss (p=0.03 by analysis of variance). We conclude that the major fatty acids are oxidized in proportion to their composition in adipose triglyceride. The significant reduction in the concentration of 18∶3ω3 during weight loss is unique among fatty acids. Its accelerated removal from adipose tissue indicates either a preferential step in β-oxidation or a defined need during supplemented fasting which exceeds its rate of provision from adipose stores.

Effects of biotin deficiency on plasma and tissue fatty acid composition: evidence for abnormalities in rats.

ABSTRACT: Abnormalities of fatty acid composition have been detected in the plasma of patients who developed frank biotin deficiency during parenteral nutrition. We sought to determine which abnormalities of fatty acid composition, if any, would be replicated in the biotindeficient rat and to determine the relative temporal relationships of these abnormalities to biotin nutritional status. We measured fatty acid compositions of the phospholipids extracted from plasma, heart, and liver and assessed biotin nutritional status longitudinally in biotin-deficient and biotin-treated rats during progressive biotin deficiency. In the biotin-deficient group, significant increases relative to the biotin-treated group were detected in all three tissues in the odd-chain fatty acids 15:0 and 17:0. In the biotindeficient rats, significant increases in 18:2ω6 in liver and 18:3ω6 in plasma and liver and significant decreases in 22:5ω6 were detected in plasma and liver. The constellation of fatty acid abnormalities observed in the biotin-deficient rats was not identical to that observed in biotin-deficient patients, but abnormalities in composition of odd-chain fatty acids were detected in both human and rat and therefore are attributable to biotin deficiency per se. The abnormalities in fatty acid composition were already present by wk 4 on the egg white diet; the cutaneous findings appeared between wk 3 and 6. These observations are consistent with the hypothesis that an abnormality in fatty acid metabolism may play a pathogenetic role in the cutaneous manifestations of biotin deficiency.

Simplified derivatization for determining sphingolipid fatty acyl composition by gas chromatography—mass spectrometry

A simple procedure for simultaneously derivatizing non-hydroxy and hydroxy fatty acids prior to GC analysis [I. Ciucanu and F. Kerek, J. Chromatogr., 284 (1984) 179] has been evaluated for its usefulness in determining sphingolipid acyl composition. The method uses methyl iodide in polar aprotic solvents to generate methyl esters of carboxyl groups and methyl ethers of hydroxyl groups. Methylation efficiency is examined as a function of hydroxyl group presence and location in free fatty acids as well as a function of 2-hydroxy fatty acid chain length. Conditions are also reported for efficient saponification and derivatization of sphingolipid fatty acyl chains as is illustrated using bovine brain galactosylceramide.

Fatty acid pattern of tissue phospholipids in copper and iron deficiencies

Because copper and iron have been reported to be essential cofactors in Δ9 desaturation of fatty acids, the effects of different dietary intakes of copper and iron on tissue fatty acids were studied. Male Long-Evans rats (ten per group) were fed diets containing adequate, deficient or excess copper or iron. On day 42 of the dietary regimen, the animals were killed and tissues and blood were removed for analysis of metals and fatty acids of phospholipids. Compared with the copper-adequate rats, the copper-deficient rats showed increased 18∶0 in liver and decreased 16∶1ω7 in liver, heart and serum. There were no differences for 16∶0 or 18∶1ω9. Intake of excess copper did not cause an increase in products of Δ9 desaturation. Comparisons between iron-deficient and iron-adequate rats showed that iron deficiency increased 18∶2ω6 in liver and serum and decreased 20∶4ω6 in serum only. Relative percentages of 16∶0, 18∶0, 16∶1ω7 and 18∶1ω9 in liver and serum phospholipids were similar for both groups. Intake of excess iron caused a decrease in 18∶2ω6; and 16∶0 and 18∶1ω9 were higher in the liver of the iron-excess group than the iron-deficient group. This study did not support the requirement for copper or iron in the Δ9 desaturation of fatty acids as expressed in phospholipids of liver, heart and serum.

A Review of Scales to Assess Family Needs

Public Law 99-457 requires an Individual Family Service Plan (IFSP) rather than an Individualized Education Plan (IEP) for families with children (birth to 2 years) who have developmental delays or who are at-risk for developmental delays. The importance of a family focus, however, extends beyond the infant and toddler population into the preschool and school-age population as well. One of the components that is specified as part of IFSP development is the assessment of family needs and priorities. This article presents a review and evaluation of published and unpublished assessment instruments that are currently available for assessing family needs. Fifteen scales that have been mentioned in the literature as possible instruments to use in assessing family needs were reviewed in terms of administration format, content validity, and psychometric characteristics.

Polyunsaturated fatty acids of serum lipids in myocardial infarction.

Two groups of volunteers had blood drawn for serum analysis of fatty acids. The first group was comprised of patients admitted to the hospital with possible myocardial infarction (MI). Blood was drawn at admission and at 12, 24 and 48 hr. These patients were subsequently divided into three groups, those with MI, those without (No MI) and those taking prostaglandin inhibitors (PGI), on the basis of the cardiac enzymes, electrocardiograms and clinical history. A fourth group of Normal nonstressed people was also drawn at 0, 12, 24 and 48 hr for comparison. Fatty acid composition of phospholipids (PL), nonesterified fatty acids (NEFA), triglycerides (TG) and cholesteryl esters (CE) was determined by capillary gas chromatography (GC), and comparison were made between the MI, No MI, PGI and Normal groups. Total NEFA were significantly elevated in patients admitted for possible MI compared with Normals. Those patients with MI had marginally higher levels of NEFA than the No MI group at each sampling time, but this difference was not statistically significant. The MI, No MI and PGI groups had significantly different fatty acid patterns in NEFA with reduced percentages of arachidonic acid (AA) than controls. The fatty acid patterns in the four lipid classes showed few significant differences comparing the MI, No MI and PGI groups. The regular use of prostaglandin inhibitors before hospitalization for chest pain was associated with a reduced frequency of MI (p<0.002). NEFA levels, nonesterified AA levels and fatty acid patterns in this group did not differ from those patients not taking prostaglandin inhibitors.

Determination of ester carbonyl 18O/16O ratios in phospholipids by gas chromatography-mass spectrometry

A method is described for the quantitation of 18O enrichment in phospholipid acyl groups. Methyl esters are prepared by transesterification with sodium hydroxide in methanol and are hydrogenated prior to gas chromatography-mass spectrometry (GC-MS). Estimation of 18O content of the resulting esters is made using the m/z 74 and m/z 76 fragments, which contain both the ester oxygens. The accuracy of the method is demonstrated with synthetic methyl esters and phosphatidylcholines containing a known amount of 18O.