The present study addresses the question whether nervonic acid (24:1n-9) accumulation in sphingomyelin (SM) of red blood cells (RBC) could yield information on cerebrum maturation in premature infants. The study included 28 premature eutrophic infants of 31.5 wk gestational age. Eleven were fed with human milk, nine with a regular formula and eight with an alpha-linolenate-enriched formula. The fatty acid composition of the SM fraction was determined by gas-liquid chromatography on a 50-m fused silica capillary column. At 32 wk gestational age, the main fatty acids in SM were 16:0, 18:0, 20:0, 22:0, 24:0 and 24:1n-9. After five weeks of feeding, at week 37 of postconceptional age, the most striking variation was a rise in 24:1n-9, from 9.9 +/- 0.7 to 12.8 +/- 0.9 (P < 0.02), regardless of regimen in all three feeding groups. The rise in 24:1n-9 after birth in premature eutrophic infants is the beginning of a trend toward the higher levels in 24:1n-9 observed in mature newborns and older infants. The 24:1n-9 level in SM of RBC from premature infants may reflect 24:1n-9 levels in SM of brain and could thus reflect brain maturity.

Objective: To evaluate the polyunsaturated fatty acid (PUFA) status in non-institutionalised elderly women and to detect a possible essential fatty acid bioconversion defect. Design and subjects: The fatty acid composition of total plasma lipids, plasma triglycerides (TG), cholesterol esters (CE), phospholipids (PL), and erythrocytes was determined by capillary column gas-liquid chromatography in a sample of 200 non-institutionalised healthy elderly women over 75 years of age. The data were compared with those of a control group of 50 young female volunteers aged 20 ± 48 y. Results: In elderly women, the n-6 series precursor, linoleic acid (18:2 n-6), was lower in TG and CE (P 0.029 and 0.014, respectively). In CE, this fatty acid was highly correlated with vegetable and vegetal fat intakes (P`0.0001), suggesting a lower dietary supply than in controls. Higher percentages of 16:1 n-7 were found in all the plasma lipid fractions in elderly women, especially in CE (P`0.0001). The ratios 20:4 n-6a20:3 n-6 and 22:6 n-3a20:5 n-3 were signi®cantly lower in PL from elderly women (P`0.005 and P`0.002, respectively), raising the question of the ef®ciency of the terminal steps of 20:4 n-6 and 22:6 n-3 biosynthesis. Dietary investigations in elderly women indicated that a high dietary protein intake via meat probably contributed to the supply of 20:4 n-6 and thus maintained the status of this fatty acid, despite the suspected altered biosynthesis. Conclusion: The PUFA status in the elderly women group could be more fragile and dependent on exogenous supply of long-chain PUFAs than previously suspected. Descriptors: non-institutionalised elderly women; polyunsaturated fatty acid; D5 desaturase; peroxisomal b oxidation; de®ciency; plasma lipid fractions; erythrocyte; capillary gas-chromatography

Objective: To investigate the effects of a milk formula supplemented with a a-linolenic acid (ALA) (18:2 n-6/ 18:3 n-3 ratio near 6/1) on plasma and red blood cell (RBC) fatty acids (FAs) in premature infants and compare with a non supplemented formula (18:2 n-6/18:3 n-3 22/1). Design and subjects: Infants of mothers who elected not to breast-feed were randomly assigned to either a high a linolenic formula (HLF: n 31) group or a low a-linolenic formula (LLF: n 32) control group. Infants fed human milk (HM: n 25) were enrolled concurrently as a reference group. Anthropometric and biological measurements were made after two days (D2) and 15 d (D15) of enteral feeding and at the 37th week (W37) of postconceptual age. In HLF, the 18:3 n-3 content was 1.95% of total FAs (0.77% of total energy) and the 18:2 n-6/18:3 n-3 ratio was near 6/1. In LLF, the 18:3 n-3 content was 0.55% of total FAs (0.22% of total energy) and the 18:2 n-6/18:3 n-3 ratio was 22/1. Results: ALA supplementation had minimal effect on the n-6 series, did not alter the anthropometric data and con®rmed the conversion of ALA into docosahexaenoic acid (DHA). Throughout the study, it maintained, the RBC membrane DHA values within the con®dence interval of those obtained in the HM group. Such was not the case with LLF Conclusion: a-linolenic acid supplementation (from Rapeseed oil and in a 18:2 n-6/18:3 n-3 ratio 6) in premature infant formula can contribute ef®ciently to the maintenance of the n-3 status in the premature newborns Descriptors: essential fatty acids; a-linolenic acid; docosahexaenoic acid; plasma; erythrocyte; preterm infant; infant formula; capillary gas chromatography; Rapeseed oil

Objective: To evaluate a-linolenic acid (ALA) (18X3 n-3) and linolenic acid (LA) (18X2 n-6) in cholesterol esters (CE) as markers of ALA and LA dietary intakes in preterm infants. Subjects: Forty-®ve preterm infants: two groups fed different formulas, the third fed human milk. Design: ALA and LA dietary intakes were precisely recorded in each infant to accurately determine the cumulative amount of ingested ALA and LA during two intervals: (i) between the second day after the ®rst signi®cant formula intake (D0) and the ®fteenth day (D15); and (ii) between D0 and the ®rst day of the 37th week of post-conception age (W37). The corresponding amounts of ingested ALA and LA were related to ALA and LA levels determined by capillary column gas ± liquid chromatography in plasma cholesterol esters at D15 and W37, respectively. Results: ALA in CE was very signi®cantly correlated to D0 ± D15 and D0 ± W37 ALA intakes (0.66; P 0.0001 and 0.70; P 0.0001), respectively. LA in CE was weakly correlated to D0 ± D15 LA intakes (0.03; P 0.01) and whatever the group (human milk or enriched formula) the correlation was lost at W37. Conclusion: In preterm infants, ALA in CE can be considered as representative of ALA dietary intakes, whereas LA in CE appears as a poor marker of LA intakes. Descriptors: a-linolenic acid; linoleic acid; dietary intake; cholesterol esters; preterm infant

The total and free fatty acid composition of plasma and lipid peroxide concentrations was studied in 32 cholestatic children with syndromatic paucity of interlobular bile ducts (Alagille’s syndrome). The mean lipid peroxide value in these patients was 8.80 ± 3.70 nmol/ml, nearly 4 times higher than the mean control value. Compared to the control group, the patients exhibited significant variations in total fatty acids, and in particular a relative decrease in linoleic acid (from 29.5 ± 6.1 % in the controls to 19.1 ± 8.03% in the patients) compensated by an increase in saturated and monounsaturated fatty acids. The plasma lipid peroxide levels were inversely correlated with the unsaturated/saturated fatty acids ratio in total fatty acids, and with the vitamin E status (vitamin E/total lipids). Most of the total and free fatty acid variations observed were largest in patients with severe jaundice. Dietary fat malabsorption and the increase in lipid peroxidation partly explain these results. Furthermore, in free fatty acids, we observed a marked increase in arachidonic acid (from 1.43 ± 0.85% in the controls to 4.27 ± 2.24% in the patients), suggesting abnormal eicosanoid synthesis.