Effects of gestational alcohol exposure on the fatty acid composition of umbilical cord serum in humans

Citation
Ym. Denkins et al., Effects of gestational alcohol exposure on the fatty acid composition of umbilical cord serum in humans, AM J CLIN N, 71(1), 2000, pp. 300S-306S
Citations number
46
Categorie Soggetti
Endocrynology, Metabolism & Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
AMERICAN JOURNAL OF CLINICAL NUTRITION
ISSN journal
00029165 → ACNP
Volume
71
Issue
1
Year of publication
2000
Supplement
S
Pages
300S - 306S
Database
ISI
SICI code
0002-9165(200001)71:1<300S:EOGAEO>2.0.ZU;2-C
Abstract
This study examined the effects of maternal periconceptional alcohol intake on polyunsaturated fatty acid (PUFA) concentrations in human neonates. The area percentage of each fatty acid in cord blood serum from 12 infants bor n to control women (who consumed <2 mt absolute ethanol/d) was compared wit h that of 9 infants born to women whose periconceptional alcohol intake ave raged greater than or equal to 30 mt absolute ethanol/d. Periconceptional a lcohol use was associated with a 30% increase in the proportion of docosahe xaenoic acid (22:6n-3) in cord blood (3.0% of total lipid in control infant s compared with 3.9% in alcohol-exposed infants; P < 0.01). The rise in the proportion of 22:6n-3 was responsible for increases in the ratio of n-3 to n-6 fatty acids and the ratio of long-chain n-3 to n-6 fatty acids (P < 0. 055). Examination of the lipid-class fatty acid profile indicated that seru m lipid alterations were localized to the cholesterol esters; 22:6n-3 in th e cholesterol esters of alcohol-exposed infants increased 54% (P < 0.011) a nd arachidonic acid increased 55% (P < 0.005). The relative fatty acyl comp osition of maternal serum showed a significant increase in 18:0 fatty acids in the alcohol-exposed group (25%, P < 0.005) but there were no changes in the other fatty acids. The increase in the proportion of 22:6n-3 was unexp ected but is consistent with the hypothesis that this essential lipid may b e conserved selectively. These results imply that the lifelong neurobehavio ral and sensory dysfunction in fetal alcohol syndrome and other alcohol-rel ated neurodevelopmental disorders may be due in part to PUFA dysregulation.