Send to

Choose Destination
Lipids. 2004 Apr;39(4):335-42.

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

Author information

Institute of Brain Chemistry and Human Nutrition, London Metropolitan University, London, N7 8DB, United Kingdom.


The activity of delta6- and delta5-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), sigman-6 metabolites (P < 0.0001), docosapentaenoic acid (22:5n-3, P < 0.0001), DHA (22:6n-3, P < 0.0001), sigman-3 (P < 0.0001), and sigman-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), sigman-6 metabolites (P < 0.05), DHA (P< 0.0001), and sigman-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.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center