Type 1 diabetes compromises plasma arachidonic and docosahexaenoic acids in newborn babies
Kebreab Ghebremeskel1, Beverley Thomas, Clara Lowy
1Institute of Brain Chemistry and Human Nutrition, London Metropolitan University, London, N7 8DB, United Kingdom. keb@kebgm.demon.co.uk
Insights
Healthy newborns of mothers with type 1 diabetes have significantly lower levels of essential fatty acids arachidonic acid (AA) and docosahexaenoic acid (DHA) at birth. These deficiencies may impact neurovisual and vascular development in infants.
Area of Science:
- Biochemistry
- Neonatal Health
- Maternal-Fetal Medicine
Background:
- Enzyme activity for arachidonic acid (AA) and docosahexaenoic acid (DHA) synthesis is reduced in diabetes.
- Type 1 diabetes in mothers may affect nutrient transfer to the fetus.
Purpose of the Study:
- To determine if neonates born to mothers with type 1 diabetes have lower plasma levels of AA and DHA at birth.
- To investigate the fatty acid composition in different plasma lipid fractions.
Main Methods:
- Cord blood samples were collected from neonates of mothers with (n=31) and without (n=59) type 1 diabetes.
- Fatty acid composition of plasma choline phosphoglycerides (CPG), triglycerides (TG), and cholesterol esters (CE) was analyzed.
Main Results:
- Neonates of diabetic mothers showed significantly lower levels of AA, adrenic acid, sigma-n-6 metabolites, docosapentaenoic acid, DHA, sigma-n-3, and sigma-n-3 metabolites in CPG.
- Lower levels of AA, sigma-n-6 metabolites, DHA, and sigma-n-3 metabolites were observed in CE.
- A non-significant reduction in AA and DHA was noted in TG.
Conclusions:
- Healthy neonates born to mothers with type 1 diabetes exhibit compromised levels of AA and DHA.
- These essential fatty acids are crucial for neurovisual and vascular development.
- Potential implications for cognitive and developmental outcomes in children of mothers with type 1 diabetes warrant further investigation.
Abstract:
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.
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