Pregnant women with gestational diabetes and with well controlled glucose levels have decreased concentrations of individual fatty acids in maternal and cord serum

Aims/hypothesis Both arachidonic acid (AA, 20:4 n-6) and docosahexaenoic acid (DHA,22:6 n-3), long-chain polyunsaturated fatty acids (LCPUFA), are involved in fetal development and, based on their percentage compositions, appear to be specifically accumulated in fetal circulation in a proposed phenomenon known as biomagnification. Discrepancies exist in the literature concerning the effect of gestational diabetes mellitus (GDM) on circulating fatty acids. Our objective was to analyse individual fatty acid concentrations in a large cohort of maternal and cord paired serum samples from pregnant women with and without GDM. Methods Overnight fasted maternal and cord blood paired samples from 84 women with GDM and well controlled blood glucose levels and 90 healthy pregnant women (controls) were drawn at term. Individual fatty acids within total serum lipids were analysed by gas chromatography and expressed both as concentrations of fatty acid (mmol/l) and as a percentage of total fatty acids. Results In the serum of overnight fasted pregnant women with GDM, the concentrations of most fatty acids were lower than in control women, except for AA and DHA, which remained the same. The concentrations of most fatty acids in cord serum were also lower in the GDM group than in the control group, except for alpha-linolenic acid (ALA,18:3 n-3), which was higher in the GDM group. In both groups, the concentrations of all fatty acids were lower in cord serum than in maternal serum. In GDM participants only, a positive and significant correlation between cord and maternal serum concentration of AA and DHA was observed. Conclusions/interpretation The expression of fatty acids in molar concentrations reveals that GDM decreases the concentration of most fatty acids in both maternal and cord serum. There is a high fetal dependence on maternal AA and DHA, but our findings do not support the existence of a fetal biomagnification of those two LCPUFA.