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

Abstract

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 α-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. Keywords Biomagnification. Cord serum. Fetal metabolism. Gestational diabetes. Polyunsaturated fatty acids Abbreviations AA Arachidonic acid (20:4 n-6) ALA α-Linolenic acid (18:3 n-3) C-section Caesarean section DGLA Dihomo-γ-linolenic acid (20:3 n-6) DHA Docosahexaenoic acid (22:6 n-3) EPA Eicosapentaenoic acid (20:5 n-3) GDM Gestational diabetes mellitus GLA γ-Linolenic acid (18:3 n-6) LA Linoleic acid (18:2 n-6) LCPUFA Long-chain polyunsaturated fatty acid(s) MUFA Monounsaturated fatty acid(s) OA Oleic acid (18:1 n-9) PA Palmitic acid (16:0) POA Palmitoleic acid (16:1) PUFA Polyunsaturated fatty acid(s) SA Stearic acid (18:0) SFA Saturated fatty acid(s) TAG Triacylglycerols Electronic supplementary material The online version of this article (

Adiponectin agonist treatment in diabetic pregnant rats

“…DHA was strongly reduced in plasma of GDM and GDM + ADI adult offspring. Reduced DHA status has been extensively described in the cord blood of GDM women ( Min et al 2005 , Pagan et al 2013 , Ortega-Senovilla et al 2020 ), but here we report the long-term deleterious consequences of GDM on the FA in the offspring. AdipoRon treatment during pregnancy did not improve the DHA level of GDM + ADI but was effective to reduce the unbalanced n-6/ n -3 PUFA ratio observed in GDM offspring.…”

Foetal hyperinsulinaemia and increased fat mass correlate negatively with circulating fatty acid concentrations in neonates of gestational diabetic mothers with dietary‐controlled glycaemia

“…20 This supports the possibility, observed herein, that under conditions of GDM, the utilization of those LCPUFA is increased by foetal tissues, and contributes to the expansion of adipose tissue. Moreover, the reduction in circulating foetal fatty acids could generate a maternal-foetus concentration gradient in favour of the foetus, 21 which could explain the lower concentration of some fatty acids observed in maternal GDM serum.…”

“…This could explain the increased utilization of AA and DHA by foetuses affected by GDM observed in other populations 20 and the higher foetal dependence on maternal AA and DHA previously reported. 21…”

“…19 However, there is no evidence relating cord serum fatty acid concentrations to foetal growth and adiposity. We have previously found that the proportions of arachidonic acid (AA, 20:4 n-6) and docosahexaenoic acid (DHA, 22:6 n-3) are lower in umbilical arterial but not in umbilical venous plasma in neonates of GDM mothers versus controls, 20 and that GDM decreases the concentration of most individual fatty acids in cord serum, 21 suggesting that there are prenatal factors that contribute to altered handling of LCPUFA in the foetus of GDM mothers.…”

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“…External factors have recently been associated with the pathogenesis of T1DM as causes and potentiators of beta cells degradation. These factors are, but not limited to, intestinal microbiota, viral infections, vaccination, cow's milk consumption, vitamin D deficiency, polyunsaturated fatty acids, glycemic index, toxins and chemicals [3][4][5][6][7]. Type 2 Diabetes mellitus (T2DM) was formerly referred to as either non-insulin-dependent diabetes or adult-induced diabetes.…”