Comparative study of maternal and cord plasma fatty acids in women with and without gestational diabetes

Thomas, Beverley (2004) Comparative study of maternal and cord plasma fatty acids in women with and without gestational diabetes. Doctoral thesis, London Metropolitan University.

Abstract

Aim/Hypothesis:
Arachidonic (AA) and Docosahexaenoic (DHA) acids are major structural and functional components of mammalian neural and vascular systems. Adequate maternal stores are required to support optimum fetal growth and development. Adverse clinical conditions can impair the maternal ability to synthesise AA and DHA during the prenatal period, and have the potential to compromise placental supply to the fetus and hence influence birth outcomes. Gestational diabetes mellitus (GDM), a transient metabolic disorder, is associated with reduced proportions of Arachidonic (AA) and Docosahexaenoic (DHA) in maternal and fetal red cell membrane phospholipids (RBC PL). It is not clear whether this abnormality in these women is restricted to red cells or is a generalised problem. Fatty acids are incorporated into RBC through an exchange of fatty acids from circulating plasma, but data on plasma fatty acid profiles in these women is scarce. We have examined maternal and cord plasma fatty acid composition in women with and without gestational diabetes. The effect of conventional nutritional and therapeutic management (diet therapy and insulin treatment), on plasma fatty acids of the gestational diabetics, was also examined.

Method:
Women were recruited and underwent a 75g oral glucose tolerance test (OGTT) between week 28-32 (Control n=40, GDM n=40). Those diagnosed as GDM were advised to reduce refined carbohydrate, total and saturated fat, and to increase complex carbohydrate and fibre. No dietary advice was given to alter polyunsaturated intake. All women completed a 4-day food record of intake and dietary assessment was carried out using a computerised nutritional database. Maternal blood was taken at time of OGTT (at diagnosis) and delivery, and cord blood at delivery. Lipids were extracted by a modification to the Folch method. Fatty acids were analysed by GC as methyl esters (FAME) and expressed as % of total fatty acids (mean ± SD). Maternal plasma lipid profile was used as a measure of dietary intake. Cord plasma lipid profile was used to indicate a shortfall in the placental supply to the fetus.

Results:
Relative to controls, newly diagnosed women with GDM, had higher (plasma choline phoshoglyceride, CPG and cholesterol esters, CE, p<0.0001) or comparable (plasma triglyceride, TG) levels of AA, and higher (TG, p<0.05) or comparable (CPG & CE) levels of DHA. Dietary assessment revealed that compared with the non-diabetics, the women with GDM had reduced intakes of dietary energy (p<0.05), total and saturated fat, and added sugar (p<0.0001). In addition, they had a concomitant increase in intake of fibre (p<0.05) and complex carbohydrate. Intake of linoleic, a-linolenic and arachidonic acids did not differ, but as a group the women with GDM consumed more DHA g/day (p<0.05) than the non-diabetics. The high DHA intake was attributed to increased fish consumption in the GDM women of Afro-Caribbean ancestry. Fatty acid composition was independent of diet or insulin treatment. There was a weak, but significant relationship between dietary LA and corresponding plasma LA, but no such association was found for dietary ALA, AA or DHA and respective plasma fatty acid. However, GDM in combination with obesity (body mass index > 25.0) appeared to influence levels of n-6 and n-3 fatty acids. Cord plasma fatty acid composition was relatively comparable between the women with and without GDM. Nevertheless, there was a trend for the n-6 and n-3 fatty acids to be reduced in the GDM group.

Conclusion:
Consistent with studies in red cells, GDM induces abnormal maternal and fetal plasma fatty acid profiles. This abnormality was independent of dietary or insulin treatment. From the current findings it is clear that GDM had an opposing effect on maternal plasma and red cell membrane PL. Hence we conclude that our previous data demonstrating striking reductions in maternal and fetal red cell membrane PL AA and DHA of women with GDM was unlikely to be the result of altered plasma lipids. Further studies are required to elucidate the other mechanisms which may be responsible.

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