In contrast to their within-pregnancy glucose tolerance, glycaemic indices at re-testing were not different between the UQ and GDM groups, although both were marginally defective compared to controls, yet still within the usual, ��currently normal�� glycaemic range. Pair-wise between-group comparisons pinpointed relatively circumscribed subsets of defined metabolite classes related to elevated diabetes risk. Those metabolite classes perturbed in the UQ compared with control women included: phospholipid subclasses, in particular phosphatidylcholines; LCFA; LCFAcarnitines; SCFA and SCFA-metabolites. Other perturbed classes included diglycerides; bile acids; steroids; CGP 57380 prostanoids; and amino acid metabolites. Most of these belong to lipid sub-classes. The greatest differences here were in the acyl carnitine class. Prominent differences in phosphatidylcholines were identified in both the control/UQ and UQ/GDM contrasts. Diacyl-phosphatidylcholines has been shown to be independently associated with increased risk of type 2 diabetes in a prospective study of type 2 diabetes patientst. Phospholipids are highly insoluble in aqueous media so these molecules will have originated in membranous structures in plasma, namely lipoproteins; this suggests that differences in phosphatidylcholine composition are related and could contribute to glucoregulatory transitions preceding hyperglycemia. Alterations in additional lipid classes including those of steroids/bile acids, and diglycerides are also probably related to Norethindrone changes in lipoprotein metabolism. Consistent with these findings, diabetes itself is associated with prominent changes in plasma lipoprotein content. This disturbance in phospholipid metabolism cannot be localised or characterised further here since the observed changes could reflect alterations in any or all of the HDL, LDL, or VLDL fractions. Prominent alterations in LDL-particle composition have previously been identified in diabetes pathogenesis, lipoproteinbound phospholipids are reportedly targets of glycoxidationmediated damage, and oxidized phospholipids can become pathogenic.