Another complex metabolic alteration change more prominent in the UQ/GDM comparison is a tendency to increased numbers of SCFA and SCFA-metabolites. Elevated SCFA and SCFA metabolites suggest their defective utilisation, as in diabetes, again occurring earlier than Norethindrone hitherto realised. Shikimate 3phosphate an obligatory intermediate in the anabolic pathway for biosynthesis of the essential aromatic amino acids, is potentially a microbial metabolite not produced in human cellular metabolism. Some SCFA-metabolites identified may originate from microbial biosynthesis. The identification of microbial metabolites in human plasma with possible links to defective glucoregulation could point to between-group differences in their production by gut microflora and/or uptake from the gut. Other identified metabolic features, as in terpenoid/quinones and teasterone/typhasterol may be of plant origin, consistent with possible differences in dietary intake and/or uptake from the gut. We also found that significantly lower circulating adiponectin levels occurred before measurable alterations in insulin or leptin levels. Adiponectin deficiency occurs from infancy, as found in the children of this cohort and may influence GDM and T2DM. It is associated with defective glycosylation and functionality, such as impaired ability to stimulate hepatic or muscle mitochondrial fatty acid oxidation via AMP kinase. Adiponectin deficiency could provide a central link between perturbed phosphatidylcholine metabolism and mitochondrial lipid UNC669 utilisation here. However, whether changes in production/secretion and/or signalling of known hormones including adiponectin really antedate or rather result from the described metabolic changes remains uncertain. It is certainly known that adiponectin deficiency can cause these changes but together with the exact nature and origin of the adiponectin deficiency observed here, requires further longitudinal study. In summary, we identified here a rather consistent pattern of metabolic perturbations in groups of women whose diabetes risk was stratified a priori by differences in their degree of glucoregulatory impairment during a previous pregnancy.