Lysophospholipid measurements could help monitor progression of tissue damage in people at risk of developing diabetes, and perhaps the response to preventive/therapeutic Azlocillin sodium salt interventions. Another significantly perturbed lipid-related signal here was for LCFA and LCFA-carnitines. Both classes tended to be lower in the UQ than in controls. Gall et al reported that medium-chain acylcarnitines decreased in concentration with increasing insulin resistance and dysglycemia. In the population-based Cooperative Health Research in the Region of Augsburg cohort, three metabolites, namely glycine had significantly altered levels in IGT individuals as compared to those with normal glucose tolerance. Acylcarnitines are biosynthesized solely in mitochondria, where they transport fatty acids into the organelle for beta-oxidation, so decreases in their plasma levels might reflect increased mitochondrial utilisation. Here, serum levels of both LCFA and LCFA-carnitines were lower in UQ compared to control women, consistent with increased rates of tissue fatty acid utilisation in the UQ group. Such changes can occur in the glucose-sparing fuel economy that emerges in diabetes. Preferential fatty-acid utilisation may contribute to systemic hyperglycemia as recognised long ago. Our data indicate that such utilisation begins much earlier in the pathogenic process than hitherto recognised. The lowering of LCFA and LCFA-carnitines coincided with a small increase in fasting plasma glucose in the UQ group, consistent with substitution of LCFA for glucose in mitochondrial oxidation. Perturbations in LCFA metabolism have been implicated in the pathogenesis of Phthalylsulfacetamide beta-cell damage in diabetes; the early onset of altered LCFA here may lead to or cause beta-cell dysfunction/ damage. Acyl carnitine levels were elevated in pregnant women who went on to develop pre-eclampsia. By contrast, this pattern is no longer evident in the UQ/GDM comparison, where LCFA tended to be higher, probably consistent with their impaired mitochondrial oxidation, typical of insulin resistance in the former GDM group.