Leukocyte ABCA1 is known to protect against atherosclerosis in animals, but our observations cannot distinguish between possible direct and indirect effects of leukocyte ABCA1 on lipid transport. ABCA1 expression was decreased in leukocytes from patients with T2DM and was directly related to the level of glycaemia. Most of the decline in gene expression occurred up to an HbA1c level of 7.5%, with little further fall above this value. Our ABCA1 expression data are compatible with and extend our previous findings in healthy men. We further demonstrate concordant changes in leukocyte ABCA1 expression and Paclitaxel 33069-62-4 protein concentrations in patients with T2DM. Our leukocyte expression results appear to contrast with the findings reported by Hoang and colleagues who did not find a difference in leukocyte ABCA1 expression between patients with diabetes and controls. This previous study was conducted in a smaller cohort with one third of patients receiving hypoglycaemic medications. ABCA1 function was assessed on the basis of the ability of the subject‘s plasma to induce cholesterol efflux from human macrophages cell lines. There were baseline differences in lipid parameters which may have had an effect on the capacity of plasma to induce cholesterol efflux. Our findings are compatible with previous data in monocytes, where reduced ABCA1 expression was observed in patients with diabetes and dyslipidaemia. Our results contrast with studies that showed reduced expression and function of ABCG1 in monocytes and macrophages in people with T2DM, but these earlier studies were not designed or conducted in drug naive patients who were free of complications. In the study by Mauldin and colleagues, information pertaining to age, other medical conditions and drug treatments was unavailable. Forty percent of participants studied by Zhou et al., had evidence of retinopathy or nephropathy and all were receiving either oral hypoglycaemic treatments or insulin treatment. It is feasible that hypoglycaemic treatments may have contributed to the observed discrepancies in the relationship between circulating glucose and ABCG1 expression. For example, insulin decreases human macrophage ABCA1 and ABCG1 gene expression in vitro. Animal studies indicate that complications such as nephropathy independently reduce macrophage ABCA1 and increase cellular cholesterol content. Treatment of nephropathy in this study restored ABCA1- mediated cholesterol efflux in macrophages. The present study has the advantage of having matched controls and patients who were drug naive and free of diabetes related complications. Skin fibroblasts were used to assess ABCA1 function in our study. Skin fibroblasts have been previously employed for this purpose, where functional consequences of ABCA1 genetic variants have been studied.