001), TNF-R1 (P=0.029) and TNF-R2 (P=0.044) than LD− patients.

Moreover, CD68 and MCP-1 gene expression showed a positive correlation with circulating FABP-4 level (P=0.022 and P=0.046, respectively) while PPAR-γ expression showed a negative correlation with circulating FABP-4 level in the HIV-1-infected group as a whole. When analyses of these relationships were carried out separately in the LD+ and LD− groups, FABP-4 remained positively correlated only with CD68 expression in the LD+ group (P=0.031). No other significant correlations with FABP-4 plasma level were observed. This study provides some meaningful insights into the involvement of FABP-4 in cART-related lipodystrophy in HIV-1-infected patients. We observed systemic overproduction of FABP-4 in cART-treated GSK-3 assay HIV-1-infected patients with lipodystrophy and found that those with a plasma FABP-4 level in the highest tertile had a higher prevalence of lipodystrophy. Furthermore, GSK2118436 solubility dmso we found that FABP-4 was one of the major determinants of the degree of insulin resistance in HIV-1-infected patients, and this association was independent of body fat distribution. We also observed a close relationship between FABP-4 and inflammatory markers both in plasma and in SAT. The biological role

of circulating FABP-4 is not well understood, but the association observed between serum FABP-4 level and the development of atherosclerosis, metabolic syndrome and type 2 diabetes suggests that plasma FABP-4 levels may parallel its tissue expression and activity. In our HIV-1-infected

cohort, FABP-4 levels were similar to those observed in the control group, despite the difference between the groups in BMI, suggesting that other inflammatory factors could play a role in the regulation of this protein in this population. The observed increase in circulating FABP-4 levels in LD+ HIV-1-infected subjects is consistent with some previous reports in which this protein was evaluated in the context of HIV-1 infection. Similar to our results, Coll and colleagues reported that the level of circulating FABP-4 was higher in HIV-1-infected patients with lipodystrophy compared with nonlipodystrophic subjects, and was closely correlated with BMI and insulin level [12]. However, in that study no measurements of inflammatory parameters or insulin resistance were made. In our cohort, findings for HIV-1-infected patients were Cyclin-dependent kinase 3 similar to those for the uninfected group, and the plasma FABP-4 level was clearly associated with BMI, HOMA-IR index, inflammatory markers and dyslipidaemia. Regarding insulin sensitivity, in an analysis of the variables associated with the HOMA-IR index, we found that FABP-4 level was one of the variables most strongly associated with insulin sensitivity, irrespective of the presence or absence of lipodystrophy. Interestingly, significant associations between FABP-4 plasma level and inflammatory markers expressed in adipose tissue were found mainly in LD+ patients.