Plasma leptin levels and digital pulse volume in obese patients without metabolic syndrome--a pilot study.

The mechanism of obesity leading to endothelial function is complex, and involves many adipokines and inflammatory cytokines. The data is especially lacking in obese patients without metabolic syndrome. We assessed the relationship among endothelial dysfunction, anthropometric indices, adipokines and inflammatory cytokines in this population. Obese patients without metabolic syndrome were included in this study. The plasma resistin, leptin, retinol-binding-protein 4 and inflammatory cytokines were examined. Endothelial function was assessed by a fingertip peripheral arterial tonometry (PAT) device. Data are expressed as the natural logarithm (ln) of the PAT ratio. Endothelial dysfunction was defined by a ln (PAT ratio) <0.30. A total of 35 patients were enrolled, 11 of whom were with endothelial dysfunction. There was a significant difference of ln leptin (p=0.007), ln [leptin/visceral fat thickness] (p=0.004) and ln [leptin/subcutaneous fat thickness] (p<0.001) between patients with and without endothelial dysfunction. Multivariate linear regression analyses showed that ln [leptin/subcutaneous fat thickness] was significantly related to the ln (PAT ratio) (p=0.002). Using ln [leptin/subcutaneous fat thickness] to detect endothelial dysfunction, the area of receiver operating characteristic curves was 0.843 (p=0.002). Using 6.10 as a cutoff point, the sensitivity and specificity to determine endothelial dysfunction were 91% and 78%, respectively. Abnormal digital vascular function occurs in obese patients without metabolic syndrome. Low plasma leptin/subcutaneous fat ratio is associated with endothelial dysfunction in this population.