Insulin resistance and not BMI is the major determinant of early vascular impairment in patients with morbid obesity.

AIM

Several factors contribute to the development of atherogenesis in patients with obesity. The aim of our study was to evaluate the different roles of insulin resistance, strictly correlated to visceral adiposity, and the body mass index (BMI), an estimate of overall adiposity, on early vascular impairment in patients with morbid obesity.

METHODS

We enrolled 65 morbidly obese subjects (BMI 44.6 ± 7 kg/m(2)) who were free of previous cardiovascular events and 28 nonobese subjects (control group) in a cross-sectional study. The presence of glycemia and insulinemia, the levels of lipids and liver parameter and the ultrasonographic assessment of the flow-mediated dilatation (FMD), carotid intima-media thickness (IMT) and visceral fat area (VFA) were evaluated in all subjects.

RESULTS

In the obese patients with a median HOMA value of ≥ 3.5, the FMD was significantly lower (p < .05) and the left carotid maximum-IMT was significantly higher (p < .05) than those observed in the group with lower HOMA values. No vascular differences were found between the two groups that were subdivided according to the BMI median value. Both the left max-IMT and FMD exhibited a significant correlation with HOMA-IR ("ρ" .292, p=0.02 , "ρ"-.292, p=0.02 respectively) but not with BMI. According to a multivariate analysis, the VFA was an independent predictor of a reduced FMD (β - .541, p.002; p of the model .002), while age (β .611 p < .0001) and HOMA-IR (β .399 p < .001) were independent predictors of the left max-IMT (p of the model .002).

CONCLUSIONS

The HOMA-IR, which is strictly related to visceral fat and is an index of metabolic impairment, and not BMI, which reflects of global adiposity, can be used to identify early vascular impairment in patients with morbid obesity.