ESPE Abstracts

Background: Cardiovascular diseases are most relevant for morbidity and mortality in obese patients. Because metabolic complications already start in childhood obesity one may expect an early manifestation of cardiovascular disease in this group as young adults. In adults fetuin A was shown to promote adipocyte inflammation and metabolic syndrome and subsequently vascular damage.

Objective and hypotheses: We evaluated the role of fetuin A in the vascular pathogenesis in an obese childhood and adolescent cohort.

Method: As part of the weight intervention trial MAINTAIN we measured a variety of obesity associated parameters including lipids, HOMA, leptin, fetuin A and intima media thickness (IMT) in 136 obese children and adolescents.

Results: While leptin was strongly correlated with BMI-SDS, fetuin A was not correlated with BMI-SDS, waist circumference or fat-mass. Neither was fetuin A correlated with GOT, GPT or triglycerides. However we found a weak correlation of fetuin A with HOMA (r=0.189, P=0.029). In contrast fetuin A was negatively and significantly correlated with IMT (r=0.308, P<0.000).

Conclusion: We found a dual role of fetuin A in obesity comorbidity parameters in a well characterized children and adolescent obesity cohort. While fetuin A was positively –however weakly- correlated with HOMA as it was expected from the so far available data in obese adult cohorts, fetuin A was negatively correlated with IMT. This negative correlation with IMT suggest that in younger obese patients the known protective role of fetuin A to inhibit vascular calcification might still be more relevant compared to the negative influence on vascular pathogenesis triggered by pro-inflammatory effects as described in adult cohorts.