ECE2016 Eposter Presentations Obesity (69 abstracts)
Dubravva University Hospital, Zagreb, Croatia.
Retinol-binding protein 4 (RBP4) is considered as an important mediator of insulin resistance and metabolic syndrome (MS). In adipose tissue (AT)) it is mainly secreted from visceral depots. The residual metabolic risk which remains beyond that caused by visceral AT seems to be hold by upper body subcutaneous AT. This large pathogenic depot might be representative by subcutaneous neck AT.
The aim of this study was to examine and to compare RBP4 gene expressions in paired superficial and deep subcutaneous neck AT. We also investigated their associations with metabolic risk factors and serum RBP4.
Samples of both superficial and deep neck subcutaneous AT were taken in 38 patients during routine neck surgery. RBP4 gene expression was analysed by RQ-PCR method. Serum was taken preoperatively to determine insulin, glucose, triglycerides, HDL-cholesterol, C-reactive protein and RBP4. Anthropometric measurements and bioelectric impedance analysis were also performed. Study participants were divided in two groups - with and without MS according to revised NCEP ATP III criteria.
RBP4 gene expressions in AT and serum level were not different between our study groups. RBP4 gene expressions were significantly lower in superficial than in deep AT in the group without MS. In patients with MS different RBP4 gene expressions between layers of AT were not present. In the whole sample of participants superficial RBP4 gene expression positively correlated with fat mass, insulin and HOMA index. Serum RBP4 did not correlate with RBP4 gene expressions, but it correlated with waist circumference, insulin, HOMA index and triglycerides.
Our results indicate that superficial and deep neck subcutaneous AT might have a different secretory profile. Superficial layers with metabolically more favourable aspects are absent in subjects with MS suggesting that dysfunctional changes occur in all layers of upper body subcutaneous AT and might contribute to insulin resistance.