Plasma VAP-1 concentration and activity during lifestyle-induced body weight reduction

Vascular adhesion protein 1 (VAP-1) is a 170 kDa glycoprotein with amine oxidase activity (SSAO-activity). Endothelial cells and adipocytes were suggested to release a soluble VAP-1 into the bloodstream. Previous data showed an association between the plasma VAP-1 with chronic liver diseases and HbA1c-values in T2DM. VAP-1-mediated generation of oxidative stress was suggested to promote cardiovascular mortality.

To estimate the role of adipocytes in VAP-1 release, we assessed VAP-1 concentration and SSAO-activity in 60 overweight patients with diagnosed metabolic syndrome during a 6-month lifestyle induced weight loss program.

The participants reduced their BMI about 12,8% (IQR 8,3%-17,1%) and the body fat mass about 23,6%. ALAT, total cholesterol, serum triglycerides, LDL, fasting blood glucose, fasting insulin, HbA1c and HOMA-index lowered significantly. However, neither the VAP-1 concentration nor the SSAO-activity changed significantly in the weight loss or control group.

We expected reduced plasma VAP-1 concentrations because the body fat mass decreased. In contrast to our expectation, VAP-1 concentration and SSAO activity remained constant. Hence, we speculate that adipocytes do not represent the main source of soluble VAP-1 in non-diabetic subjects. This assumption is in line with a recent publication (Carpene et al, 2016) concerning the missing coherence between VAP-1 concentration in adipocytes and plasma arguing against a direct release mechanism.

We conclude that plasma VAP-1 is not directly released from adipose tissue. A more complex release mechanism involving also endothelial cells and releasing factors is likely, hence soluble VAP-1 does not seem to represent a suitable biomarker for metabolic diseases.