Endocrine Abstracts

Introduction: Visfatin is a protein secreted by adipose tissue which was discovered as a protein with insulin-mimetic properties. Experimental and clinical studies demonstrated that visfatin can be involved in the pathogenesis of insulin resistance. It was demonstrated that plasma visfatin is elevated in insulin resistant states i.e. obesity, type two diabetes mellitus, PCOS. In vitro study showed that insulin inhibits visfatin release from adipocytes. The aim of the present study was to evaluate serum visfatin concentration during hyperinsulinemia (6 h hyperinsulinemic euglycemic clamp) and than during insulin resistant conditions caused by an acute elevation of NEFA (6 h hyperinsulinemic clamp combined with Intralipid –heparin infusion).

Materials and methods: The study group consisted of 19 apparently healthy male volunteers (mean age 25.1±3.1 years, BMI-26.7±4.7 kg/m²). Clinical examination, anthropometric measurements, OGTT, plasma lipids and liver enzymes activity were measured. Subjects underwent 6 h euglycemic hyperinsulinemic clamp and after one week 6 h hyperinsulinemic euglycemic clamp combined with Intralipid – heparin infusion. Measurements of serum visfatin during both clamp studies were performed.

Results: 6 h of insulin infusion during clamp resulted in significant decrease in serum visfatin concentration (P=0.0057), however after 2 h there was no change in serum visfatin concentration (P=0.097). Concomitant Intralipid-heparin infusion which caused a significant increase in NEFA concentration (P<0.0001), resulted in marked increase in serum visfatin (P=0.00035) which was already observed after 2 h of Intralipid infusion (P=0.00028). Serum visfatin during clamp study after 2 h and 6 h of Intralipid infusion were significantly higher than respective values during clamp study without elevation of NEFA (both P<0.0001). The increase of serum visfatin during Intralipid infusion (δ visfatin) was positively related to body weight (r=0.54, P=0.016), %body fat (r=0.48, P=0.036) and GGTP (r=0.56, P=0.011).

Conclusion: Our data show that plasma visfatin is differentially regulated by insulin and NEFA. One might suggest that induction of insulin resistance by NEFA suppress insulin inhibition of visfatin production by adipose tissue, resulting in plasma visfatin increase in insulin resistant conditions.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details unavailable.