Context: Recent data suggest that circulating retinol binding protein (RBP) might be involved in the pathogenesis of insulin resistance. Moreover, protein C inhibitor (PCI) which specifically binds retinoic acid was found to be increased in myocardial infarction survivors who are also insulin-resistant.

Objective: The objective of this study was to investigate the association of insulin resistance with plasma retinol binding factors (RBP) and PCI active antigen.

Design and Setting: This was a clinical study.

Patients: Nondiabetic humans with high (IS; n = 20, f/m = 14/6, age: 47.2 ± 1.9 years, BMI: 26 ± 1 kg/m²) and low (IR; n = 20, f/m = 14/6, age: 45.5 ± 1.7 years, BMI: 28 ± 1 kg/m²) insulin-stimulated glucose-disposal (M) participated in this study.

Main Outcome Measures: M was measured by 2-h hyperinsulinemic-(40 mU|b1min^-1|b1m^-2)-isoglycemic clamp-tests. Measurements of RBP were performed using a nephelometric method and validated using quantitative Western blotting.

Results: M (80–120 min) was higher in IS (10.9 ± 0.6 mg|b1min^-1|b1kg^-1) than in IR (4.0 ± 0.2; P < 10^-12). Fasting plasma RBP concentrations were comparable between IS and IR measured by both, nephelometry (IS: 4.4 ± 0.3; IR: 4.6 ± 0.3 mg/dl, P = 0.6) and quantitative Western blot (IS 7.9±0.5, IR 8.3±0.6 mg/dl; P = 0.6). Fasting plasma PCI active antigen was similar in both groups. Plasma RBP and PCI were not significantly related to M. RBP was positively correlated with uric acid (r = 0.488, P = 0.003), triglycerides (r = 0.592, P < 0.001), prealbumin (r = 0.63, P < 0.0001) and vitamin A (r = 0.75, P < 10^-6).

Conclusions: Our data demonstrate that healthy, insulin-resistant humans do not show altered plasma retinol binding factors, such as RBP and PCI. Both do not significantly correlate with insulin sensitivity. Thus, our findings do not support the hypothesis of insulin sensitivity modulation by proteins involved in retinol transport.