ECE2007 Poster Presentations (1) (659 abstracts)
Circulating retinol binding protein 4 and protein C inhibitor are not related to insulin resistance
Miriam Promintzer 1 , Michael Krebs 1 , Anton Luger 1 , Martin Georg Bischof 1 , Peter Nowotny 1 , Christoph Binder 2 , Harald Esterbauer 2 & Christian Anderwald 1
1Division of Endocrinology and Metabolism, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria; 2Clinical Institute of Medical and Chemical Laboratory Diagnostics, Medical University Vienna, Vienna, Austria.
Recent data suggest that circulating retinol binding protein-4 (RBP4) is involved in the pathogenesis of insulin resistance in rodents and humans. Moreover, protein C inhibitor (PCI) which specifically binds retinoic acid was found to be increased in myocardial infarction survivors who are also insulin-resistant.
Therefore, we investigated the association of insulin resistance with plasma retinol binding factors (RBP4 and PCI active antigen) in 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), measured by 2-h hyperinsulinemic-(40 mU•min-1•m-2)-isoglycemic clamp-tests.
M (80–120 min) was higher in IS (10.9±0.6 mg•min-1•kg-1) than in IR (4.0±0.2; P<10–12). Fasting plasma RBP4 concentrations were comparable in IS (4.4±0.3 mg/dl) and IR (4.6±0.3). Fasting plasma PCI active antigen was similar in both groups (IS: 106.6±15.6%; IR: 95.3±4.0%). Plasma RBP4 and PCI were not significantly related to M.
In conclusion, our data demonstrate that healthy, nondiabetic, insulin-resistant humans do not show altered plasma retinol binding factors, such as RBP4 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.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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