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Division of Diabetes, Nutrition, and Metabolic Disorders, Department of Medicine, C.H.U. Sart- Tilman, B-4000 Liège, Belgium; and Clinical Physiology Unit, School of Medicine, University of Granada, Granada, Spain
Address correspondence and requests for reprints to: Prof. A. J. Scheen, Division of Diabetes, Nutrition, and Metabolic Disorders, Department of Medicine, C.H.U. Sart Tilman, B-4000 Liège 1, Belgium.
Abstract
Inhibition of tumor necrosis factor (TNF)-
results in a marked
increase in insulin sensitivity in obese rodents. We investigated the
influence of a TNF antagonist [Ro 45-2081, a recombinant fusion
protein that consists of the soluble TNF-receptor (p55) linked to the
Fc portion of human IgG1] on insulin sensitivity of patients with
android obesity. Seven patients (five women and two men; mean ±
SD age, 41 ± 4 yr; body mass index, 36.1 ± 4.7
kg/m2; waist to hip ratio, 0.99 ± 0.11) were studied
(three patients with normal glucose tolerance and four patients with
impaired glucose tolerance or mild diabetes; all were
hyperinsulinemic). Each patient underwent two consecutive euglycemic
hyperinsulinemic glucose-clamp tests: 48 h after injection of
placebo and 48 h after a single iv injection of 50 mg Ro 45-2081.
In both tests, steady-state plasma glucose and insulin levels were
similar. Insulin-mediated glucose disposal (2.23 ± 0.74
vs. 2.38 ± 0.99
mg/kg-1·min-1) and glucose metabolic
clearance rate (2.28 ± 0.85 vs. 2.48 ± 1.03
mL/kg-1·min-1) were similar after placebo
and after the drug. Indirect calorimetry showed no difference in
substrate oxidation rates between the two experimental conditions. In
conclusion, under the conditions of this study, no improvement in
insulin sensitivity was observed in obese insulin-resistant patients
following a single iv administration of a recombinant TNF receptor: Fc
fusion protein.
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