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Acute and Chronic Exposure to Tumor Necrosis Factor- Fails to Affect Insulin-Stimulated Glucose Metabolism of Isolated Rat Soleus Muscle¹

Department of Medicine III (C.F., S.N., M.R., M.B., W.W.), Division of Endocrinology & Metabolism, and Department of Medical & Chemical Laboratory Diagnostics (O.W.), University of Vienna, Vienna, Austria A-1090

Address all correspondence and requests for reprints to: Clemens Fürnsinn, Ph.D., Department of Medicine III, Division of Endocrinology and Metabolism, Währinger Gürtel 18–20, A-1090 Vienna, Austria. E-mail: clemens.fuernsinn{at}akh-wien.ac.at

To better understand the effects of tumor necrosis factor- (TNF) on insulin sensitivity, direct interaction of the peptide with freshly isolated rat soleus muscle strips was investigated. Muscles were exposed to TNF at concentrations ranging from 0.01–5 nmol/liter. Rates of insulin-stimulated (5 or 100 nmol/liter) glucose metabolism were determined after periods of TNF preexposure of 30 min, 6 h, and 24 h. Independent of exposure time, TNF failed to exert any significant effect on rates of ³H-2-deoxy-glucose transport (stimulation by 100 nmol/liter insulin after preincubation without vs. with 5 nmol/liter TNF, cpm/mg·h: 30 min, 779 ± 29 vs. 725 ± 29; 6 h, 652 ± 56 vs. 617 ± 60; 24 h, 911 ± 47 vs. 936 ± 31) or glucose incorporation into glycogen (µmol/g·h: 30 min, 5.19 ± 0.22 vs. 5.25 ± 0.41; 6 h, 2.08 ± 0.10 vs. 2.09 ± 0.17; 24 h, 2.51 ± 0.21 vs. 2.41 ± 0.26). In parallel, TNF neither affected insulin-stimulated rates of glucose oxidation (CO₂ production) and anaerobic glycolysis (lactate release), nor muscle glycogen content. In conclusion, these findings do not support the hypothesis of muscle insulin desensitization by TNF via autocrine or paracrine mechanisms. The obtained data favor the concept that TNF-dependent muscle insulin resistance in vivo depends on indirect effects rather than direct interaction of the peptide with skeletal muscle.

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