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

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Abstract
To better understand the effects of tumor necrosis factor-a (TNFa) on insulin sensitivity, direct interaction of the peptide with freshly isolated rat soleus muscle strips was investigated. Muscles were ex- posed to TNFa 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 TNFa preexposure of 30 min, 6 h, and 24 h. Independent of exposure time, TNFa failed to exert any significant effect on rates of 3H-2-deoxy-glucose transport (stimula- tion by 100 nmol/liter insulin after preincubation without vs. with 5 nmol/liter TNFa, cpm/mgzh: 30 min, 779 6 29 vs. 725 6 29; 6 h, 652 6 56 vs. 617 6 60; 24 h, 911 6 47 vs. 936 6 31) or glucose incorporation into glycogen (mmol/gzh: 30 min, 5.19 6 0.22 vs. 5.25 6 0.41; 6 h, 2.08 6 0.10 vs. 2.09 6 0.17; 24 h, 2.51 6 0.21 vs. 2.41 6 0.26). In parallel, TNFa neither affected insulin-stimulated rates of glucose oxidation (CO2 production) and anaerobic glycolysis (lactate release), nor mus- cle glycogen content. In conclusion, these findings do not support the hypothesis of muscle insulin desensitization by TNFa via autocrine or paracrine mechanisms. The obtained data favor the concept that TNFa-dependent muscle insulin resistance in vivo depends on indi- rect effects rather than direct interaction of the peptide with skeletal muscle. (Endocrinology 138: 2674 -2679, 1997)

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