Administration of tumor necrosis factor (TNF-α) increases whole body glucose kinetics and stimulates in vivo glucose uptake by several tissues. Because circulating catecholamines are also increased after TNF-α administration, the present study was conducted to examine the potential role of the adrenergic system in eliciting these changes. Rats given 150 μg TNF- α/kg by intravenous infusion over a 30-min period exhibited an increased rate of glucose appearance (glucose R(a)). Combined α- and β-adrenergic blockade (phentolamine and propranolol infusion) prevented the TNF-α-induced increase in glucose R(a) without influencing plasma glucagon or corticosterone levels. TNF-α infusion also increased in vivo glucose utilization (R(g)), measured with 2-deoxy-[14C]glucose, in spleen (86%), liver (80%), skin (47%), ileum (71%), lung (53%), and heart (112%). Adrenergic blockade prevented the tissue R(g) increase in the spleen, liver, and skin; partially reduced it in the ileum; but did not abrogate it in the lung or heart. The effect of blockade was primarily due to inhibition of the TNF-α-induced increase in hepatic glucose output. Whereas the adrenergic system plays a major role on the effect of TNF-α on whole body glucose production, its importance in directly mediating TNF-α's effect on tissue glucose uptake is minimal.
|Original language||English (US)|
|Journal||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|Issue number||4 31-4|
|Publication status||Published - Jan 1 1992|
All Science Journal Classification (ASJC) codes
- Physiology (medical)