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Am J Physiol Regul Integr Comp Physiol 262: R628-R635, 1992;
0363-6119/92 $5.00
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AJP - Regulatory, Integrative and Comparative Physiology, Vol 262, Issue 4 628-R635, Copyright © 1992 by American Physiological Society

ARTICLES

Attenuation of glucose metabolic changes resulting from TNF-alpha administration by adrenergic blockade

G. J. Bagby, C. H. Lang, N. Skrepnik and J. J. Spitzer
Department of Physiology, Louisiana State University Medical Center, New Orleans 70112.

Administration of tumor necrosis factor (TNF-alpha) increases whole body glucose kinetics and stimulates in vivo glucose uptake by several tissues. Because circulating catecholamines are also increased after TNF-alpha administration, the present study was conducted to examine the potential role of the adrenergic system in eliciting these changes. Rats given 150 micrograms TNF-alpha/kg by intravenous infusion over a 30-min period exhibited an increased rate of glucose appearance (glucose Ra). Combined alpha- and beta-adrenergic blockade (phentolamine and propranolol infusion) prevented the TNF-alpha-induced increase in glucose Ra without influencing plasma glucagon or corticosterone levels. TNF-alpha infusion also increased in vivo glucose utilization (Rg), 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 Rg 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-alpha-induced increase in hepatic glucose output. Whereas the adrenergic system plays a major role on the effect of TNF-alpha on whole body glucose production, its importance in directly mediating TNF-alpha's effect on tissue glucose uptake is minimal.


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