Inhibitory effect of tumor necrosis factor [alpha] on gluconeogenesis in perfused rat liver

• Published in: Molecular and cellular biochemistry Vol. 375; no. 1-2; p. 89
• Main Authors: Da Rocha, Aline Franco, Liboni, Thaís Fernanda, Moreira, Carolina Campos; Lima, Miksza, Daniele Romani, de Souza, Camila Oliveira, de Fatima Silva, Flaviane, Borba-murad, Glaucia Regina, Bazotte, Roberto Barbosa, de Souza, Helenir Medri
• Format: Journal Article
• Language: English
• Published: New York Springer Nature B.V 01-03-2013
• Subjects: Biochemistry; Cytokines; Liver; Metabolism; Rodents; Urea
• ISSN: 0300-8177; 1573-4919
• DOI: 10.1007/s11010-012-1531-4

Tumor necrosis factor [alpha] (TNF[alpha]) is a cytokine involved in many metabolic responses in both normal and pathological states. Considering that the effects of TNF[alpha] on hepatic gluconeogenesis are inconclusive, we investigated the influence of this cytokine in gluconeogenesis from various glucose precursors. TNF[alpha] (10 μg/kg) was intravenously injected in rats; 6 h later, gluconeogenesis from alanine, lactate, glutamine, glycerol, and several related metabolic parameters were evaluated in situ perfused liver. TNF[alpha] reduced the hepatic glucose production (p < 0.001), increased the pyruvate production (p < 0.01), and had no effect on the lactate and urea production from alanine. TNF[alpha] also reduced the glucose production (p < 0.01), but had no effect on the pyruvate production from lactate. In addition, TNF[alpha] did not alter the hepatic glucose production from glutamine nor from glycerol. It can be concluded that the TNF[alpha] inhibited hepatic gluconeogenesis from alanine and lactate, which enter in gluconeogenic pathway before the pyruvate carboxylase step, but not from glutamine and glycerol, which enter in this pathway after the pyruvate carboxylase step, suggesting an important role of this metabolic step in the changes mediated by TNF[alpha].[PUBLICATION ABSTRACT]