| Autor: |
da Rocha, Aline Franco, Liboni, Thaís Fernanda, Kurauti, Mirian Ayumi, de Souza, Camila Oliveira, Miksza, Daniele Romani, Moreira, Carolina Campos Lima, Borba-Murad, Glaucia Regina, Bazotte, Roberto Barbosa, de Souza, Helenir Medri |
| Zdroj: |
Pharmacological Reports; May 2014, Vol. 66 Issue: 3 p380-385, 6p |
| Abstrakt: |
Background: Tumor necrosis factor alpha (TNFa) is implicated in the development of insulin resistance in obesity, type 2 diabetes and cancer. However, its ability to modulate the action of insulin on glycogen catabolism in the liver is controversial. The aim of the present study was to investigate whether TNFa acutely affects the suppression by insulin of hepatic glucose production (HGP) and glycogenolysis stimulated by cyclic adenosine monophosphate (cAMP). Methods: TNFa (10 µg/kg) was injected intravenously to rats and, 1 or 6 h later, their livers were subjected to in situperfusion with cAMP (3 µM), in the presence or absence of physiological (20 µU/mL) or supraphysiological (500 µU/mL) concentrations of insulin. Results: The injection of TNFa, 1 or 6 h before liver perfusion, had no direct effect on the action of cAMP in stimulating HGP and glycogenolysis. However, when TNFa was injected 1 h, but not 6 h, before liver perfusion it completely abolished (p< 0.05) the suppressive effect of 20 µU/mL insulin on HGP and glycogenolysis stimulated by cAMP. Furthermore, the injection of TNFa 1 h or 6 h before liver perfusion did not influence the suppression of cAMP-stimulated HGP and glycogenolysis by 500 µU/mL insulin. Conclusion: TNFa acutely abolished the suppressive effect of physiological, but not supraphysiological, levels of insulin on HGP and glycogenolysis stimulated by cAMP, suggesting an important role of this mechanism to the increased HGP in several pathological states. |
| Databáze: |
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