ArticleThe Biochemical journal2004
Tumour necrosis factor alpha decreases glucose-6-phosphatase gene expression by activation of nuclear factor kappaB.
Article in The Biochemical journal, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 36 citations in OpenAlex.
- Article
- Detection of a novel, primate-specific 'kill switch' tumor suppression mechanism that may fundamentally control cancer risk in humans: an unexpected twist in the basic biology of TP53.Endocrine-related cancer · 2018Review
- Glucose homeostasis in two degrees of sepsis lethality induced by caecum ligation and puncture in mice.International journal of experimental pathology · 2017Article
- Article
- Acute low-dose endotoxin treatment results in improved whole-body glucose homeostasis in mice.Metabolism: clinical and experimental · 2017Article
- Investigation of salicylate hepatic responses in comparison with chemical analogues of the drug.Biochimica et biophysica acta · 2016Article
- Adiponectin signaling in the liver.Reviews in endocrine & metabolic disorders · 2014Review
- Article
- Inhibitory effect of tumor necrosis factor α on gluconeogenesis in perfused rat liver.Molecular and cellular biochemistry · 2013Article
- Animal models of ricin toxicosis.Current topics in microbiology and immunology · 2012Article
- Mycobacterium tuberculosis-infected human monocytes down-regulate microglial MMP-2 secretion in CNS tuberculosis via TNFα, NFκB, p38 and caspase 8 dependent pathways.Journal of neuroinflammation · 2011Article
- Peroxisome proliferator-activated receptor {alpha} is responsible for the up-regulation of hepatic glucose-6-phosphatase gene expression in fasting and db/db Mice.The Journal of biological chemistry · 2011Article
- Lipopolysaccharide inhibition of glucose production through the Toll-like receptor-4, myeloid differentiation factor 88, and nuclear factor kappa b pathway.Hepatology (Baltimore, Md.) · 2009Article
- ABINs inhibit EGF receptor-mediated NF-kappaB activation and growth of EGF receptor-overexpressing tumour cells.Oncogene · 2008Article
- Inhibition of NF-kappaB activation by the histone deacetylase inhibitor 4-Me2N-BAVAH induces an early G1 cell cycle arrest in primary hepatocytes.Cell proliferation · 2007Article
- Amelioration of glucose tolerance by hepatic inhibition of nuclear factor kappaB in db/db mice.Diabetologia · 2007Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The key insulin-regulated gluconeogenic enzyme G6Pase (glucose-6-phosphatase) has an important function in the control of hepatic glucose production. Here we examined the inhibition of G6Pase gene transcription by TNF (tumour necrosis factor) in H4IIE hepatoma cells. TNF decreased dexamethasone/dibtuyryl cAMP-induced G6Pase mRNA levels. TNFalpha, but not insulin, led to rapid activation of NFkappaB (nuclear factor kappaB). The adenoviral overexpression of a dominant negative mutant of IkappaBalpha (inhibitor of NFkappaB alpha) prevented the suppression of G6Pase expression by TNFalpha, but did not affect that by insulin. The regulation of G6Pase by TNF was not mediated by activation of the phosphoinositide 3-kinase/protein kinase B pathway, extracellular-signal-regulated protein kinase or p38 mitogen-activated protein kinase. Reporter gene assays demonstrated a concentration-dependent down-regulation of G6Pase promoter activity by the transient overexpression of NFkappaB. Although two binding sites for NFkappaB were identified within the G6Pase promoter, neither of these sites, nor the insulin response unit or binding sites for Sp proteins, was necessary for the regulation of G6Pase promoter activity by TNFalpha. In conclusion, the data indicate that the activation of NFkappaB is sufficient to suppress G6Pase gene expression, and is required for the regulation by TNFalpha, but not by insulin. We propose that NFkappaB does not act by binding directly to the G6Pase promoter.
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