High levels of glucose-6-phosphatase gene and protein expression reflect an adaptive response in proliferating liver and diabetes.

@article{Haber1995HighLO,
  title={High levels of glucose-6-phosphatase gene and protein expression reflect an adaptive response in proliferating liver and diabetes.},
  author={Barbara A. Haber and S Chin and E Chuang and Wieneke A. Buikhuisen and A Naji and Rebecca A. Taub},
  journal={The Journal of clinical investigation},
  year={1995},
  volume={95 2},
  pages={
          832-41
        }
}
  • B. Haber, S. Chin, +3 authors R. Taub
  • Published 1 February 1995
  • Biology, Medicine
  • The Journal of clinical investigation
The regenerating liver after partial hepatectomy is one of the few physiologic models of cellular proliferation in the adult animal. During hepatic regeneration, the animal is able to maintain metabolic homeostasis despite the acute loss of two thirds of hepatic tissue. In examining the molecular mechanisms regulating hepatic regeneration, we isolated novel immediate-early genes that are rapidly induced as the remnant liver undergoes the transition from its normal quiescent state into the G1… 
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Hepatocellular expression of glucose-6-phosphatase is unaltered during hepatic regeneration.
TLDR
Data indicate that, although this hepatocyte IEG is transcriptionally regulated, the physiologically important level of regulation is posttranscriptional, which highlights the importance of correlating gene expression of IEG with protein expression and physiological function.
Hepatocellular expression of glucose-6-phosphatase is unaltered during hepatic regeneration.
TLDR
Data indicate that, although this hepatocyte IEG is transcriptionally regulated, the physiologically important level of regulation is posttranscriptional, which highlights the importance of correlating gene expression of IEG with protein expression and physiological function.
Upregulation of hepatic glucose 6-phosphatase gene expression in rats treated with an inhibitor of glucose-6-phosphate translocase.
TLDR
It is suggested that the significant upregulation of Glc-6-Pase gene expression observed after treatment of rats in vivo with an inhibitor of the glucose- 6-phosphate translocase is caused predominantly either by S 3483 per se or by the compound-induced changes of intracellular carbohydrate metabolism.
Perturbation of Fuel Homeostasis Caused by Overexpression of the Glucose-6-phosphatase Catalytic Subunit in Liver of Normal Rats*
TLDR
It is shown that Zucker diabetic fatty rats (fa/fa), which are known to exhibit impaired suppression of hepatic glucose output, have 2.4-fold more glucose-6-phosphatase activity in liver than lean controls, and overexpression of G6Pase in liver is sufficient to perturb whole animal glucose and lipid homeostasis, possibly contributing to the development of metabolic abnormalities associated with diabetes.
Induction of Hepatic Glucose-6-Phosphatase Gene Expression by Lipid Infusion
TLDR
The data indicate that the in vivo gene expression of Glc-6-Pase in the liver is regulated by circulating lipids independent of insulin and thus that prolonged hyperlipidemia may contribute to the increased production of glucose via increased expression of this protein.
Gene expression of glucokinase regulatory protein in regenerating rat liver
TLDR
A decrease in the content of regulatory protein and the glucokinase activity, and an increase in the molar ratio of these two proteins correlate with the observed decrease in glycolytic flux, providing further evidence that the phosphorylation of glucose is a control point in the glycoleytic/gluconeogenic flux during liver regeneration.
Expression and function of growth-induced genes during liver regeneration
Ontogeny of the murine glucose-6-phosphatase system.
TLDR
This study strongly supports the multicomponent model for the G6Pase system, and in situ hybridization analysis demonstrated that, in addition to the liver and kidney, the intestine expressed G 6Pase.
Insulin resistance and the transcription of the glucose-6-phosphatase gene in newborn dogs.
TLDR
The reduced rate of suppression of transcription of the liver G6Pase gene by insulin in newborn dogs may reflect the unsuppressed neonatal hepatic gluconeogenesis due to insulin resistance and that the physiological roles of IGF-1 seemed to be intact in newborn Dogs and may be not responsible for neonatal hyperglycemia.
Interleukin-6-Induced STAT3 and AP-1 Amplify Hepatocyte Nuclear Factor 1-Mediated Transactivation of Hepatic Genes, an Adaptive Response to Liver Injury
TLDR
The results demonstrate that the two classes of transcription factors, growth induced (STAT3 and AP-1) and tissue specific (HNF-1), can interact as an adaptive response to liver injury to amplify expression of hepatic genes important for the homeostatic response during organ repair.
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TLDR
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TLDR
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TLDR
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TLDR
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