scholarly journals PROFILING OF GENE EXPRESSION IN RAT LIVER AND RAT PRIMARY CULTURED HEPATOCYTES TREATED WITH PEROXISOME PROLIFERATORS

2006 ◽  
Vol 31 (5) ◽  
pp. 471-490 ◽  
Author(s):  
Kotaro TAMURA ◽  
Atsushi ONO ◽  
Toshikazu MIYAGISHIMA ◽  
Taku NAGAO ◽  
Tetsuro URUSHIDANI
Keyword(s):  
Gene Expression ◽  
Rat Liver ◽  
Peroxisome Proliferators ◽  
Cultured Hepatocytes ◽  
Primary Cultured Hepatocytes

Hormonal Regulation of Aldolase B Gene Expression in Rat Primary Cultured Hepatocytes

1998 ◽  
Vol 350 (2) ◽  
pp. 291-297 ◽  
Author(s):  
Jun-itsu Ito ◽  
Takejiro Kuzumaki ◽  
Kaoru Otsu ◽  
Yoshihito Iuchi ◽  
Kiichi Ishikawa
Keyword(s):  
Gene Expression ◽  
Hormonal Regulation ◽  
Cultured Hepatocytes ◽  
Primary Cultured Hepatocytes ◽  
Aldolase B

Gene Expression Profiles in Rat Liver Slices Exposed to Hepatocarcinogenic Enzyme Inducers, Peroxisome Proliferators, and 17α-Ethinylestradiol

2006 ◽  
Vol 25 (5) ◽  
pp. 379-395 ◽  
Author(s):  
Gisela Werle-Schneider ◽  
Andreas Wölfelschneider ◽  
Marie Charlotte von Brevern ◽  
Julia Scheel ◽  
Thorsten Storck ◽  
...  
Keyword(s):  
Gene Expression ◽  
Rat Liver ◽  
Mode Of Action ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Peroxisome Proliferators ◽  
Liver Slices ◽  
Enzyme Inducers

Transcription profiling is used as an in vivo method for predicting the mode-of-action class of nongenotoxic carcinogens. To set up a reliable in vitro short-term test system DNA microarray technology was combined with rat liver slices. Seven compounds known to act as tumor promoters were selected, which included the enzyme inducers phenobarbital, α-hexachlorocyclohexane, and cyproterone acetate; the peroxisome proliferators WY-14,643, dehydroepiandrosterone, and ciprofibrate; and the hormone 17 α-ethinylestradiol. Rat liver slices were exposed to various concentrations of the compounds for 24 h. Toxicology-focused TOXaminer™ DNA microarrays containing approximately 1500 genes were used for generating gene expression profiles for each of the test compound. Hierarchical cluster analysis revealed that (i) gene expression profiles generated in rat liver slices in vitro were specific allowing classification of compounds with similar mode of action and (ii) expression profiles of rat liver slices exposed in vitro correlate with those induced after in vivo treatment (reported previously). Enzyme inducers and peroxisome proliferators formed two separate clusters, confirming that they act through different mechanisms. Expression profiles of the hormone 17 α-ethinylestradiol were not similar to any of the other compounds. In conclusion, gene expression profiles induced by compounds that act via similar mechanisms showed common effects on transcription upon treatment in vivo and in rat liver slices in vitro.

scholarly journals Regulation of IGFBP-2 expression during fasting

2015 ◽  
Vol 467 (3) ◽  
pp. 453-460 ◽  
Author(s):  
Hye Suk Kang ◽  
Mi-Young Kim ◽  
Seung-Jae Kim ◽  
Jae-Ho Lee ◽  
Yong-Deuk Kim ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Promoter ◽  
Biological Action ◽  
Peroxisome Proliferator ◽  
Cultured Hepatocytes ◽  
Peroxisome Proliferator Activated Receptor ◽  
Akt Phosphorylation ◽  
Primary Cultured Hepatocytes ◽  
Igf Binding ◽  
Responsive Element

Insulin-like growth factor (IGF)-binding protein-2 (IGFBP-2), one of the most abundant circulating IGFBPs, is known to attenuate the biological action of IGF-1. Although the effect of IGFBP-2 in preventing metabolic disorders is well known, its regulatory mechanism remains unclear. In the present study, we demonstrated the transcriptional regulation of the Igfbp-2 gene by peroxisome-proliferator-activated receptor (PPAR) α in the liver. During fasting, both Igfbp-2 and PPARα expression levels were increased. Wy14643, a selective PPARα agonist, significantly induced Igfbp-2 gene expression in primary cultured hepatocytes. However, Igfbp-2 gene expression in Pparα null mice was not affected by fasting or Wy14643. In addition, through transient transfection and chromatin immunoprecipitation assay in fasted livers, we determined that PPARα bound to the putative PPAR-responsive element between −511 bp and −499 bp on the Igfbp-2 gene promoter, indicating that the Igfbp-2 gene transcription is activated directly by PPARα. To explore the role of PPARα in IGF-1 signalling, we treated primary cultured hepatocytes with Wy14643 and observed a decrease in the number of IGF-1 receptors (IGF-1Rs) and in Akt phosphorylation. No inhibition was observed in the hepatocytes isolated from Pparα null mice. These results suggest that PPARα controls IGF-1 signalling through the up-regulation of hepatic Igfbp-2 transcription during fasting and Wy14643 treatment.

scholarly journals Amylin impairment of insulin effects on glycogen synthesis and phosphoenolpyruvate carboxykinase gene expression in rat primary cultured hepatocytes

1994 ◽  
Vol 304 (2) ◽  
pp. 449-453 ◽  
Author(s):  
S Baqué ◽  
J J Guinovart ◽  
A M Gómez-Foix
Keyword(s):  
Gene Expression ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Glycogen Synthase ◽  
Glycogen Synthesis ◽  
Mrna Level ◽  
Rat Hepatocytes ◽  
Synthesis Rate ◽  
Cultured Hepatocytes ◽  
Glycogen Accumulation ◽  
Primary Cultured Hepatocytes

The ability of amylin to impair hepatic insulin action is controversial. We have found that the effect of amylin in primary cultured hepatocytes is strongly dependent on the culture conditions. Only in hepatocytes preincubated in the presence of fetal serum did amylin, at concentrations ranging from 1 to 100 nM, reduce insulin-stimulated glycogen synthesis rate and glycogen accumulation without showing direct effects. Neither basal glycogen synthase nor glycogen phosphorylase activity was modified by amylin treatment. Nevertheless, amylin (100 nM) blocked the activation of glycogen synthase by insulin. Amylin also proved capable of opposing the reduction in the expression of the phosphoenolpyruvate carboxykinase (PEPCK) gene induced by insulin, whereas the basal mRNA level of PEPCK was unaffected by amylin treatment. Thus, these results show that, in cultured rat hepatocytes, amylin is indeed able to interfere with insulin regulation of glycogenesis and PEPCK gene expression, favouring the hypothesis that amylin may modulate liver sensitivity to insulin.

Inverse gene expression patterns for macrophage activating hepatotoxicants and peroxisome proliferators in rat liver

2004 ◽  
Vol 67 (11) ◽  
pp. 2141-2165 ◽  
Author(s):  
Michael McMillian ◽  
Alex Y Nie ◽  
J.Brandon Parker ◽  
Angelique Leone ◽  
Michael Kemmerer ◽  
...  
Keyword(s):  
Gene Expression ◽  
Rat Liver ◽  
Expression Patterns ◽  
Gene Expression Patterns ◽  
Peroxisome Proliferators
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