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G Paumgartner - One of the best experts on this subject based on the ideXlab platform.

  • increased serum Deoxycholic Acid levels in men with colorectal adenomas
    Gastroenterology, 1993
    Co-Authors: E Bayerdorffer, Thomas Ochsenkühn, G A Mannes, Werner O Richter, Baldur Wiebecke, Wolfgang Kopcke, G Paumgartner
    Abstract:

    Abstract Background: Epidemiological and animal studies have suggested that the secondary bile Acid Deoxycholic Acid is cocarcinogenic in colorectal cancer, but this hypothesis was not confirmed by case-control studies investigating fecal bile Acids. Methods: Individual serum bile Acid concentrations were investigated in 25 men and 25 women with colorectal adenomas and in an equal number of age- and sex-matched controls by gas-liquid chromatography. Results: Deoxycholic Acid levels were significantly higher in the sera of men with colorectal adenomas (1.70 ± 0.59 vs. 1.16 ± 0.39 μmol/L, P P

C J Steer - One of the best experts on this subject based on the ideXlab platform.

  • Posttranscriptional regulation of mRNA levels in rat liver associated with Deoxycholic Acid feeding.
    American Journal of Physiology-gastrointestinal and Liver Physiology, 1995
    Co-Authors: B T Kren, C M Rodrigues, K D Setchell, C J Steer
    Abstract:

    We investigated the effects of bile Acid feeding on the mRNA levels and transcriptional activity of genes involved in various facets of hepatic cell function. Rats were maintained for 10 days on standard diet supplemented with combinations of 1 and 0.4% Deoxycholic Acid and ursoDeoxycholic Acid. Significant reductions in mRNA levels for liver fatty Acid binding protein, albumin, the asialoglycoprotein receptor, connexins 32 and 26, and cytochromes P-450IIB1 and P-450IIE1 were associated with 1% Deoxycholic Acid feeding. Conversely, the 1% Deoxycholic Acid-fed animals exhibited increased mRNA levels for cholesterol 7 alpha-hydroxylase, 3-hydroxy-3-methylglutaryl-CoA reductase, multidrug resistance, procollagens, extracellular matrix, protooncogenes, tumor suppressors, and cyclins. The 0.4% Deoxycholic Acid-fed animals exhibited increased mRNA levels for c-jun, H-ras, p53, cyclins D1 and D3, fibronectin, and procollagens alpha 1(I) and alpha 1(III). Transcriptional rate changes could not account for the obs...

  • Regulation of bile Acid synthesis by Deoxycholic Acid in the rat: Different effects on cholesterol 7α-hydroxylase and sterol 27-hydroxylase
    Hepatology, 1995
    Co-Authors: Sarah Shefer, B T Kren, C J Steer, Gerald Salen, L B Nguyen, Thomas T. Chen, G. Stephen Tint, Ashok K. Batta
    Abstract:

    Abstract We examined the effects of feeding Deoxycholic Acid (1% and 0.4% of diet), alone and in combination with ursoDeoxycholic Acid, on serum and biliary bile Acid concentrations, hepatic morphology, and the activities and steady-state messenger RNA (mRNA) levels of HMG-CoA reductase and cholesterol 7α-hydroxylase in the rat. Feeding 1% Deoxycholic Acid increased serum bile Acid concentrations (cholestasis), produced portal triad inflammation, bile duct proliferation, and severe hepatocyte necrosis with nuclear pleomorphism. Hepatic damage was prevented when ursoDeoxycholic Acid (1%) was combined with the Deoxycholic Acid (1%), or when Deoxycholic Acid intake was reduced to 0.4%. HMG-CoA reductase and cholesterol 7α-hydroxylase activities were markedly inhibited (-56% and -55%, respectively) with either 1% or 0.4% Deoxycholic Acid. UrsoDeoxycholic Acid alone produced an insignificant decline in HMG-CoA reductase and cholesterol 7α-hydroxylase activities, and when combined with 1% Deoxycholic Acid did not lessen the inhibitory effect of the latter. Steady state mRNA levels increased 20-fold for HMG-CoA reductase and 53-fold for cholesterol 7α-hydroxylase in rats fed 1% Deoxycholic Acid. In contrast, 0.4% Deoxycholic Acid decreased HMG-CoA reductase mRNA levels 76%, and cholesterol 7α-hydroxylase mRNA levels 82%. UrsoDeoxycholic Acid alone did not affect HMG-CoA reductase or cholesterol 7α-hydroxylase steady-state mRNA levels. Steady-state mRNA levels and activities of sterol 27-hydroxylase, a key enzyme in the alternative Acidic pathway of bile Acid synthesis, did not change with either high or low doses of Deoxycholic Acid. In conclusion, 1% Deoxycholic Acid induced hepatocyte destruction and regeneration associated with increased mRNA levels for HMG-CoA reductase and cholesterol 7α-hydroxylase, but significantly suppressed both enzyme activities. Thus, high-dose Deoxycholic Acid uncouples HMG-CoA reductase and cholesterol 7α-hydroxylase mRNA levels from enzyme function. In contrast, lower-dose Deoxycholic Acid (0.4%) inhibited both activities and mRNA levels of HMG-CoAreductase and cholesterol 7α-hydroxylase. Adding 1% ursoDeoxycholic Acid to 1% Deoxycholic Acid prevented the rise in mRNA levels but did not lessen the inhibitory effect of the latter. This inhibition occurred without change in hepatic histology, which suggests a regulatory role for Deoxycholic Acid that is independent of liver damage. Conversely, sterol 27-hydroxylase activity and mRNA levels are not affected by Deoxycholic Acid treatments.

  • Posttranscriptional regulation of mRNA levels in rat liver associated with Deoxycholic Acid feeding.
    The American journal of physiology, 1995
    Co-Authors: B T Kren, C M Rodrigues, K D Setchell, C J Steer
    Abstract:

    We investigated the effects of bile Acid feeding on the mRNA levels and transcriptional activity of genes involved in various facets of hepatic cell function. Rats were maintained for 10 days on standard diet supplemented with combinations of 1 and 0.4% Deoxycholic Acid and ursoDeoxycholic Acid. Significant reductions in mRNA levels for liver fatty Acid binding protein, albumin, the asialoglycoprotein receptor, connexins 32 and 26, and cytochromes P-450IIB1 and P-450IIE1 were associated with 1% Deoxycholic Acid feeding. Conversely, the 1% Deoxycholic Acid-fed animals exhibited increased mRNA levels for cholesterol 7 alpha-hydroxylase, 3-hydroxy-3-methylglutaryl-CoA reductase, multidrug resistance, procollagens, extracellular matrix, protooncogenes, tumor suppressors, and cyclins. The 0.4% Deoxycholic Acid-fed animals exhibited increased mRNA levels for c-jun, H-ras, p53, cyclins D1 and D3, fibronectin, and procollagens alpha 1(I) and alpha 1(III). Transcriptional rate changes could not account for the observed changes in steady-state mRNA levels. UrsoDeoxycholic Acid feeding had no significant effect on gene expression and almost completely inhibited the changes associated with 1% Deoxycholic Acid when coadministered. The results indicate that dietary ingestion of Deoxycholic Acid profoundly affects hepatic gene expression in the rat, and regulation occurs primarily at the posttranscriptional level.

E Bayerdorffer - One of the best experts on this subject based on the ideXlab platform.

  • increased serum Deoxycholic Acid levels in men with colorectal adenomas
    Gastroenterology, 1993
    Co-Authors: E Bayerdorffer, Thomas Ochsenkühn, G A Mannes, Werner O Richter, Baldur Wiebecke, Wolfgang Kopcke, G Paumgartner
    Abstract:

    Abstract Background: Epidemiological and animal studies have suggested that the secondary bile Acid Deoxycholic Acid is cocarcinogenic in colorectal cancer, but this hypothesis was not confirmed by case-control studies investigating fecal bile Acids. Methods: Individual serum bile Acid concentrations were investigated in 25 men and 25 women with colorectal adenomas and in an equal number of age- and sex-matched controls by gas-liquid chromatography. Results: Deoxycholic Acid levels were significantly higher in the sera of men with colorectal adenomas (1.70 ± 0.59 vs. 1.16 ± 0.39 μmol/L, P P

Ashok K. Batta - One of the best experts on this subject based on the ideXlab platform.

  • Regulation of bile Acid synthesis by Deoxycholic Acid in the rat: Different effects on cholesterol 7α-hydroxylase and sterol 27-hydroxylase
    Hepatology, 1995
    Co-Authors: Sarah Shefer, B T Kren, C J Steer, Gerald Salen, L B Nguyen, Thomas T. Chen, G. Stephen Tint, Ashok K. Batta
    Abstract:

    Abstract We examined the effects of feeding Deoxycholic Acid (1% and 0.4% of diet), alone and in combination with ursoDeoxycholic Acid, on serum and biliary bile Acid concentrations, hepatic morphology, and the activities and steady-state messenger RNA (mRNA) levels of HMG-CoA reductase and cholesterol 7α-hydroxylase in the rat. Feeding 1% Deoxycholic Acid increased serum bile Acid concentrations (cholestasis), produced portal triad inflammation, bile duct proliferation, and severe hepatocyte necrosis with nuclear pleomorphism. Hepatic damage was prevented when ursoDeoxycholic Acid (1%) was combined with the Deoxycholic Acid (1%), or when Deoxycholic Acid intake was reduced to 0.4%. HMG-CoA reductase and cholesterol 7α-hydroxylase activities were markedly inhibited (-56% and -55%, respectively) with either 1% or 0.4% Deoxycholic Acid. UrsoDeoxycholic Acid alone produced an insignificant decline in HMG-CoA reductase and cholesterol 7α-hydroxylase activities, and when combined with 1% Deoxycholic Acid did not lessen the inhibitory effect of the latter. Steady state mRNA levels increased 20-fold for HMG-CoA reductase and 53-fold for cholesterol 7α-hydroxylase in rats fed 1% Deoxycholic Acid. In contrast, 0.4% Deoxycholic Acid decreased HMG-CoA reductase mRNA levels 76%, and cholesterol 7α-hydroxylase mRNA levels 82%. UrsoDeoxycholic Acid alone did not affect HMG-CoA reductase or cholesterol 7α-hydroxylase steady-state mRNA levels. Steady-state mRNA levels and activities of sterol 27-hydroxylase, a key enzyme in the alternative Acidic pathway of bile Acid synthesis, did not change with either high or low doses of Deoxycholic Acid. In conclusion, 1% Deoxycholic Acid induced hepatocyte destruction and regeneration associated with increased mRNA levels for HMG-CoA reductase and cholesterol 7α-hydroxylase, but significantly suppressed both enzyme activities. Thus, high-dose Deoxycholic Acid uncouples HMG-CoA reductase and cholesterol 7α-hydroxylase mRNA levels from enzyme function. In contrast, lower-dose Deoxycholic Acid (0.4%) inhibited both activities and mRNA levels of HMG-CoAreductase and cholesterol 7α-hydroxylase. Adding 1% ursoDeoxycholic Acid to 1% Deoxycholic Acid prevented the rise in mRNA levels but did not lessen the inhibitory effect of the latter. This inhibition occurred without change in hepatic histology, which suggests a regulatory role for Deoxycholic Acid that is independent of liver damage. Conversely, sterol 27-hydroxylase activity and mRNA levels are not affected by Deoxycholic Acid treatments.

  • Regulation of bile Acid synthesis by Deoxycholic Acid in the rat: different effects on cholesterol 7 alpha-hydroxylase and sterol 27-hydroxylase.
    Hepatology (Baltimore Md.), 1995
    Co-Authors: Sarah Shefer, Gerald Salen, L B Nguyen, G. Stephen Tint, B T Kren, C J Steer, T Chen, Ashok K. Batta
    Abstract:

    We examined the effects of feeding Deoxycholic Acid (1% and 0.4% of diet), alone and in combination with ursoDeoxycholic Acid, on serum and biliary bile Acid concentrations, hepatic morphology, and the activities and steady-state messenger RNA (mRNA) levels of HMG-CoA reductase and cholesterol 7 alpha-hydroxylase in the rat. Feeding 1% Deoxycholic Acid increased serum bile Acid concentrations (cholestasis), produced portal triad inflammation, bile duct proliferation, and severe hepatocyte necrosis with nuclear pleomorphism. Hepatic damage was prevented when ursoDeoxycholic Acid (1%) was combined with the Deoxycholic Acid (1%), or when Deoxycholic Acid intake was reduced to 0.4%. HMG-CoA reductase and cholesterol 7 alpha-hydroxylase activities were markedly inhibited (-56% and -55%, respectively) with either 1% or 0.4% Deoxycholic Acid. UrsoDeoxycholic Acid alone produced an insignificant decline in HMG-CoA reductase and cholesterol 7 alpha-hydroxylase activities, and when combined with 1% Deoxycholic Acid did not lessen the inhibitory effect of the latter. Steady-state mRNA levels increased 20-fold for HMG-CoA reductase and 53-fold for cholesterol 7 alpha-hydroxylase in rats fed 1% Deoxycholic Acid. In contrast, 0.4% Deoxycholic Acid decreased HMG-CoA reductase mRNA levels 76%, and cholesterol 7 alpha-hydroxylase mRNA levels 82%. UrsoDeoxycholic Acid alone did not affect HMG-CoA reductase or cholesterol 7 alpha-hydroxylase steady-state mRNA levels. Steady-state mRNA levels and activities of sterol 27-hydroxylase, a key enzyme in the alternative Acidic pathway of bile Acid synthesis, did not change with either high or low doses of Deoxycholic Acid.(ABSTRACT TRUNCATED AT 250 WORDS)

Sabrina G Fabi - One of the best experts on this subject based on the ideXlab platform.