Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The possible induction of fatty liver by Rifampicin has been investigated by oral administration of two different doses (200 and 400 mg/kg/24 h) of this antibiotic for a period of 8 days to male and female Rats. The results obtained are more constant and more coherent in male than in female. It is the 400 mg/kg/24 h dose which is more effective, leading to an increase of lipids, triglycerides and cholesterol in the liver and a decrease of serum triglycerides. A dose-effect relationship may exist. These preliminary data lead us to believe that Rifampicin may inhibit the synthesis of the protein moiety of lipoproteins, such as alpha-Amanitin, which is also a RNA-polymerase inhibitor.
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PMID:[Liver steatogenic power of high doses of rifampicin in rats]. 9 90

The steatogenic effect on the liver of Rifampicin, a potent inhibitor of the DNA-dependent RNA polymerase in bacteria, was investigated in male and female rats which received either 200 mg or 400 mg of Rifampicin/kg/24 h for 8 days. The determination of total lipids (TL), triglycerides (TG), total cholesterol (TC) and phospholipids (PL) showed a significant increase of TL, TG and TC in the liver at a dose of 400 mg. There was better reproducibility in the male whose blood TG and PL were significantly decreased. These results showed that fatty liver can be induced by very high doses of Rifampicin in rats. A blockage of the very low density lipoproteins (VLDL) biosynthesis and/or secretion can be expected. As a potent steatogenic toxin, alpha-amanitin, is a strong inhibitor of RNA polymerase II in eukariotic cells, a relationship between the RNA polymerase inhibition induced by both of substances and a subsequent inhibition of the biosynthesis of the protein moiety of lipoproteins can be considered. Nevertheless Rifampicin is at present not considered as an inhibitor in eukariotic cells and it will be of great interest to test such a possibility with the high doses used in these experiments, in further work.
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PMID:Fatty liver induced by high doses of rifampicin in the rat: possible relation with an inhibition of RNA polymerases in eukariotic cells. 28 41

The purpose of this work was to study if the steatogenic effect on the liver of Rifampicin, which is an inhibitor of the RNA polymerases DNA dependent in bacteria, can be prevented by an anabolic steroid: 19 nortestosterone phenylproprionate (19-NTPP) which probably stimulates the RNA polymerase activity in eukariotic cells. 19-NTPP (25 mg/kg/24 h, i.p.) was administered to male and both intact and ovariectomized female rats for 8 days prior to the administration of Rifampicin (400 mg/kg/24 h for 8 days). In male rats, 19-NTPP does not prevent the Rifampicin-induced fatty liver. On the contrary, in female rats, 19-NTPP exerts a partial protective effect in intact as well as in ovariectomized animals. These results show that the protective effect of 19-NTPP against Rifampicin fatty liver is less complete and little specific, comparated to the protective effect obtained against another steatogenic compound in female rats: alpha-Amanitin, which is a potent inhibitor of RNA polymerase II in eukariotic cells. In conclusion, the inhibitor effect of Rifampicin on the hepatic apolipoprotein biosynthesis appears as less specific and more intricate than the comparable effect of alpha-Amanitin.
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PMID:Study of the protective effect of an anabolic steroid, 19-nortestosterone phenylpropionate (19-NTPP) on the fatty liver induced by high doses of rifampicin in the rat. 693 30