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 effects of the administration of different fatty liver inducing drugs on the serum lipoprotein lipase activating ability was investigated in rats. Addition of serum from 2-mercaptoethanol-, 2-mercaptoacetate-, ethionine- or D-galactosamine- treated rats failed to activate heart and adipose tissue lipoprotein lipase from control rats. The activating effect of serum was only slightly reduced in isopropanol-treated rats, whereas it was found unaffected in ethanol-treated ones. Electrophoresis of the lipoproteins and of the very low density lipoproteins (VLDL) fraction of sera from 2-mercaptoethanol-, 2-mercaptoacetate-, isopropanol-, ethionine- and D-galactosamine-treated rats suggest that the lack of lipoprotein lipase activation ability of these sera is most probably related to the impairing effects of these drugs upon VLDL metabolism, i.e. reduction of VLDL secretion in the case of 2-mercaptoethanol, 2-mercaptoacetate and isopropanol, production of abnormal VLDL in the case of D-galactosamine and both decreased VLDL secretion and production of abnormal VLDL in the case of ethionine.
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PMID:Loss of the lipoprotein lipase activating ability of rat serum after administration of some fatty liver inducing drugs. 8 Sep 91

2-Mercaptoethanol-induced fatty liver involves an increased free fatty acid mobilization which is primarily due to an inhibition of free fatty acid reesterification in adipose tissue. Furthermore, increased free fatty acid mobilization as well as fatty liver induction are not induced by 2-mercaptoethanol per se but result most probably from 2-mercaptoacetate through oxidation of 2-mercaptoethanol.
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PMID:Role and mechanism of peripheral fatty acid mobilization in 2-mercaptoethanol-induced fatty liver. 89 14

The intraperitoneal administration of 2-mercaptoethanol or 2-mercaptoacetate (40 muM/100 g body weight) to the rat induces a fatty liver, a marked and early increase of free fatty acids and a decrease of triacylglycerol and phospholipids in the blood. These changes are accompanied by a decrease of the ketone body level and the beta-hydroxybutyrate/acetoacetate ratio in the liver. Under the same experimental conditions, however, administration of 2-mercaptopropionate fails to induce a fatty liver and does not modify the hepatic ketone body level or the blood triacylglycerol and free fatty acid levels. These results led us to conclude that fatty liver induction is not a general feature of foreign thiols, and suggest that increased peripheral fat mobilization as well as decreased hepatic lipoprotein synthesis and/or release are responsible for the 2-mercaptoethanol- and 2-mercaptoacetate-induced fatty liver.
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PMID:Is fatty liver induction a general feature of the administration of foreign sulfhydryl compounds? 93 53