Effect of diisopropyl 1,3-dithiol-2-ylidenemalonate (NKK-105) on fatty liver induced by carbon tetrachloride.
The therapeutic effect of diisopropyl 1,3-dithiol-2-ylidenemalonate (NKK-105) on the fatty liver induced by carbon tetrachloride (CCl4) was studied. The recovery from elevated liver triglyceride levels induced by CCl4 required over 20 days in 35 week-old rats, but 14 days in 6 week-old rats. This indicates that 35 week-old rats are useful for studying the therapeutic effect of NKK-105 on fatty liver. In rats with CCl4-induced fatty liver, NKK-105 lowered the hepatic triglyceride level, accelerated the rate of triglyceride release from the liver, enhanced the incorporation of 14C-leucine into microsomal protein, and increased the RNA content in microsomes. These data suggest that NKK-105 exerts a curative effect on CCl4-induced fatty liver by improving the impaired protein synthesis and by promoting lipoprotein secretion.
D000818:Animals; D002251:Carbon Tetrachloride; D002252:Carbon Tetrachloride Poisoning; D005234:Fatty Liver / Q000139:chemically induced / Q000188:drug therapy*; D008074:Lipoproteins / Q000378:metabolism; D008099:Liver / Q000032:analysis; D008297:Male; D008314:Malonates / Q000627:therapeutic use*; D008862:Microsomes, Liver / Q000378:metabolism; D014176:Protein Biosynthesis; D051381:Rats; D013876:Thiophenes / Q000627:therapeutic use*; D014280:Triglycerides / Q000032:analysis / Q000378:metabolism
D008074:Lipoproteins; D008314:Malonates; D013876:Thiophenes; D014280:Triglycerides; D002251:Carbon Tetrachloride; C024808:diisopropyl 1,3-dithiol-2-ylidenemalonate