Fatty liver in hypervitaminosis A: synthesis and release of hepatic triglycerides.
Feeding large doses (30,000 IU/100 g body wt per day) of vitamin A to young rats for 2 days produced fatty liver, caused a stimulation of oxidation and esterification of [1-14C]palmitate by liver slices, and increased the activity of hepatic palmitoyl-CoA synthetase. Under similar conditions, however, release of hepatic triglycerides into the plasma, as judged from the post-Triton triglyceridemia, remained unaffected. It is indicated by the present findings that excessive intake of vitamin A produces fatty liver by stimulating the synthesis of triglycerides in liver without affecting the rate of secretion of hepatic triglycerides. An involvement of altered oxidation of fatty acids in the liver can also be ruled out because in hypervitaminosis A this process is increased rather than decreased as required for fatty liver production.
D000090:Acetoacetates / Q000378:metabolism; D000818:Animals; D002245:Carbon Dioxide / Q000378:metabolism; D003066:Coenzyme A Ligases / Q000378:metabolism; D004951:Esterification; D005234:Fatty Liver / Q000139:chemically induced*; D006986:Hypervitaminosis A; D066298:In Vitro Techniques; D050356:Lipid Metabolism; D008055:Lipids / Q000097:blood; D008099:Liver / Q000378:metabolism*; D010084:Oxidation-Reduction; D010168:Palmitates / Q000378:metabolism; D051381:Rats; D014280:Triglycerides / Q000378:metabolism*
D000090:Acetoacetates; D008055:Lipids; D010168:Palmitates; D014280:Triglycerides; D002245:Carbon Dioxide; D003066:Coenzyme A Ligases