title: Lipogenic enzyme gene expression in rat liver during development after birth.
abstract: The time courses and the regulation of lipogenic enzyme gene expression during development after birth have been investigated. The mRNA concentrations and activities of liver lipogenic enzymes (acetyl-CoA carboxylase, fatty acid synthase, malic enzyme, glucose-6-phosphate dehydrogenase, and ATP-citrate lyase) were very low in all the suckling rats, regardless of dietary fat of the mothers. After weaning to the same diet as the mothers, the mRNA and enzyme levels were greatly increased by the fat-free or hydrogenated fat diet but not so greatly increased by the corn or fish oil diet. The mRNA concentrations of all the groups reached maximum at 4-6 weeks old and then decreased, usually to 40-60% of the maximal levels. It appeared that the gene expression after weaning is subject to strong nutritional regulation, as well as developmental regulation. The plasma levels of triiodothyronine and insulin were low during suckling. Malic enzyme mRNA level was increased by triiodothyronine treatment even during suckling, but the absolute increase was much less than after weaning. Thus, the gene expression of lipogenic enzymes during suckling appeared to be suppressed by nutritional and hormonal regulation, or may not be sufficiently developed. On the other hand, the hepatic triacylglycerol levels were increased slightly at 2 weeks old and greatly at 3 weeks. As the gene expression of lipogenic enzymes was still low at that time, the major triacylglycerols appear to be obtained from milk and accumulated in preparation for weaning.
authors.affiliation: Tezukayama Gakuin College, Osaka.
authors.forename: N
authors.initials: N
authors.lastname: Eritani
authors.forename: H
authors.initials: H
authors.lastname: Fukuda
authors.forename: Y
authors.initials: Y
authors.lastname: Matsumura
mesh_terms: D001275:ATP Citrate (pro-S)-Lyase / Q000235:genetics*; D000103:Acetyl-CoA Carboxylase / Q000235:genetics; D000818:Animals; D000833:Animals, Suckling; D004041:Dietary Fats / Q000008:administration & dosage; D064429:Fatty Acid Synthases / Q000235:genetics; D005260:Female; D015870:Gene Expression; D005954:Glucosephosphate Dehydrogenase / Q000235:genetics; D007328:Insulin / Q000097:blood; D008055:Lipids / Q000096:biosynthesis*; D008099:Liver / Q000201:enzymology* / Q000254:growth & development; D008291:Malate Dehydrogenase / Q000235:genetics; D010743:Phospholipids / Q000378:metabolism; D011247:Pregnancy; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D014280:Triglycerides / Q000378:metabolism; D014284:Triiodothyronine / Q000097:blood / Q000494:pharmacology; D014886:Weaning
chemical_list: D004041:Dietary Fats; D007328:Insulin; D008055:Lipids; D010743:Phospholipids; D012333:RNA, Messenger; D014280:Triglycerides; D014284:Triiodothyronine; D008291:Malate Dehydrogenase; D005954:Glucosephosphate Dehydrogenase; D064429:Fatty Acid Synthases; D001275:ATP Citrate (pro-S)-Lyase; D000103:Acetyl-CoA Carboxylase