Apolipoprotein A-IV messenger ribonucleic acid abundance is regulated in a tissue-specific manner.
The influence of development and estrogen, thyroid hormone, corticosteroid, and fibrate administration on apolipoprotein (apo) A-IV mRNA levels in the liver and intestine and on serum or plasma concentrations of apo A-IV was studied in the rat. Treatment of ovariectomized rats with ethinyl estradiol provoked a dose-dependent decrease in liver apo A-IV mRNA levels, whereas intestinal apo A-IV mRNA did not change. The serum apo A-IV concentration decreased in a dose-dependent manner. Administration of L-T4 increased liver apo A-IV mRNA levels more than 2-fold, while n-propylthiouracil (PTU) decreased these levels more than 4-fold. Intestinal apo A-IV mRNA levels remained constant upon L-T4 treatment, but increased after PTU. Change in thyroid hormone levels caused no significant alteration of plasma apo A-IV levels. Hydrocorticsone increased liver and intestinal apo A-IV mRNA levels 2- and 1.5-fold, respectively, without changing plasma apo A-IV. Liver and intestinal apo A-IV mRNA underwent opposite changes during development. Intestinal apo A-IV mRNA decreased gradually during the period of weaning, while liver apo A-IV mRNA was undetectable before day 20 of life and rose to adult levels thereafter. Both L-T4 and hydrocortisone were able to increase liver apo A-IV mRNA prematurely when rat pups were treated from day 9 on. Hypothyroidism induced by PTU, on the other hand, was able to delay the developmental rise in liver apo A-IV mRNA. The hypolipidemic drug clofibrate reduced liver apo A-IV mRNA more than 10-fold without changing the intestinal levels. Plasma apo A-IV decreased by one third. Ethinyl estradiol, thyroid hormones, and clofibrate regulate apo A-IV mRNA abundance in a tissue-specific manner. Only liver, not intestinal, apo A-IV mRNA levels respond to treatment. Furthermore, opposing changes in liver and intestinal apo A-IV mRNA levels occur during development, and thyroid hormones and glucocorticoids are able to accelerate the developmental changes in liver apo A-IV mRNA.
Staels
B
B
Department of Developmental Biology, Katholieke Universiteit, Leuven, Belgium.
van Tol
A
A
Verhoeven
G
G
Auwerx
J
J
D000818:Animals; D001054:Apolipoproteins A / Q000097:blood / Q000235:genetics*; D002994:Clofibrate / Q000494:pharmacology; D004997:Ethinyl Estradiol / Q000494:pharmacology; D005260:Female; D005938:Glucocorticoids / Q000494:pharmacology; D006854:Hydrocortisone / Q000494:pharmacology; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000254:growth & development; D008099:Liver / Q000254:growth & development / Q000378:metabolism; D008297:Male; D010052:Ovariectomy; D011441:Propylthiouracil / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D013974:Thyroxine / Q000494:pharmacology
D001054:Apolipoproteins A; D005938:Glucocorticoids; D012333:RNA, Messenger; C022205:apolipoprotein A-IV; D004997:Ethinyl Estradiol; D011441:Propylthiouracil; D002994:Clofibrate; D013974:Thyroxine; D006854:Hydrocortisone