Low-density lipoprotein catabolism does not respond to estrogen in the fetal and newborn rat.
The elimination of native and methylated low-density lipoprotein (LDL) from serum and the effect of estradiol on the serum LDL-apoB pool, the uptake of homologous [125I]-LDL into liver and adrenals, and the fractional catabolic rate (FCR) of [125I]-LDL was studied in fetal (22nd day of gestation), newborn (15th day postpartum), and adult rats. In fetal rats the receptor-mediated LDL decay accounted only for 47%, whereas in adults it was calculated to 65%. In the latter, estrogen caused (1) a diminution of the serum LDL-apoB pool by 85%; (2) an enhancement of the LDL uptake into the liver and the adrenals by 5- and 10-fold, respectively, and (3) an acceleration of the [125I]-LDL decay in the serum with a rise of the FCR by 3-fold. In contrast, neither the LDL pool and uptake nor the LDL elimination (FCR) did respond to estrogen in fetal and newborn rats. In summary, the LDL catabolism of the rat is insensitive towards estrogen in the late gestational period and during the first 2 weeks of postnatal life [3].
Plonné
D
D
Institute of Pathological Biochemistry, Friedrich-Schiller University, Jena, FRG.
Winkler
L
L
Schröter
A
A
Dargel
R
R
D000311:Adrenal Glands / Q000737:chemistry; D000818:Animals; D000831:Animals, Newborn / Q000378:metabolism; D001055:Apolipoproteins B / Q000737:chemistry / Q000378:metabolism; D004967:Estrogens / Q000494:pharmacology*; D005260:Female; D005333:Fetus / Q000378:metabolism; D008077:Lipoproteins, LDL / Q000737:chemistry / Q000378:metabolism*; D008099:Liver / Q000737:chemistry; D051381:Rats; D017208:Rats, Wistar
D001055:Apolipoproteins B; D004967:Estrogens; D008077:Lipoproteins, LDL