A Marked Increase in Latency of Fetal Rat Liver UDP-Glucuronosyltransferase Accompanies the Fluidization of the Microsomal Membrane in the Perinatal Period

1989 ◽  
Vol 12 (1) ◽  
pp. 30-34 ◽  
Author(s):  
Jaime Kapitulnik ◽  
Mira Tshershedsky
Keyword(s):  
Rat Liver ◽  
Perinatal Period ◽  
Microsomal Membrane ◽  
Fetal Rat ◽  
Fetal Rat Liver ◽  
Udp Glucuronosyltransferase

scholarly journals Glucocorticoids increase the fluidity of the fetal-rat liver microsomal membrane in the perinatal period

1986 ◽  
Vol 239 (1) ◽  
pp. 41-45 ◽  
Author(s):  
J Kapitulnik ◽  
E Weil ◽  
R Rabinowitz
Keyword(s):  
Fatty Acids ◽  
Rat Liver ◽  
Perinatal Period ◽  
Fatty Acyl ◽  
Microsomal Membrane ◽  
Fatty Acyl Moiety ◽  
Pregnant Rats ◽  
Fetal Rat ◽  
Fetal Rat Liver ◽  
Membrane Fluidization

Dexamethasone, a synthetic glucocorticoid, was administered to pregnant rats during the last week of pregnancy in order to examine its effects on the fluidity of the developing fetal-rat liver microsomal membrane. This early prenatal exposure to dexamethasone, which preceded the natural appearance of fetal corticosteroids, markedly accelerated the normal perinatal course of fluidization of this membrane. The lipid apparent microviscosity, which was determined by measurement of fluorescence polarization, decreased in 21-days-old treated fetuses to values that were indistinguishable from those of untreated newborn rats. This dexamethasone-mediated acceleration of membrane fluidization was associated with an increase in the index of unsaturation of the fatty acyl moiety of microsomal lipids. Dexamethasone caused a significant increase in the microsomal content of polyunsaturated fatty acids (arachidonic and linoleic acid), which was accompanied by a decrease in content of monoenoic fatty acids (oleic and palmitoleic acid). This early exposure in utero to dexamethasone precociously induced the changes in fatty acid composition of fetal-rat liver microsomal lipids that normally occur between the last day of pregnancy and the first day of extra-uterine life. These results suggest that endogenous glucocorticoids play a major role in the perinatal fluidization of the rat liver microsomal membrane.

Increasing inhibition of hepatic protein secretion by colchicine during development

1984 ◽  
Vol 247 (3) ◽  
pp. G311-G318
Author(s):  
S. S. Kaufman ◽  
D. J. Tuma ◽  
M. F. Sorrell ◽  
J. A. Vanderhoof
Keyword(s):  
Rat Liver ◽  
Protein Secretion ◽  
Plasma Protein ◽  
Perinatal Period ◽  
Late Gestation ◽  
Maximum Effect ◽  
Rat Development ◽  
Fetal Rat ◽  
Full Participation ◽  
Fetal Rat Liver

Colchicine and other antimicrotubular drugs have been shown to impair plasma protein secretion by fetal rat liver at late gestation (day 21) markedly less than by the mature organ. In the present study, the effect of colchicine on plasma protein secretion by liver slices was determined at several times during rat development. Secretion of [14C]leucine-labeled albumin and [3H]glucosamine-labeled glycoproteins was only minimally impaired (20%) by colchicine (50 microM) on gestation day 19. Inhibition of protein secretion increased to about 40% just before birth and remained unchanged throughout the perinatal period. Inhibition increased thereafter until the maximum effect (75%) was first observed 28 days after birth. Studies in which [3H]-colchicine was used indicated that neither reduced colchicine levels in tissue nor reduced affinity of tubulin for colchicine caused the diminished impairment of secretion in immature liver. These findings suggest that participation of microtubules in liver plasma protein secretion is reduced during development and that full participation is delayed beyond the perinatal period in this species.

Effects of Steroids on Fetal Rat Liver

1969 ◽  
Vol 27 ◽  
pp. 350-351
Author(s):  
F. G. Zaki
Keyword(s):  
Liver Injury ◽  
Rat Liver ◽  
Fetal Liver ◽  
Dosage Level ◽  
Maternal Plasma ◽  
Methyl Prednisolone ◽  
Fetal Rat ◽  
Toxic Agents ◽  
Fetal Rat Liver ◽  
Neonatal Liver

Fetal and neonatal liver injury induced by agents circulating in maternal plasma, even though well recognized, its morphological manifestations are not yet established. As part of our studies of fetal and neonatal liver injury induced by maternal nutritional disorders, metabolic impairment and toxic agents, the effects of two anti-inflammatory steroids have been recently inves tigated.Triamcinolone and methyl prednisolone were injected each in a group of rats during pregnancy at a-dosage level of 2 mgm three times a week. Fetal liver was studied at 18 days of gestation. Litter size and weight markedly decreased than those of control rats. Stillbirths and resorption were of higher incidence in the triamcinolone group than in those given the prednisolone.

Changes in the properties of fetal rat liver during organ culture

In Vitro ◽  
1979 ◽  
Vol 15 (8) ◽  
pp. 579-586
Author(s):  
Carl Monder ◽  
Alena Hatle Coufalik
Keyword(s):  
Organ Culture ◽  
Rat Liver ◽  
Fetal Rat ◽  
Fetal Rat Liver

Hormonal control of fructose 2,6-bisphosphate concentration and of phosphofructokinase 2 in the rat liver during development

1986 ◽  
Vol 6 (6) ◽  
pp. 513-518 ◽  
Author(s):  
Christian Schubert ◽  
Hans-Joachim Boehme ◽  
Eberhard Hofmann
Keyword(s):  
Rat Liver ◽  
Total Activity ◽  
Hormonal Control ◽  
Developmental Changes ◽  
Adrenal Hormones ◽  
Phosphorylation State ◽  
Exogenous Glucose ◽  
Substrate Supply ◽  
Fetal Rat ◽  
Fetal Rat Liver

In fetal rat liver the concentration of fructose 2,6-bisphosphate is decreased by administration of glucagon. The glucagon effect, i.e., the phosphorylation state of phosphofructokinase 2, dominates over the substrate supply. Insulin was found to increase fructose 2,6-bisphosphate only when exogenous glucose is supplied simultaneously. The total activity of phosphofructokinase 2 exhibits remarkable developmental changes. It is high at term, moderate in the fetal as well as in the mature organ, and low during suckling. The level of the enzyme during development is controlled by pancreatic and adrenal hormones.

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