Post-Natal Changes in Blood Glucose, Phosphopyruvate Carboxylase and Tyrosine Aminotransferase after Normal Birth and Premature Delivery in the Rat

Marco, P.N. Di; Ghisalberti, Ann V.; Pearce, P. Helen; Oliver, I.T.

doi:10.1159/000240922

Cited by 29 publications

(27 citation statements)

References 25 publications

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“…Since maturation is accompanied by induction of the expression of adult liver-specific genes, we examined the expression of such genes in fetal hepatocytes following glucocorticoid treatment. In rat liver, the gluconeogenic enzyme TAT and the acute-phase protein AGP are -two adult liver-specific proteins (10,35). RLA209-15 cells did not express either the TAT or the AGP gene products at 33 or 40°C.…”

Section: Resultsmentioning

confidence: 97%

“…Thus, maturation of fetal hepatocytes can be monitored by a decrease in expression of the AFP gene and an increase in expression of the albumin and transferrin genes. In addition, the induction of adult liver-specific genes such as tyrosine aminotransferase (TAT) (10) and a1-acid glycoprotein (AGP) (35), which are present in low or undetectable levels in fetal liver but which increase suddenly after birth, indicates that the fetal cells have differentiated or matured into adult cells.…”

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confidence: 99%

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Regulation of rat liver maturation in vitro by glucocorticoids.

Chou¹,

Wan²,

Sakiyama³

1988

Mol. Cell. Biol.

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The biochemistry of liver maturation was studied by using the RLA209-15 fetal rat hepatocyte line that is temperature sensitive for maintenance of the differentiated fetal liver phenotype. At 33°C these cells were dedifferentiated; but at 40°C they were phenotypically differentiated and, like normal fetal hepatocytes, synthesized moderate levels of albumin and transferrin, high levels of authentic (69,000 and 73,000 molecular weight) rat fetal a-fetoprotein (AFP), and low levels of a 65,000-molecular-weight variant AFP. Our results indicated that administration of glucocorticoid hormones to RLA209-15 cells at 40°C induced a series of events associated with normal hepatocyte maturation; synthesis of fetal AFP was inhibited, whereas the synthesis of variant AFP, albumin, transferrin, tyrosine aminotransferase, and al-acid glycoprotein was induced.,The variant AFP was produced by RLA209-15 cells at both temperatures and was encoded by an mRNA of 1.7 kilobases (kb). The fetal AFP was encoded by an mRNA of 2.2 kb. Normal adult rat liver contained three AFP mRNAs of 2.2 (minor), 1.7, and 1.5 kb. The 1.7-kb adult liver AFP mRNA comigrated with the RNA found in RLA209-15 cells, and both directed the synthesis of a 50,000-molecular-weight precursor polypeptide of the variant AFP. Administration of glucocorticoids to RLA209-15 cells grown at 33°C stimulated synthesis of both the fetal and variant AFPs, but the levels of the 2.2-kb AFP mRNA were preferentially increased. RLA209-15 cells contained two glucocorticoid receptor mRNAs of 6.8 and 4.5 kb. The glucocorticoid-mediated maturation described above was blocked by the antiglucocorticoid RU486.

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Section: Resultsmentioning

confidence: 97%

mentioning

confidence: 99%

Regulation of rat liver maturation in vitro by glucocorticoids.

Chou¹,

Wan²,

Sakiyama³

1988

Mol. Cell. Biol.

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“…Different exposition times of the micrograph films were used to ensure that bands fetuses were delivered by cesarean section. 22 A suspension of fetal hepatocytes was prepared by a nonperfusion collagenase were not saturated. Quantification of the films was performed by laser densitometry (Molecular Dynamics), using dispersion method that involved incubation (3 g/flask) of chopped fetal liver for 30 minutes at 37ЊC with 30 mL of the hybridization with a b-actin probe (0.6 kb EcoRI/HindIII fragment isolated from a VC 18 vector) as an internal stanCa Measurement of Lactatedehydrogenase Activity.…”

Section: P]deoxycitidine Test (Sigma)mentioning

confidence: 99%

Bacterial lipopolysaccharide antagonizes transforming growth factor β1-induced apoptosis in primary cultures of hepatocytes

1996

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Incubation of primary cultures of fetal hepatocytes with lipopolysaccharide (LPS) elicited the expression of nitric oxide (NO) synthetase as well as antagonized the apoptotic cell death evoked by treating the cells with transforming growth factor beta 1 (TGF-beta 1). In addition to LPS, exposure of the cells to chemical NO donors also protected against apoptotic cell death when assayed at concentrations in the low micromolar range. Treatment of hepatocytes with large concentrations of NO donors promoted both apoptotic and necrotic cell death. These results suggest that NO synthesis by hepatocytes might be involved in the protection against apoptotic death.

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“…Foetal rats were delivered by surgical delivery without anaesthesia as previously described [9] . Animals were killed by cervical fracture, the livers quickly excised and kept in ice-cold buffer until the entire litter had been killed.…”

Section: Preparation Of Homogenates and Subcellular Fractionsmentioning

confidence: 99%

“…The cyclic AMP concentration in rat liver increases after birth [6,7] at a time when there is an increase in activity of several liver enzymes which are thought to be induced by cyclic AMP [8,9]. The largest increase in cyclic AMP however, was only about 2-fold during the first hour after delivery [6,7] .…”

Section: Introductionmentioning

confidence: 99%