The Effects of Dexamethasone on Nucleic Acid Synthesis and Cell Numbers in Rat Fetuses<sup>1</sup>)

R, Klepac

doi:10.1055/s-0029-1210244

Cited by 2 publications

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“…The pattern of fetal glycogen concentration results from the relationship of two parameters: the rate of glycogen deposition and organ protein content. During the last days of pregnancy fetal organs nd their protein contents increased in rat fetuses' (Klepac, 1982(Klepac, , 1983. Injected dexamethasone strongly depressed fetal growth, especially growth of fetal adrenal glands and their protein level (Kiepac, 1982(Kiepac, , 1983.…”

Section: Discussionmentioning

confidence: 99%

“…There is a lot of data on glycogen metabolism in fetal liver, while very little is known about the regulation of glycogen metabolism in the other fetal tissues. Dexamethasone administered to pregnant rats inhibited fetal growth and depressed nucleic acids synthesis in various fetal tissues (Klepac, 1982(Klepac, , 1983. Simultaneously, it decreased the fetal adrenal steroidogenesis and plasmacorticosterone level (Kiepac et al, 1978;Klepac and Milkovió, 1979;Paul and D'Angelo, 1972).…”

Section: Introductionmentioning

confidence: 99%

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Effect of Dexamethasone on Glycogen Deposition in Pregnant Rats and Their Fetuses¹)

R¹

2009

Exp Clin Endocrinol Diabetes

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Glycogen deposition was determined in pregnant rats and their fetuses twenty four hrs after maternal treatment with dexamethasone in the final days of pregnancy. Dexamethasone increases glycogen accumulation in the fetal liver, heart, adrenal glands and thymus. Simultaneously, it increases the glycogen concentration in maternal liver. In this study, dexamethasone did not change the glycogen level in the fetal kidneys, brain, placenta, lung and maternal adrenal glands. These results show that dexamethasone accelerated glycogen deposition in some fetal tissues. It is possible that dexamethasone activated enzymes of glycogen synthesis or potentiated the action of fetal corticosterone on induction of glycogen accumulation in fetal rat tissues.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effect of Dexamethasone on Glycogen Deposition in Pregnant Rats and Their Fetuses¹)

R¹

2009

Exp Clin Endocrinol Diabetes

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Effect of dexamethasone, 2-bromopalmitate and clofibrate on L-FABP mediated hepatoma proliferation

Rajaraman

Burczynski

2004

Journal of Pharmacy and Pharmacology

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Cytosolic liver fatty acid binding protein (L-FABP) is involved in many intracellular functions including cellular mitogenesis. We investigated the role of L-FABP and the plasma membrane liver fatty acid binding proteins (L-FABP(pm)) in the modulation of hepatoma growth and proliferation, hypothesizing that agents that affect either the content of, or ligand binding to, L-FABP would affect hepatocellular mitogenesis. L-FABP expressing 1548-rat hepatoma cells were treated with 0.5 microM dexamethasone or 500 microM clofibrate for 4 days to downregulate and upregulate L-FABP expression, respectively. The competitive inhibitor 2-bromopalmitate (BrPA, 600 microM) was used to inhibit ligand binding to L-FABP. The peripherally present plasma membrane fatty acid transporter was inactivated by treating cells with 1:50 rabbit antisera (FABP-Ab) raised against L-FABP. Western blot analysis was used to monitor L-FABP levels while [(3)H]-thymidine incorporation and growth curves were used to monitor hepatocellular proliferation. [(3)H]-Palmitate clearance studies were performed using monolayer cultures. Palmitate clearance in dexamethasone-, BrPA- and FABP-Ab-treated cells was significantly reduced when compared with control (P < 0.05), while clofibrate treatment moderately increased the rate. [(3)H]-Thymidine incorporation by dexamethasone- and BrPA-treated cells was significantly lower than control (P < 0.05), suggesting that hepatocellular proliferation was inhibited. Clofibrate treatment did not statistically affect growth rate. Lowering L-FABP using dexamethasone or interfering with its activity using BrPA significantly affected hepatocellular proliferation. This may be due to the non-availability of long-chain fatty acids or other intracellular mediators that are transported by L-FABP to the nucleus.

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The Effects of Dexamethasone on Nucleic Acid Synthesis and Cell Numbers in Rat Fetuses¹)

Cited by 2 publications

References 6 publications

Effect of Dexamethasone on Glycogen Deposition in Pregnant Rats and Their Fetuses¹)

Effect of Dexamethasone on Glycogen Deposition in Pregnant Rats and Their Fetuses¹)

Effect of dexamethasone, 2-bromopalmitate and clofibrate on L-FABP mediated hepatoma proliferation

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The Effects of Dexamethasone on Nucleic Acid Synthesis and Cell Numbers in Rat Fetuses1)

Cited by 2 publications

References 6 publications

Effect of Dexamethasone on Glycogen Deposition in Pregnant Rats and Their Fetuses1)

Effect of Dexamethasone on Glycogen Deposition in Pregnant Rats and Their Fetuses1)

Effect of dexamethasone, 2-bromopalmitate and clofibrate on L-FABP mediated hepatoma proliferation

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The Effects of Dexamethasone on Nucleic Acid Synthesis and Cell Numbers in Rat Fetuses¹)

Effect of Dexamethasone on Glycogen Deposition in Pregnant Rats and Their Fetuses¹)

Effect of Dexamethasone on Glycogen Deposition in Pregnant Rats and Their Fetuses¹)