scholarly journals Effects of Cholera Enterotoxin, Glucagon, and Dibutyryl Cyclic Amp on Rat Liver Alkaline Phosphatase, Bile Flow, and Bile Composition

1976 ◽  
Vol 70 (4) ◽  
pp. 577-581 ◽  
Author(s):  
Alfred L. Baker ◽  
Marshall M. Kaplan
Keyword(s):  
Alkaline Phosphatase ◽  
Cyclic Amp ◽  
Rat Liver ◽  
Bile Flow ◽  
Dibutyryl Cyclic Amp ◽  
Bile Composition ◽  
Cholera Enterotoxin

scholarly journals Evidence for a dual effect of dibutyryl cyclic AMP on the synthesis of tyrosine aminotransferase in rat liver.

1982 ◽  
Vol 257 (5) ◽  
pp. 2386-2390 ◽  
Author(s):  
T Noguchi ◽  
M Diesterhaft ◽  
D Granner
Keyword(s):  
Cyclic Amp ◽  
Rat Liver ◽  
Tyrosine Aminotransferase ◽  
Dibutyryl Cyclic Amp ◽  
Dual Effect

scholarly journals Factors that prevent the premature appearance of glucokinase in neonatal rat liver

1980 ◽  
Vol 186 (3) ◽  
pp. 817-826 ◽  
Author(s):  
M J O Wakelam ◽  
M B Allen ◽  
D G Walker
Keyword(s):  
Angiotensin Ii ◽  
Cyclic Amp ◽  
Insulin Release ◽  
Rat Liver ◽  
Neonatal Rat ◽  
Oral Glucose ◽  
Dibutyryl Cyclic Amp ◽  
Simultaneous Treatment ◽  
Physiological Factors ◽  
Glucose Administration

1. The physiological factors that prevent the precocious appearance of glucokinase activity in the 13-day-old rat that can be induced by oral glucose administration were explored. 2. Evidence is presented that the galactose component of milk sugar is inhibitory. In the absence of this inhibitory galactose, the amount of glucose necessary to effect appreciable induction is greater than that present in milk. 3. The induction is prevented both by administration of mannoheptulose, which inhibits insulin release, and by excess insulin; the amount of insulin available therefore seems to be critical. 4. The inhibition of induction by galactose does not appear to be via competition with glucose but by enhancing insulin release and thereby making this excessive. The relative amounts of glucose and insulin appear to be important in regulating glucokinase induction. 5. The precocious induction of glucokinase by glucose is inhibited by simultaneous treatment with approriate amounts of adrenaline, glucagon, dibutyryl cyclic AMP or isoprenaline but not by vasopressin or angiotensin II. 6. No single cause of glucokinase induction in neonatal rat liver can be recognized. The process is subject to regulation by many factors at a time subsequent to when competence to synthesize the enzyme has been established.

Effect of epinephrine and dibutyryl cyclic AMP on Δ5-desaturation activity of rat liver microsomes

Lipids ◽  
1980 ◽  
Vol 15 (12) ◽  
pp. 1064-1066 ◽  
Author(s):  
I. N. T. de Gomez Dumm ◽  
M. J. T. de Alaniz ◽  
R. R. Brenner
Keyword(s):  
Cyclic Amp ◽  
Rat Liver ◽  
Liver Microsomes ◽  
Rat Liver Microsomes ◽  
Dibutyryl Cyclic Amp ◽  
Desaturation Activity

scholarly journals Interaction of hydrocortisone and dibutyryl cyclic AMP in the induction of tyrosine amino-transferase and phosphoenolpyruvate carboxy-kinase in rat liver

FEBS Letters ◽  
1974 ◽  
Vol 46 (1-2) ◽  
pp. 158-161 ◽  
Author(s):  
W. Krone ◽  
W.B. Huttner ◽  
H.J. Seitz ◽  
W. Tarnowski
Keyword(s):  
Cyclic Amp ◽  
Rat Liver ◽  
Dibutyryl Cyclic Amp

scholarly journals Hepatic thiol and glutathione efflux under the influence of vasopressin, phenylephrine and adrenaline

1985 ◽  
Vol 226 (2) ◽  
pp. 545-549 ◽  
Author(s):  
H Sies ◽  
P Graf
Keyword(s):  
Plasma Membrane ◽  
Cyclic Amp ◽  
Rat Liver ◽  
Isolated Perfused Rat Liver ◽  
Peripheral Inflammation ◽  
Perfused Rat Liver ◽  
Dibutyryl Cyclic Amp ◽  
Hormone Dependence ◽  
Experimental Shock ◽  
Hormone Effects

Thiol and glutathione (GSH) efflux across the sinusoidal plasma membrane in isolated perfused rat liver was stimulated by addition of hormones such as vasopressin, phenylephrine and adrenaline, whereas glucagon or dibutyryl cyclic AMP were without effect. Phenylephrine and adrenaline effects were sensitive to prazosin and phentolamine, respectively. The increase in thiol efflux was largely accounted for by an increase in GSH efflux. Thiol efflux and the hormone effects were abolished in GSH-depleted liver. Biliary GSH efflux was diminished upon hormone addition. The newly discovered hormone-dependence of GSH release across the sinusoidal plasma membrane may explain the known loss of GSH during conditions of experimental shock (traumatic or endotoxin) and stress and peripheral inflammation.

scholarly journals The effect of bromodeoxyuridine and dibutyryl cyclic AMP on the induction of placental alkaline phosphate in human choriocarcinoma cells

1981 ◽  
Vol 198 (1) ◽  
pp. 29-35 ◽  
Author(s):  
T A Hamilton ◽  
H H Sussman
Keyword(s):  
Alkaline Phosphatase ◽  
Cyclic Amp ◽  
Polyacrylamide Gel Electrophoresis ◽  
Specific Protein ◽  
Placental Alkaline Phosphatase ◽  
Dibutyryl Cyclic Amp ◽  
Specific Enzyme ◽  
Alkaline Phosphate ◽  
Choriocarcinoma Cells ◽  
Human Choriocarcinoma Cells

The effect of 5-bromo-2′-deoxyuridine (BrdUrd) and dibutyryl cyclic AMP (Bt2cAMP) on the expression of the placental isoenzyme of human alkaline phosphatase was examined in BeWo choriocarcinoma cells. By using a combination of specific immunoprecipitation and polyacrylamide-gel electrophoresis of cells labelled either metabolically with [35S]methionine or cell-surface-labelled with 125I, both BrdUrd (5 micrograms/ml) and 1 mM-Bt2cAMP were shown to result in the enhanced accumulation of a specific protein. This protein has immunochemical identity and co-electrophoreses with placental alkaline phosphatase in two-dimensional gels. These results clearly demonstrate that the induction of placental alkaline phosphatase activity in choriocarcinoma cells treated with these agents is a consequence of the accumulation of specific enzyme protein rather than of altered catalytic activity.

scholarly journals Regulation of coenzyme A biosynthesis by glucagon and glucocorticoid in adult rat liver parenchymal cells

1980 ◽  
Vol 188 (1) ◽  
pp. 175-184 ◽  
Author(s):  
Colleen M. Smith ◽  
C. Richard Savage
Keyword(s):  
Cyclic Amp ◽  
Rat Liver ◽  
Maximum Effect ◽  
Maximal Effect ◽  
Dibutyryl Cyclic Amp ◽  
Liver Parenchymal ◽  
Adult Rat ◽  
Intracellular Mechanism ◽  
Inhibitor Of Protein Synthesis ◽  
Parenchymal Cells

We studied the effects of glucagon, dibutyryl cyclic AMP and dexamethasone on the rate of [14C]pantothenate conversion to CoA in adult rat liver parenchymal cells in primary culture. The presence of 30nm-glucagon increased the rate by about 1.5-fold relative to control cultures (range 1.4–2.3) and 2.4-fold relative to cultures containing 1–3m-i.u. of insulin/ml. The half-maximal effect was obtained at 3nm-glucagon. Dibutyryl cyclic AMP plus theophylline also enhanced the rate by about 1.5-fold. Dexamethasone acted synergistically with glucagon; glucagon at 0.3nm had no effect when added alone, but resulted in a 1.7-fold enhancement when added in the presence of dexamethasone (maximum effect at 50nm). The 1.4-fold enhancement caused by the addition of saturating glucagon concentrations was increased to a 3-fold overall enhancement by the addition of dexamethasone. However, dexamethasone added alone over the range 5nm to 5μm had no effect on the rate of [14C]pantothenate conversion to CoA. The stimulatory effect of dibutyryl cyclic AMP plus theophylline was also enhanced by the addition of dexamethasone. Changes in intracellular pantothenate concentration or radioactivity could not account for the stimulatory effects of glucagon, dibutyryl cyclic AMP or dexamethasone. Addition of 18μm-cycloheximide, an inhibitor of protein synthesis, decreased the rate of incorporation of [14C]pantothenate into CoA and the enhancement of this rate by glucagon and dibutyryl cyclic AMP plus theophylline in a reversible manner. These results demonstrate an influence of glucagon, dibutyryl cyclic AMP and glucocorticoids on the intracellular mechanism regulating total CoA concentrations in the liver.

scholarly journals The adaptive behaviour of isoenzyme forms of rat liver alanine amino transferases during development

1972 ◽  
Vol 128 (2) ◽  
pp. 403-413 ◽  
Author(s):  
Keith Snell ◽  
Deryck G. Walker
Keyword(s):  
Cyclic Amp ◽  
Rat Liver ◽  
In Utero ◽  
Adaptive Behaviour ◽  
Intragastric Administration ◽  
Aminotransferase Activity ◽  
Dibutyryl Cyclic Amp ◽  
Neonatal Development ◽  
Foetal Liver ◽  
Glyoxylate Aminotransferase

1. The activities of the mitochondrial and cytosol isoenzyme forms of l-alanine–glyoxylate and l-alanine–2-oxoglutarate aminotransferases were determined in rat liver during foetal and neonatal development. 2. The mitochondrial glyoxylate aminotransferase activity begins to develop in late-foetal liver, increases rapidly at birth to a peak during suckling and then decreases at weaning to the adult value. 3. The cytosol glyoxylate aminotransferase and the mitochondrial and cytosol 2-oxoglutarate aminotransferase activities first appear prenatally, increase further after birth and then rise to the adult values during weaning. 4. In foetal liver the mitochondrial glyoxylate aminotransferase and the cytosol 2-oxoglutarate aminotransferase activities are increased after injection in utero of glucagon, dibutyryl cyclic AMP (6-N,2′-O-dibutyryladenosine 3′:5′-cyclic monophosphate) or thyroxine. The cytosol glyoxylate aminotransferase and the mitochondrial 2-oxoglutarate aminotransferase activities are increased after injection in utero of cortisol or thyroxine. 5. After birth the further normal increases in the mitochondrial and cytosol 2-oxoglutarate aminotransferase activities can be hastened by cortisol injection, whereas the increase in cytosol glyoxylate aminotransferase activity requires cortisol treatment together with the intragastric administration of casein. 6. The results are discussed with reference to the metabolic patterns and the changes in regulatory stimuli (hormonal and dietary) that occur during the period of development.

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