The Effect of Nicotinic Acid, 5-Methylpyrazole-3-carboxylic Acid (U-19425), and Dibutyryl Cyclic AMP on Renal Gluconeogenesis

1971 ◽  
Vol 49 (2) ◽  
pp. 102-105
Author(s):  
Andrew Issekutz
Keyword(s):  
Carboxylic Acid ◽  
Cyclic Amp ◽  
Nicotinic Acid ◽  
Kidney Cortex ◽  
Dibutyryl Cyclic Amp ◽  
Renal Gluconeogenesis ◽  
Minimal Concentration ◽  
Cortex Slices ◽  
Glucose Formation ◽  
Kidney Cortex Slices

The effects of nicotinic acid, 5-methylpyrazole-3-carboxylic acid (U-19425), and dibutyryl (DB-) cyclic AMP on gluconeogenesis from lactate, oxalacetate, and glycerol were studied in kidney cortex slices. DB-cyclic AMP stimulated glucose formation from lactate (+67%), but not from oxalacetate or glycerol. Nicotinic acid and U-19425 inhibited gluconeogenesis from all three substrates by 30–63%. DB-cyclic AMP stimulated gluconeogenesis from lactate in the presence of either inhibitor. DB-cyclic AMP abolished the inhibition by either drug on glucose formation from oxalacetate or glycerol. It is concluded that nicotinic acid and U-19425 may inhibit gluconeogenesis by decreasing the cyclic AMP level within the cells, and that a minimal concentration of cyclic AMP may be functional above the triose phosphate level.

scholarly journals Inhibition of renal gluconeogenesis in rats by ochratoxin

1979 ◽  
Vol 180 (3) ◽  
pp. 681-684 ◽  
Author(s):  
H Meisner ◽  
P Selanik
Keyword(s):  
Ochratoxin A ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Kidney Cortex ◽  
Hexokinase Activity ◽  
Renal Gluconeogenesis ◽  
Cortex Slices ◽  
Kidney Cortex Slices

In kidney-cortex slices from rats fed on 2.0 mg of ochratoxin A/kg per day for 2 days, gluconeogenesis from pyruvate is decreased by 26%, and renal phosphoenolpyruvate carboxykinase activity is lowered by about 55%. Gluconeogenesis from 10 mM-lactate or 20 mM-malate or -glutamine is also significantly decreased. Hepatic phosphoenolpyruvate carboxykinase is unchanged or increased, and hexokinase activity in kidney and liver remains unaffected. We conclude that ochratoxin A in vivo is an inhibitor of renal phosphoenolpyruvate carboxykinase activity, which is responsible, at least in part, for the block in renal gluconeogenesis.

scholarly journals Renal gluconeogenesis. The effect of diet on the gluconeogenic capacity of rat-kidney-cortex slices

1963 ◽  
Vol 86 (1) ◽  
pp. 22-27 ◽  
Author(s):  
HA KREBS ◽  
DAH BENNETT ◽  
P DE GASQUET ◽  
P GASQUET ◽  
T GASCOYNE ◽  
...  
Keyword(s):  
Rat Kidney ◽  
Kidney Cortex ◽  
Rat Kidney Cortex ◽  
Renal Gluconeogenesis ◽  
Cortex Slices ◽  
Kidney Cortex Slices

scholarly journals Gluconeogenesis in the kidney cortex. Flow of malate between compartments

1970 ◽  
Vol 116 (3) ◽  
pp. 493-502 ◽  
Author(s):  
R. Rognstad
Keyword(s):  
Dehydrogenase Activity ◽  
Malate Dehydrogenase ◽  
Paper Chromatography ◽  
Analytical Methods ◽  
Specific Radioactivity ◽  
Kidney Cortex ◽  
Cortex Slices ◽  
Glucose Formation ◽  
Kidney Cortex Slices

1. Kidney-cortex slices from starved rats were incubated with l-[U-14C]lactate or l-[U-14C]malate plus unlabelled acetate and the specific radioactivity of the glucose formed was determined. In parallel experiments the specific radioactivity of the glucose formed from [1-14C]acetate plus unlabelled l-lactate and l-malate was determined. 2. By analytical methods the major products formed from the substrates were measured. The glucose formed was purified by paper chromatography for determination of specific radioactivity. 3. The specific radioactivity of the glucose formed from l-[U-14C]lactate agrees with predictions of a model based on interaction of the gluconeogenic and the oxidative pathways. 4. The specific radioactivity of the glucose formed from l-[U-14C]malate agrees with the predicted value if rapid malate exchange between the cytosol and mitochondria is assumed. 5. The rate of malate exchange between compartments was estimated to be rapid and at least several times the rate of glucose formation. 6. The specific radioactivity of the glucose formed from [1-14C]acetate plus unlabelled l-lactate or l-malate agrees with the predictions from the model, again assuming rapid malate exchange between compartments. 7. Malate exchange between compartments together with reversible malate dehydrogenase activity in the mitochondria and cytosol also tends to equilibrate isotopically the NADH pool in these compartments. 3H from compounds such as l-[2-3H]lactate, which form NAD3H in the cytosol, appears in part in water; and 3H from dl-β-hydroxy[3-3H]butyrate, which forms NAD3H in the mitochondria, appears in part in glucose, largely on C-4.

scholarly journals The interrelationship of the concentration of hydrogen ions, bicarbonate ions, carbon dioxide and calcium ions in the regulation of renal gluconeogenesis in the rat

1973 ◽  
Vol 136 (3) ◽  
pp. 445-453 ◽  
Author(s):  
George A. O. Alleyne ◽  
Hernando Flores ◽  
Anne Roobol
Keyword(s):  
Phosphoenolpyruvate Carboxylase ◽  
Rat Kidney ◽  
Respiratory Acidosis ◽  
Kidney Cortex ◽  
Rat Kidney Cortex ◽  
Bicarbonate Ions ◽  
Cortex Slices ◽  
Glucose Formation ◽  
Kidney Cortex Slices

1. The interrelationship of acidosis and Ca2+on the stimulation of gluconeogenesis by rat kidney-cortex slices was studied. 2. Ca2+stimulated gluconeogenesis from glutamine, glutamate, 2-oxoglutarate, succinate, malate, pyruvate, lactate and fructose, but not from galactose. 3. The [Ca2+] needed for optimum gluconeogenesis was about 2mm, but at this concentration, acidosis, produced in vitro by a decrease of [HCO3−] in the medium at constant pCO2 or by an increase in pCO2 at constant [HCO3−], did not stimulate gluconeogenesis. 4. In the absence of Ca2+, acidosis (low [HCO3−]) stimulated gluconeogenesis from glutamine, glutamate, 2-oxoglutarate, succinate, malate, pyruvate and lactate but not from fructose or galactose. With succinate as substrate, the stimulatory effect of acidosis (low [HCO3−]) disappeared at Ca2+concentrations above 1.0mm. 5. The [HCO3−] was the most important determinant of the acidosis effect since a decrease of pH caused by an increase in pCO2 did not uniformly stimulate gluconeogenesis, whereas a decrease in [HCO3−] without a change in pH consistently stimulated glucose formation in a way similar to the stimulation produced by acidosis (low [HCO3−]) in the absence of Ca2+. 6. Acidosis in vitro inhibited the rate of decrease of activity of phosphoenolpyruvate carboxylase in slices, and Ca2+caused an increase in the activity of fructose 1-phosphate aldolase. 7. Respiratory acidosis in vitro caused an increase in the activity of phosphoenolpyruvate carboxylase in kidney cortex and an increase in gluconeogenesis from glutamine. 8. Possible points of interaction between Ca2+, H+and HCO3−with the gluconeogenic sequence are discussed.

scholarly journals Glucose metabolism in the newborn rat. Hormonal effects in vivo

1973 ◽  
Vol 134 (4) ◽  
pp. 899-906 ◽  
Author(s):  
Keith Snell ◽  
Deryck G. Walker
Keyword(s):  
Cyclic Amp ◽  
Intraperitoneal Injection ◽  
Actinomycin D ◽  
Specific Radioactivity ◽  
Liver Glycogen ◽  
Newborn Rats ◽  
Dibutyryl Cyclic Amp ◽  
Lactate Formation ◽  
Glucose Formation

1. The concentrations of liver glycogen and plasma d-glucose were measured in caesarian-delivered newborn rats at time-intervals up to 3h after delivery after treatment of the neonatal rats with glucagon, dibutyryl cyclic AMP, cortisol or cortisol+dibutyryl cyclic AMP. Glycogenolysis was promoted by glucagon or dibutyryl cyclic AMP in the third hour after birth but not at earlier times. Cortisol and dibutyryl cyclic AMP together (but neither agent alone) promoted glycogenolysis in the second hour after birth, but no hormone combination was effective in the first postnatal hour. 2. The specific radioactivity of plasma d-glucose was measured as a function of time for up to 75 min after the intraperitoneal injection of d-[6-14C]glucose and d-[6-3H]glucose into newborn rats at delivery and after treatment with glucagon or actinomycin D. Glucagon-mediated hyperglycaemia at this time was due to an increased rate of glucose formation and a decreased rate of glucose utilization. Actinomycin D prevented glucose formation and accelerated the rate of postnatal hypoglycaemia. 3. The specific radioactivity of plasma l-lactate and the incorporation of 14C into plasma d-glucose was measured as a function of time after the intraperitoneal injection of l-[U-14C]lactate into glucagon- or actinomycin D-treated rats immediately after delivery. The calculated rates of lactate formation were unchanged by either treatment, but lactate utilization was stimulated by glucagon administration. Glucagon stimulated and actinomycin D diminished 14C incorporation into plasma d-glucose. 4. The factors involved in the initiation of glycogenolysis and gluconeogenesis in the rat immediately after birth are discussed.

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