scholarly journals Inhibition of renal gluconeogenesis in rats by ochratoxin

1979 ◽  
Vol 180 (3) ◽  
pp. 681-684 ◽  
Author(s):  
H Meisner ◽  
P Selanik

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.

1963 ◽  
Vol 86 (1) ◽  
pp. 22-27 ◽  
Author(s):  
HA KREBS ◽  
DAH BENNETT ◽  
P DE GASQUET ◽  
P GASQUET ◽  
T GASCOYNE ◽  
...  

1971 ◽  
Vol 49 (2) ◽  
pp. 102-105
Author(s):  
Andrew Issekutz

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.


1962 ◽  
Vol 203 (4) ◽  
pp. 655-661 ◽  
Author(s):  
E. C. Foulkes

In kidney cortex slices from rats and rabbits, cell K is known to be distributed between a diffusible compartment (Kd) and a nondiffusible pool (Knd). In the cold, Knd fails to exchange with extracellular Na or K despite the high permeability of the outer cell membrane to both Na and K. The Knd compartment is freely accessible only to metabolically linked K fluxes, whereas both active and passive fluxes occur into Kd. The distribution of K between Kd and Knd is altered by ouabain, cyanide, dinitrophenol, Ca, and other agents. This effect occurs in the absence of changes in the total K content of the cells and may represent an intracellular action of the drugs. The response of Knd to alterations in pH in vitro corresponds to the influence of acidosis or K deficiency in vivo. Together with the previous finding of a functional difference between Kd and Knd in vitro, the fact that the distribution of cellular potassium between two compartments can be altered by treatment of intact animals, as well as in slices, suggests that this potassium compartmentation may possess physiological significance.


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