Metabolism of maltose in perfused rat liver and in isolated hepatocytes

1976 ◽  
Vol 168 (3) ◽  
pp. 157-163 ◽  
Author(s):  
U. Sprandel ◽  
G. Wolfram ◽  
R. Scholz
Keyword(s):  
Rat Liver ◽  
Isolated Hepatocytes ◽  
Perfused Rat Liver

Enhanced cytotoxicity of imidacloprid by biotransformation in isolated hepatocytes and perfused rat liver

2020 ◽  
Vol 164 ◽  
pp. 183-190
Author(s):  
Paulo F.V. Bizerra ◽  
Anilda R.J.S. Guimarães ◽  
Camila A. Miranda ◽  
Rodrigo P. Constantin ◽  
Karina S. Utsunomiya ◽  
...  
Keyword(s):  
Rat Liver ◽  
Isolated Hepatocytes ◽  
Perfused Rat Liver

scholarly journals NH4+ metabolism and the intracellular pH in isolated perfused rat liver

1993 ◽  
Vol 293 (3) ◽  
pp. 667-673 ◽  
Author(s):  
J Zange ◽  
J Gronczewski ◽  
A W H Jans
Keyword(s):  
Intracellular Ph ◽  
Rat Liver ◽  
Isolated Hepatocytes ◽  
Isolated Perfused Rat Liver ◽  
Small Range ◽  
Perfused Rat Liver ◽  
Atp Content ◽  
Intracellular Acidification ◽  
Subsequent Conversion ◽  
Intracellular Alkalinization

The effects of NH4+ on the intracellular pH (pHi) and on the ATP content in isolated perfused rat liver were studied by 31P n.m.r. spectroscopy. In the initial phase of perfusion an average pHi of 7.29 +/- 0.04 was estimated. The presence of low (0.5 mmol/l) and high (10 mmol/l) doses of NH4Cl induced significant intracellular acidification by -0.06 +/- 0.03 and -0.11 +/- 0.03 pH unit respectively. This effect was in contrast with the transient intracellular alkalinization observed in preliminary studies on isolated hepatocytes, which was caused by a passive entry of NH3 by non-ionic diffusion and subsequent conversion into NH4+. During application of 0.5 mmol/l NH4Cl the liver released 0.54 +/- 0.06 mumol of urea/min per g into the perfusate. When the intracellular availability of HCO3- was decreased by acetazolamide (0.5 mmol/l) or by removal of HCO3- from the perfusion medium, the decrease in pHi by NH4Cl application was significantly lower than under control conditions. Furthermore, synthesis of urea was significantly inhibited by the decrease in intracellular HCO3-. Under these conditions, 10 mmol/l NH4Cl caused the transient alkalinization that was expected because of the passive uptake of uncharged NH3. Therefore, it is concluded that the intracellular acidification induced by NH4Cl is caused by the continuous utilization of intracellular HCO3- via the synthesis of urea. This metabolic effect on pHi dominates the effects of passive NH3 entry. The rate of urea formation depends on continuous efflux of H+, which is strictly limiting the degree of intracellular acidification within a small range. If the extrusion of H+ by the Na+/H+ exchanger was inhibited by amiloride (0.5 mmol/l) during the NH4Cl application, the decrease in pHi was amplified and the formation of urea was significantly inhibited. The application of NH4Cl at 0.5 or 10 mmol/l decreased the ATP content by 11% or 22% respectively.

scholarly journals Rapid Ca2+ influx induced by the action of dibutylhydroquinone and glucagon in the perfused rat liver

1997 ◽  
Vol 323 (2) ◽  
pp. 463-467 ◽  
Author(s):  
Tanya L. APPLEGATE ◽  
Ari KARJALAINEN ◽  
Fyfe L. BYGRAVE
Keyword(s):  
Endoplasmic Reticulum ◽  
Electron Transport ◽  
Rat Liver ◽  
Sodium Azide ◽  
Isolated Hepatocytes ◽  
Atp Depletion ◽  
Perfused Rat Liver ◽  
Total Calcium ◽  
Combined Administration ◽  
Prior Administration

Glucagon induces a slight Ca2+ efflux when administered to the perfused rat liver. However, the hormone promotes rapid and significant Ca2+ influx after the prior administration of 2,5-di(t-butyl)-1,4-hydroquinone (BHQ), an agent that promotes Ca2+ release from the endoplasmic reticulum (ER). The concentrations of glucagon that promote Ca2+ influx are similar to those that promote glycogenolysis and gluconeogenesis in isolated hepatocytes. The permeable analogue of cAMP, but not that of cGMP, is able to duplicate the Ca2+-mobilizing effects of glucagon. The influx of Ca2+ into liver is blocked by Ni2+. Administration of sodium azide, an inhibitor of mitochondrial electron transport, also blocks the BHQ plus glucagon-induced Ca2+ influx and this is reversed when azide administration is terminated. The actions of azide are evident within 60 s after administration or withdrawal, and also occur when either oligomycin or fructose is co-administered; this provides evidence for an effect of azide independent of cellular ATP depletion. Measurement of total calcium in mitochondria that were isolated rapidly from perfused livers after the combined administration of glucagon and BHQ confirmed that large quantities of extracellular Ca2+ had entered these organelles. These experiments provide evidence that in the perfused rat liver the artificial emptying of the ER Ca2+ pool allows glucagon to promote rapid and sustained Ca2+ influx that seems to terminate in mitochondria.

Effect of indomethacin on the uptake, metabolism and excretion of 3-oxocholic acid: Studies in isolated hepatocytes and perfused rat liver

1991 ◽  
Vol 1084 (3) ◽  
pp. 247-250 ◽  
Author(s):  
H. Takikawa ◽  
J.C. Fernandez-Checa ◽  
J. Kuhlenkamp ◽  
A. Stolz ◽  
M. Ookhtens ◽  
...  
Keyword(s):  
Rat Liver ◽  
Isolated Hepatocytes ◽  
Perfused Rat Liver

scholarly journals Inhibition of proteolysis by cell swelling in the liver requires intact microtubular structures

1995 ◽  
Vol 308 (2) ◽  
pp. 529-536 ◽  
Author(s):  
S vom Dahl ◽  
B Stoll ◽  
W Gerok ◽  
D Häussinger
Keyword(s):  
Cell Volume ◽  
Rat Liver ◽  
Rat Hepatocytes ◽  
Isolated Hepatocytes ◽  
Cell Swelling ◽  
Perfused Rat Liver ◽  
Volume Changes ◽  
Isolated Rat Hepatocytes ◽  
Microtubule Inhibitors ◽  
Microtubular Structures

In the perfused rat liver, proteolysis is inhibited by cell swelling in response to hypo-osmotic media, glutamine and insulin. Colchicine, an inhibitor of microtubules, did not affect cell swelling in response to these agonists. However, the antiproteolytic action of these effectors was largely blunted in the presence of colchicine or the microtubule inhibitors colcemid and taxol. On the other hand, inhibition of proteolysis by phenylalanine, asparagine or NH4Cl, i.e. compounds which exert their antiproteolytic effects by mechanisms distinct from cell swelling, was not sensitive to colchicine. Swelling-induced inhibition of proteolysis was not affected by cytochalasin B. The anti-proteolytic effect of hypo-osmotic cell swelling and insulin was largely abolished in freshly isolated rat hepatocytes; however, it reappeared upon cultivation of the hepatocytes for 6-10 h. The restoration of the sensitivity of proteolysis to cell volume changes was accompanied by a progressive reorganization of microtubule structures, as shown by immunohistochemical staining for tubulin. It is concluded that intact microtubules are required for the control of proteolysis by cell volume, but not for the control of proteolysis by phenylalanine, asparagine or NH4Cl. These findings may explain why others [Meijer, Gustafson, Luiken, Blommaart, Caro, Van Woerkom, Spronk and Boon (1993) Eur. J. Biochem. 215, 449-454] failed to detect an antiproteolytic effect of hypo-osmotic exposure of freshly isolated hepatocytes. This effect, however, which is consistently found in the intact perfused rat liver, also reappeared in isolated hepatocytes when they were allowed to reorganize their microtubular structures in culture.

Effects of Ca2+ agonists on cytosolic Ca2+ in isolated hepatocytes and on bile secretion in the isolated perfused rat liver

Hepatology ◽  
1992 ◽  
Vol 15 (1) ◽  
pp. 107-116 ◽  
Author(s):  
Michael H. Nathanson ◽  
Anil Gautam ◽  
Rafael Bruck ◽  
Carlos M. Isales ◽  
James L. Boyer
Keyword(s):  
Rat Liver ◽  
Isolated Hepatocytes ◽  
Bile Secretion ◽  
Isolated Perfused Rat Liver ◽  
Perfused Rat Liver

Oxygen consumption by rat liver: effects of taurocholate and sulfobromophthalein transport, glucagon, and cation substitution

1983 ◽  
Vol 244 (5) ◽  
pp. G523-G531
Author(s):  
R. W. van Dyke ◽  
J. L. Gollan ◽  
B. F. Scharschmidt
Keyword(s):  
Oxygen Consumption ◽  
Rat Liver ◽  
Large Fraction ◽  
Isolated Hepatocytes ◽  
Rectal Gland ◽  
Isolated Perfused Rat Liver ◽  
Cation Substitution ◽  
Perfused Rat Liver ◽  
Oxygen Utilization ◽  
Bile Formation

The proportion of total hepatic energy utilized for bile formation and transport of taurocholate (TC) and conjugated sulfobromophthalein (cBSP) has not been defined previously. To study this question we have measured changes in oxygen consumption by the isolated perfused rat liver and freshly isolated hepatocytes occurring in response to TC and cBSP administration, cation substitution, and glucagon infusion. The basal rates of bile formation and oxygen consumption varied considerably among different livers, and there was little or no relationship between these two variables. Administration of either TC or cBSP to the perfused liver elicited a marked choleresis but failed to alter steady-state oxygen consumption even at maximal rates of TC or cBSP transport. Similarly, incubation of hepatocytes with TC or cBSP did not alter oxygen consumption. In contrast, inhibition of Na-K-ATPase by removal of sodium and/or potassium from the medium reduced oxygen consumption by perfused rat liver and isolated hepatocytes by 27-37%, and glucagon administration increased oxygen consumption in both systems by 31-40%. These findings indicate that the oxygen requirement for bile formation and even maximal rates of TC and cBSP transport is small compared with that for the metabolic changes induced by glucagon or for hepatic Na-K-ATPase activity. This is in contrast to other epithelial tissues, such as kidney and rectal gland, in which oxygen utilization for transepithelial solute and water transport constitutes a large fraction of both total and Na-K-ATPase-dependent oxygen consumption.

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