scholarly journals The characteristics and site of inhibition of gluconeogenesis in rat liver cells by bacterial endotoxin. Stimulation of phosphofructokinase-1

1987 ◽  
Vol 242 (3) ◽  
pp. 721-728 ◽  
Author(s):  
R G Knowles ◽  
J P McCabe ◽  
S J Beevers ◽  
C I Pogson
Keyword(s):  
Enzyme Activities ◽  
Pyruvate Carboxylase ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Liver Cells ◽  
Atp Content ◽  
Rat Liver Cells ◽  
Endogenous Substrates ◽  
And Control ◽  
Control Coefficients ◽  
Stimulation Of

The characteristics and site of inhibition of gluconeogenesis by endotoxin were investigated in liver cells isolated from control and endotoxin-treated rats. Endotoxin treatment was associated with inhibition (40-50%) of gluconeogenesis from lactate plus pyruvate over a range of concentrations of substrate and of oleate and with or without glucose or glucagon. Similar inhibition was observed with asparagine, proline, glutamine, alanine and a substrate mixture, but not with glycerol, glyceraldehyde, dihydroxyacetone or endogenous substrates. There was no change in cellular ATP content or in the rates of ketogenesis or ureogenesis from asparagine, proline or glutamine. Other effects on isotopic fluxes, metabolite contents, enzyme activities and control coefficients were consistent with the suggestion that the effects of endotoxin on gluconeogenesis are exerted at the level of phosphofructokinase-1, and not at phosphoenolpyruvate carboxykinase, pyruvate kinase, pyruvate carboxylase or glucokinase.

scholarly journals Streptozotocin-induced diabetes impairs Mg2+ homeostasis and uptake in rat liver cells

2004 ◽  
Vol 286 (2) ◽  
pp. E184-E193 ◽  
Author(s):  
Theresa E. Fagan ◽  
Christie Cefaratti ◽  
Andrea Romani
Keyword(s):  
Liver Cells ◽  
Atp Content ◽  
Sprague Dawley ◽  
Uptake Mechanism ◽  
Diabetes Onset ◽  
Kinase C ◽  
Sprague Dawley Rats ◽  
Rat Liver Cells ◽  
Streptozotocin Induced Diabetes ◽  
Stimulation Of

Male Sprague-Dawley rats rendered diabetic by streptozotocin injection presented 10 and 20% decreases in total hepatic Mg2+ content at 4 and 8 wk, respectively, following diabetes onset. This decrease was associated with a parallel decrease in K+ and ATP content and an increase in Na+ level. In diabetic liver cells, the Mg2+ extrusion elicited by α1-adrenoceptor stimulation was markedly reduced compared with nondiabetic livers, whereas that induced by β-adrenoceptor stimulation was unaffected. In addition, diabetic hepatocytes did not accumulate Mg2+ following stimulation of protein kinase C pathway by vasopressin, diacylglycerol analogs, or phorbol 12-myristate 13-acetate derivates despite the reduced basal content in cellular Mg2+. Experiments performed in purified plasma membrane from diabetic livers located the defect at the level of the bidirectional Na+/Mg2+ exchanger operating in the basolateral domain of the hepatocyte cell membrane, which could extrude but not accumulate Mg2+ in exchange for Na+. The impairment of Mg2+ uptake mechanism, in addition to the decrease in cellular ATP level, can contribute to explaining the decrease in liver Mg2+ content observed under diabetic conditions.

Chronic EtOH administration alters liver Mg2+homeostasis

2003 ◽  
Vol 284 (1) ◽  
pp. G57-G67 ◽  
Author(s):  
Andrew Young ◽  
Christie Cefaratti ◽  
Andrea Romani
Keyword(s):  
Adrenergic Receptor ◽  
Prolonged Exposure ◽  
Liver Cells ◽  
Chronic Alcohol ◽  
Atp Content ◽  
Chronic Alcohol Consumption ◽  
Kinase C ◽  
And Control ◽  
Total Tissue ◽  
Stimulation Of

Ethanol (EtOH) administration to rats for 4 wk markedly decreased Mg2+ content in several tissues, including liver. Total cellular Mg2+ accounted for 26.8 ± 2.4 vs. 36.0 ± 1.4 nmol Mg2+/mg protein in hepatocytes from EtOH-fed and control rats, respectively, and paralleled a 13% decrease in cellular ATP content. Stimulation of α1- or β-adrenergic receptor or acute EtOH administration did not elicit an extrusion of Mg2+ from liver cells of EtOH-fed rats while releasing 5% of total tissue Mg2+ content from hepatocytes of control rats. Despite the 25% decrease in Mg2+ content, hepatocytes from EtOH-fed rats did not accumulate Mg2+following stimulation of protein kinase C signaling pathway, whereas control hepatocytes accumulated ∼2 nmol Mg2+ · mg protein−1 · 4 min−1. Together, these data indicate that Mg2+ homeostasis and transport are markedly impaired in liver cells after prolonged exposure to alcohol. The inability of liver cells, and possibly other tissues, to accumulate Mg2+ can help explain the reduction in tissue Mg2+ content following chronic alcohol consumption.

Effects of Hypophysectomy on the Fine Structure of Rat Liver Cells

1967 ◽  
Vol 25 ◽  
pp. 156-157
Author(s):  
Robert R. Cardell
Keyword(s):  
Electron Microscopy ◽  
Fine Structure ◽  
Rat Liver ◽  
Liver Cell ◽  
Anterior Pituitary ◽  
Liver Cells ◽  
Biochemical Studies ◽  
Liver Functions ◽  
Rat Liver Cells ◽  
And Control

Hypophysectomy of the rat renders this animal deficient in the hormones of the anterior pituitary gland, thus causing many primary and secondary hormonal effects on basic liver functions. Biochemical studies of these alterations in the rat liver cell are quite extensive; however, relatively few morphological observations on such cells have been recorded. Because the available biochemical information was derived mostly from disrupted and fractionated liver cells, it seemed desirable to examine the problem with the techniques of electron microscopy in order to see what changes are apparent in the intact liver cell after hypophysectomy. Accordingly, liver cells from rats which had been hypophysectomized 5-120 days before sacrifice were studied. Sham-operated rats served as controls and both hypophysectomized and control rats were fasted 15 hours before sacrifice.

scholarly journals Differential effects of tryptophan on glucose synthesis in rats and guinea pigs

1978 ◽  
Vol 176 (3) ◽  
pp. 817-825 ◽  
Author(s):  
S A Smith ◽  
K R F Elliott ◽  
C I Pogson
Keyword(s):  
Rat Liver ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Glucose Production ◽  
Rat Hepatocytes ◽  
Liver Cells ◽  
Isolated Rat Hepatocytes ◽  
Rat Liver Cells ◽  
Glucose Output ◽  
Isolated Rat

1. Tryptophan inhibition of gluconeogenesis in isolated rat liver cells is characterized by a 20 min lag period before linear rates of glucose output are attained. 2. Half-maximal inhibition of gluconeogenesis in isolated rat hepatocytes is produced by approx. 0.1 mM-tryptophan. 3. Tryptophan inhibits gluconeogenesis from all substrates giving rise to oxaloacetate, but stimulates glycerol-fuelled glucose production. 4. Gluconeogenesis in guinea-pig hepatocytes is insensitive to tryptophan. 5. Changes in metabolite concentrations in rat liver cells are consistent with a locus of inhibition at the step catalysed by phosphoenolpyruvate carboxykinase. 6. Inhibition of gluconeogenesis persists in cells from rats pretreated with tryptophan in vivo. 7. Tryptophan has no effect on urea production from alanine, but decreases [1-14C]palmitate oxidation to 14CO2 and is associated with an increased [hydroxybutyrate]/[acetoacetate] ratio. 8. These results are discussed with reference to the control of gluconeogenesis in various species.

In vitro stimulation of rat liver cells by homologous partial hepatectomy serum

In Vitro ◽  
1971 ◽  
Vol 7 (1) ◽  
pp. 1-5 ◽  
Author(s):  
Lynne P. Rutzky ◽  
William G. Taylor ◽  
Robert W. Pumper
Keyword(s):  
Partial Hepatectomy ◽  
Rat Liver ◽  
Liver Cells ◽  
Rat Liver Cells ◽  
Stimulation Of

scholarly journals Effect of treatment of rats with dexamethasone in vivo on gluconeogenesis and metabolite compartmentation in subsequently isolated hepatocytes

1984 ◽  
Vol 219 (1) ◽  
pp. 117-123 ◽  
Author(s):  
E H Allan ◽  
M A Titheradge
Keyword(s):  
Pyruvate Carboxylase ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Intact Cell ◽  
Isolated Hepatocytes ◽  
Dexamethasone Treatment ◽  
Acetyl Coa ◽  
General Activation ◽  
Effect Of Treatment ◽  
Stimulation Of

Hepatocytes prepared from rats treated with dexamethasone for 2 or 3h and maintained in the presence of 10 microM-dexamethasone in the preparation and incubation buffers showed significantly elevated rates of gluconeogenesis compared with those prepared from control animals. Dexamethasone treatment also increased the sensitivity of the cells to glucagon and the catecholamines. Analysis of the concentrations of metabolites in the gluconeogenic pathway indicated that dexamethasone decreased the intracellular concentration of pyruvate and increased those of phosphoenolpyruvate, acetyl-CoA and citrate, suggesting a stimulation of the reaction(s) converting pyruvate into phosphoenolpyruvate. This was substantiated by analysis of the pattern of metabolites found in the mitochondrial compartment after digitonin fractionation of the cells. Inclusion of 3-mercaptopicolinate in the incubation enhanced the effect of the hormone on the distribution of metabolites. Thus, in the absence of an effect of the steroid at the level of phosphoenolpyruvate carboxykinase or pyruvate kinase, dexamethasone treatment still increased the formation of malate, aspartate and citrate from pyruvate, indicating a stimulation in the intact cell of pyruvate carboxylase. It is suggested that the stimulation of pyruvate carboxylase is a result of a general activation of mitochondrial function, with an increase in the intramitochondrial concentrations of acetyl-CoA and ATP, a decrease in glutamate and an enhanced intramitochondrial [ATP]/[ADP] ratio.

Activation of Na+- and Ca2+-dependent Mg2+ extrusion by α1- and β-adrenergic agonists in rat liver cells

2000 ◽  
Vol 279 (5) ◽  
pp. G943-G950 ◽  
Author(s):  
Theresa E. Fagan ◽  
Andrea Romani
Keyword(s):  
Adrenergic Receptor ◽  
Liver Cells ◽  
Adrenergic Agonists ◽  
Experimental Conditions ◽  
Rat Liver Cells ◽  
Rat Livers ◽  
Cellular Ca ◽  
Adrenergic Receptor Agonist ◽  
Dependent Mechanism ◽  
Stimulation Of

The administration of selective α1 (phenylephrine)-, β (isoproterenol)-, or mixed (epinephrine) adrenergic agonists induces a marked Mg2+extrusion from perfused rat livers. In the absence of extracellular Ca2+, phenylephrine does not induce a detectable Mg2+ extrusion, isoproterenol-induced Mg2+mobilization is unaffected, and epinephrine induces a net Mg2+ extrusion that is lower than in the presence of extracellular Ca2+ and quantitatively similar to that elicited by isoproterenol. In the absence of extracellular Na+, no Mg2+ is extruded from the liver irrespective of the agonist used. Similar results are observed in perfused livers stimulated by glucagon or 8-chloroadenosine 3′,5′-cyclic monophosphate. In the absence of extracellular Na+ or Ca2+, adrenergic-induced glucose extrusion from the liver is also markedly decreased. Together, these results indicate that liver cells extrude Mg2+ primarily via a Na+-dependent mechanism. This extrusion pathway can be activated by the increase in cellular cAMP that follows the stimulation by glucagon or a specific β-adrenergic receptor agonist or, alternatively, by the changes in cellular Ca2+ induced by the stimulation of the α1-adrenoceptor. In addition, the stimulation of the α1-adrenoceptor appears to activate an auxiliary Ca2+-dependent Mg2+extrusion pathway. Finally, our data suggest that experimental conditions that affect Mg2+ mobilization also interfere with glucose extrusion from liver cells.

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