scholarly journals The stimulation of tricarboxylic acid-cycle flux by α-adrenergic agonists in perfused rat liver

1986 ◽  
Vol 233 (2) ◽  
pp. 321-324 ◽  
Author(s):  
W M Taylor ◽  
E van de Pol ◽  
F L Bygrave
Keyword(s):  
Rat Liver ◽  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Perfused Rat Liver ◽  
Adrenergic Agonists ◽  
Acid Cycle ◽  
Total Tissue ◽  
Stimulation Of

Output of 14CO2 from 1-14C-labelled glutamate, 2-oxoglutarate or octanoate and from 4-methyl-2-oxo[2-14C]pentanoate was increased by more than 100% after infusion of phenylephrine into perfused livers of fed rats. Infusion of ethanol or sorbitol raised 3-hydroxybutyrate/acetoacetate ratios and decreased the output of 14CO2. Increases in 14CO2 output induced by phenylephrine were observed in the presence or absence of ethanol or sorbitol and were accompanied by elevated 3-hydroxybutyrate/acetoacetate ratios under all conditions examined. Phenylephrine had no effect on total tissue ATP/ADP ratios in livers from fed or starved rats. The data suggest that phenylephrine-induced increases in tricarboxylic acid-cycle flux do not arise from lowered matrix NADH/NAD+ or ATP/ADP ratios.

scholarly journals The Ca2+-mobilizing actions of vasopressin and angiotensin differ from those of the α-adrenergic agonist phenylephrine in the perfused rat liver

1985 ◽  
Vol 232 (3) ◽  
pp. 911-917 ◽  
Author(s):  
J G Altin ◽  
F L Bygrave
Keyword(s):  
Plasma Membrane ◽  
Rat Liver ◽  
Similar Amount ◽  
Perfused Rat Liver ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Hormone Administration ◽  
Sensitive Electrode ◽  
Stimulation Of

A Ca2+-sensitive electrode was used to study net Ca2+-flux changes induced by the administration of phenylephrine, vasopressin and angiotensin to the perfused rat liver. The studies reveal that, although the Ca2+ responses induced by vasopressin and angiotensin are similar, they are quite different from the Ca2+ fluxes induced by phenylephrine. The administration of phenylephrine is accompanied by a stimulation of a net amount of Ca2+ efflux (140 nmol/g of liver). A re-uptake of a similar amount of Ca2+ occurs only after the hormone is removed. In contrast, the administration of vasopressin or angiotensin to livers perfused with 1.3 mM-Ca2+ induces the release of a relatively small amount of Ca2+ (approx. 40 nmol/g of liver) during the first 60 s. This is followed by a much larger amount of Ca2+ uptake (70-140 nmol/g of liver) after 1-2.5 min of hormone administration, and a slow efflux or loss of a similar amount of Ca2+ over a period of 6-8 min. At lower concentrations of perfusate Ca2+ (less than 600 microM) these hormones induce only a net efflux of the ion. These results suggest that at physiological concentrations of extracellular Ca2+ the mechanism by which alpha-adrenergic agonists mobilize cellular Ca2+ is different from that involving vasopressin and angiotensin. It seems that the hormones may have quite diverse effects on Ca2+ transport across the plasma membrane and perhaps organellar membranes in liver.

scholarly journals The redistribution of carbon label by the reactions involved in glycolysis, gluconeogenesis and the tricarboxylic acid cycle in rat liver

1968 ◽  
Vol 110 (2) ◽  
pp. 313-335 ◽  
Author(s):  
D. F. Heath
Keyword(s):  
Carbon Dioxide ◽  
Steady State ◽  
Rat Liver ◽  
Tricarboxylic Acid Cycle ◽  
Specific Radioactivity ◽  
Tricarboxylic Acid ◽  
State Theory ◽  
Variable Rate ◽  
Acid Cycle ◽  
Constant Rate

A scheme is presented that shows how the reactions involved in gluconeogenesis, glycolysis and the tricarboxylic acid cycle are linked in rat liver. Equations are developed that show how label is redistributed in aspartate, glutamate and phosphopyruvate when it is introduced as specifically labelled pyruvate or glucose either at a constant rate (steady-state theory) or at a variable rate (non-steady-state theory). For steady-state theory the fractions of label introduced as specifically labelled pyruvate that are incorporated into glucose and carbon dioxide are also given, and for both theories the specific radioactivities of aspartate and glutamate relative to the specific radioactivity of the substrate. The theories allow for entry of label into the tricarboxylic acid cycle via both oxaloacetate and acetyl-CoA, for 14CO2 fixation and for loss of label from the tricarboxylic acid cycle in glutamate, but not for losses in citrate. They also allow for incomplete symmetrization of label in oxaloacetate due to incomplete equilibration with fumarate both in the extramitochondrial part of the cell and in the mitochondrion on entry of oxaloacetate into the tricarboxylic acid cycle. In the latter case failure both of oxaloacetate to equilibrate with malate and of malate to equilibrate with fumarate are considered.

scholarly journals Stimulation of [1-14C]oleate oxidation to 14CO2 in isolated rat hepatocytes by the catecholamines, vasopressin and angiotensin. A possible mechanism of action

1983 ◽  
Vol 212 (1) ◽  
pp. 85-91 ◽  
Author(s):  
M C Sugden ◽  
D I Watts
Keyword(s):  
Phosphoenolpyruvate Carboxykinase ◽  
Tricarboxylic Acid Cycle ◽  
Rat Hepatocytes ◽  
Tricarboxylic Acid ◽  
Isolated Rat Hepatocytes ◽  
Acid Cycle ◽  
14Co2 Production ◽  
Oxoglutarate Dehydrogenase ◽  
Stimulation Of

Adrenaline, noradrenaline, vasopressin and angiotensin increased 14CO2 production from [1-14C]oleate by hepatocytes from fed rats but not by hepatocytes from starved rats. The hormones did not increase 14CO2 production when hepatocytes from fed rats were depleted of glycogen in vitro. Increased 14CO2 production from]1-14C]oleate in response to the hormones was observed when hepatocytes from starved rats were incubated with 3-mercaptopicolinate, an inhibitor of phosphoenolpyruvate carboxykinase. 3-Mercaptopicolinate inhibited uptake and esterification of [1-14C]oleate, slightly increased 14CO2 production from [1-14C]oleate and greatly increased the [3-hydroxybutyrate]/[acetoacetate] ratio. In the presence of 3-mercaptopicolinate 14CO2 production in response to the catecholamines was blocked by the α-antagonist phentolamine and required extracellular Ca2+. The effects of vasopressin and angiotensin were also Ca2+-dependent. The actions of the hormones of 14CO2 production from [I-14C]oleate by hepatocytes from starved rats in the presence of 3-mercaptopicolinate thus have the characteristics of the response to the hormones found with hepatocytes from fed rats incubated without 3-mercaptopicolinate. The stimulatory effects of the hormones on 14CO2 production from [1-14C]oleate were not the result of decreased esterification (as the hormones increased esterification) or increased β-oxidation. It is suggested that the effect of the hormones to increase 14CO2 production from [1-14C]oleate are mediated by CA2+-activation of NAD+-linked isocitrate dehydrogenase, the 2-oxoglutarate dehydrogenase complex, and/or electron transport. The results also demonstrate that when the supply of oxaloacetate is limited it is utilized for gluconeogenesis rather than to maintain tricarboxylic acid-cycle flux.

THE EFFECT OF NEUTRAL SALTS ON PARTICLE PREPARATIONS FROM RAT LIVER: II. EFFECTS OF NEUTRAL SALTS ON TRICARBOXYLIC ACID CYCLE REACTIONS

1965 ◽  
Vol 43 (3) ◽  
pp. 359-372 ◽  
Author(s):  
E. R. Tustanoff ◽  
H. B. Stewart
Keyword(s):  
Rat Liver ◽  
Acid Metabolism ◽  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Neutral Salt ◽  
Acid Cycle ◽  
Pyruvate Oxidation ◽  
Highly Sensitive ◽  
Osmotic Activity

In a previous paper it was shown that neutral salt or sucrose, probably as a consequence of osmotic activity, interferes with the utilization of pyruvate by washed particle preparations from rat liver. In the present paper the effects of neutral salt on reaction sequences in the tricarboxylic acid cycle have been investigated. α-Oxoglutarate utilization is inhibited by salt in a fashion that closely resembles the osmolar inhibition of pyruvate oxidation. Citrate, but not cis-aconitate or isocitrate, utilization is inhibited by salt concentrations somewhat greater than those required for inhibition of α-oxo acid metabolism. Succinate, fumarate, and malate utilization are not highly sensitive to salt inhibition, and anaerobic utilization of citrate in the presence of 1,10-phenanthroline does not appear to be affected by salt.

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