The nature of the changes in liver mitochondrial function induced by glucagon treatment of rats. The effects of intramitochondrial volume, aging and benzyl alcohol

Armston, Annie; Halestrap, Andrew P.; Scott, Robin D.

doi:10.1016/0005-2728(82)90185-2

Cited by 57 publications

(77 citation statements)

References 75 publications

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“…The stimulation of glutamine uptake and utilization may in part be the result of mitochondria1 swelling [26,27]. In contrast to urea formation from glutamine, urea formation from exogenous ammonia is inhibited.…”

Section: Resultsmentioning

confidence: 99%

Exposure of perfused liver to hypotonic conditions modifies cellular nitrogen metabolism

Häussinger

Läng

1990

J of Cellular Biochemistry

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Isolated livers were exposed to hypotonic perfusates. As shown previously, this hypotonic challenge leads to initial cell swelling, followed by volume regulatory ion fluxes, largely restoring cell volume within approximately 6 min. However, the hepatocyte is left in an altered metabolic state, which is characterized by marked stimulation of hepatic glutamine uptake and degradation and transient release of glutamate from the liver. Urea formation from glutamine and alanine is stimulated, whereas hepatic ammonia uptake and utilization for urea and glutamine synthesis decreases. These observations reveal a hitherto unrecognized factor modulating hepatic function during intestinal absorption.

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Section: Resultsmentioning

confidence: 99%

Exposure of perfused liver to hypotonic conditions modifies cellular nitrogen metabolism

Häussinger

Läng

1990

J of Cellular Biochemistry

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“…Furthermore, in bovine heart, PKA activity was detected in the matrix or the matrix side of the mitochondrial inner membrane [44,45]. However, the work of Halestrap and coworkers provided little evidence for intramitochondrial protein phosphorylation by PKA, but gave some evidence for outer membrane phosphorylation, both integral and loosely bound proteins [46-48]. The localization of RIIα to the postsynaptic region beyond the postsynaptic membrane is consistent with part of the immunostaining of NMJs in the soleus muscle [18], yet differs in part because there is no overlap with the bungarotoxin label; however, this is in agreement with another study [17].…”

Section: Discussionmentioning

confidence: 99%

PKA, PKC, and AKAP localization in and around the neuromuscular junction

et al. 2001

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Background: One mechanism that directs the action of the second messengers, cAMP and diacylglycerol, is the compartmentalization of protein kinase A (PKA) and protein kinase C (PKC). A-kinase anchoring proteins (AKAPs) can recruit both enzymes to specific subcellular locations via interactions with the various isoforms of each family of kinases. We found previously that a new class of AKAPs, dual-specific AKAPs, denoted D-AKAP1 and D-AKAP2, bind to RIα in addition to the RII subunits.

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“…This effect might be dependent on the composition of the isolation medium (Siess et al, 1981(Siess et al, , 1984(Siess et al, , 1985Siess, 1983a, b ;Halestrap et al, 1985). Osmotic and volume effects have also been considered (Armston, Halestrap & Scott, 1982;Quinlan et al, 1983;Whipps & Halestrap, 1984;Quinlan & Halestrap, 1986) as have the supply or content of malate (Bobyleva-Guarriero et al, 1986), phosphate (Siess et al, 1985) and pyrophosphate (Halestrap et al, 1985). There is circumstantial evidence that some of these changes occur in vivo: however, until clearer evidence is forthcoming that they can be important in control of respiration in intact cells and tissues they cannot be properly evaluated.…”

Section: (B) Effects In Isolated Liver Mitochondriamentioning

confidence: 99%

Control of Electron Flux Through the Respiratory Chain in Mitochondria and Cells

1987

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Summary To answer the question ‘What controls the rate of respiration?’ requires a clear definition of control and an explicit description of the limits of the system to be considered. In this review we use a neutral definition of control in which A controls B if changes in A cause changes in B. A useful system to define when discussing the control of respiration consists of the electron transport chain, the H+‐ATPase, the adenine nucleotide carrier, the intramitochondrial adenine nucleotide and phosphate pools, δp and the proton leak across the mitochondrial inner membrane. Controls operating within this system are designated internal controls and many of them are fairly well characterized. Several models have been advanced to describe the rates of these internal processes in isolated mitochondria, including control of respiration rate by cytochrome oxidase with all other steps near to equilibrium, control by the adenine nucleotide carrier or control by the extent of displacement of individual reactions from equilibrium. More recently, analysis using control theory has shown that in the resting state (state 4) most control over flux is exerted by the leak of protons through the inner membrane, whereas in more active, phosphorylating states (up to state 3) control is distributed between a number of steps, including the proton leak, the adenine nucleotide carrier and cytochrome oxidase. This approach seems a very useful framework within which to pose further questions. This system may be treated as a ‘black box’ interacting with its environment (the rest of the mitochondrion and the experimental cuvette or living cell) through the redox states of NAD, Q and O2 and through the phosphorylation state of the extramitochondrial adenine nucleotides. Very few external effectors cross the system boundary; the only well‐characterized ones are long‐chain fatty acyl‐CoA, which inhibits the adenine nucleotide carrier, and fatty acids, which activate a specific uncoupling protein found only in the inner membrane of mitochondria from brown adipose tissue. At this level respiration rate is determined only by the internal properties of the ‘black box’, by the redox states of NAD, Q and O2, and by the phosphorylation status of the extramitochondrial adenine nucleotide pool. Within a cell the rate of respiration is controlled primarily by the rates of reactions feeding electrons to the electron transport chain (through their effects on NADH/NAD and QH2/Q ratios) and by the rates of reactions consuming or producing ATP (through the cytosolic phosphorylation potential or ATP/ADP ratio). Control of reducing equivalent supply occurs through availability of oxidizable substrates (determined by diet and hormonal status), through regulation of pathways such as glycolysis or fatty acid catabolism and, importantly, through Ca2+ activation of intramitochondrial dehydrogenases. Hormonal control over respiration can occur at all the levels mentioned. Hormones may alter the kinetic properties of the oxidative phosphorylation system by alterin...

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The nature of the changes in liver mitochondrial function induced by glucagon treatment of rats. The effects of intramitochondrial volume, aging and benzyl alcohol

Cited by 57 publications

References 75 publications

Exposure of perfused liver to hypotonic conditions modifies cellular nitrogen metabolism

Exposure of perfused liver to hypotonic conditions modifies cellular nitrogen metabolism

PKA, PKC, and AKAP localization in and around the neuromuscular junction

Control of Electron Flux Through the Respiratory Chain in Mitochondria and Cells

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