Stimulation of hepatic mitochondrial calcium transport by elevated plasma insulin concentrations

Dorman, D M; Barritt, Greg J.; Bygrave, Fyfe L.

doi:10.1042/bj1500389

Cited by 44 publications

(28 citation statements)

References 30 publications

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“…Moreover, other experiments in this laboratory (V. Prpic, T. L. Spencer & F. L. Bygrave, unpublished work) have shown that glucagon administration to rats in vivo, which offsets the uncoupling action of Ca2+ on isolated mitochondria described above, is without effect on the Ca2+ efflux seen here (see also Dorman et al, 1975).…”

Section: Discussionmentioning

confidence: 66%

Calcium ion cycling in rat liver mitochondria

Ramachandran

Bygrave

1978

Biochemical Journal

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1. Addition of N-ethylmaleimide to rat liver mitochondria respiring with succinate as substrate decreases both the initial rate of Ca(2+) transport and the ability of mitochondria to retain Ca(2+). As a result, Ca(2+) begins to leave the mitochondria soon after it has entered. Half-maximal effects occur at an N-ethylmaleimide concentration of about 100nmol/mg of protein. 2. The efflux of Ca(2+) induced by N-ethylmaleimide is not prevented by Mg(2+) or by Ruthenium Red at concentrations known to prevent Ca(2+) efflux when exogenous phosphate also is present. Swelling of mitochondria does not accompany N-ethylmaleimide-induced Ca(2+) efflux. 3. Addition of Ca(2+) to rat liver mitochondria in the presence of N-ethylmaleimide produces an immediate decrease in DeltaE (membrane potential), which decreases further to only a slight extent over the next 8min. Concomitant with this is an immediate increase and then levelling off of the -59DeltapH (transmembrane pH gradient). 4. Preincubation of rat liver mitochondria with p-chloromercuribenzenesulphonate, which by contrast with N-ethylmaleimide is unable to penetrate the inner mitochondrial membrane, also prevents Ca(2+) retention. The DeltaE and -59DeltapH respond to Ca(2+) addition in a manner similar to that which occurs when N-ethylmaleimide is present. Subsequent addition of mercaptoethanol produces an immediate increase in both DeltaE and -59DeltapH. At the same time Ca(2+) is rapidly accumulated by the organelles. 5. The above data are interpreted as indicating that under the conditions of Ca(2+) efflux seen here, the mitochondria retain their functional integrity. This contrasts with the uncoupling effect of Ca(2+) seen in the presence of P(i), which generally leads to a loss of mitochondrial integrity. We suggest that a unique mechanism of Ca(2+) cycling is able to take place when mitochondria have been treated with N-ethylmaleimide.

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Section: Discussionmentioning

confidence: 66%

Calcium ion cycling in rat liver mitochondria

Ramachandran

Bygrave

1978

Biochemical Journal

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“…As mentioned in the Introduction, recent work has provided evidence that mitochondrial Ca2+ transport might be a site for insulin [5] and glucagon [6] action in vivo. It seems quite significant in this regard that that at the time of birth marked changes in the plasma levels of both insulin [ 191 and glucagon [20] occur in the rat.…”

Section: Discussionmentioning

confidence: 99%

“…That this process plays an important physiological role in the control of cell Cap in vivo [3,4] has received impetus from studies showing that Cap transport in liver mitochondria might be a target for hormone action in vivo [5,6] , that Ca2' transport in tumour mitochondria may to some extent be deranged and that Ca2' transport in mitochondria isolated from flightmuscle of the blowfly changes markedly with development [lo].…”

Section: Introductionmentioning

confidence: 99%

Development of mitochondrial calcium transport activity in rat liver

Bygrave

Ash

1977

FEBS Letters

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“…(2) Insulin also counteracted the activation of phosphorylase by phenylephrine, suggesting that it might affect Ca2+ concentration, which, as indicated above, seems to play a role in the action of the aadrenergic agonist. It is of interest to recall that hepatic mitochondrial Ca2+ transport is stimulated in rats treated with insulin (Dormann et al, 1975).…”

Section: Effect Of Insulinmentioning

confidence: 99%

Hormonal and ionic control of the glycogenolytic cascade in rat liver

Werve¹,

Hue²,

Hers³

1977

Biochemical Journal

199

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1. A parallel dose-dependent activation of histone kinase, phosphorylase kinase and phosphorylase was observed in isolated hepatocytes incubated in the presence of glucagon; the effect of suboptimal concentrations of glucagon was antagonized by insulin. 2. An activation of phosphorylase which was not accompanied by a stable change in the activity of phosphorylase kinase was observed in hepatocytes incubated with phenylephrine, isoproterenol or vasopressin as well as on decapitation of unanesthetized animals. A dissociation of the two enzymic activities was also observed in hepatocytes incubated in the presence of a high concentration of glucose, in which phosphorylase was strongly inactivated with no change in the activity of phosphorylase kinase. 3. The activation of phosphorylase by phenylephrine in isolated hepatocytes was counteracted by insulin, greatly decreased by the absence of Ca2+ from the incubation medium, and completely suppressed by the replacement of Na+ by K+. 4. In a liver extract, phosphorylase kinase could also be activated by trypsin. Control, glucagon-activated or trypsin-activated phosphorylase kinase was inhibited by about 70% by EGTA and the activity was restored by the addition of Ca2+. 5. The mechanisms that control the activity of phosphorylase kinase and of phosphorylase are discussed.

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Stimulation of hepatic mitochondrial calcium transport by elevated plasma insulin concentrations

Cited by 44 publications

References 30 publications

Calcium ion cycling in rat liver mitochondria

Calcium ion cycling in rat liver mitochondria

Development of mitochondrial calcium transport activity in rat liver

Hormonal and ionic control of the glycogenolytic cascade in rat liver

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