Effects of the calcium ionophore A-23187 on the regulation of sugar transport in muscle

Bihler, I.; Charles, Paul T.; Sawh, P.C.

doi:10.1016/0143-4160(80)90034-2

Cited by 29 publications

(10 citation statements)

References 14 publications

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“…This compound is a highly lipophilic molecule which distributes into the lipid phase of cell membranes. It is conceivable that it could cause a redistribution of the Ca bound to membranes, as already suggested by Bilher, Charles & Sawh (1980). Finally, while the results reported in this study strengthen the hypothesis that noradrenaline or ATP regulate the Na-K pump activity by removing the inhibitory effect of Ca on the pump there is no indication of the molecular mechanism involved in the interaction.…”

Section: Discussioncontrasting

confidence: 52%

Mechanism of action of noradrenaline on the sodium‐potassium pump in isolated rat liver cells.

Berthon¹,

Burgess²,

Capiod³

et al. 1983

The Journal of Physiology

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SUMMARY1. Noradrenaline, which mobilizes Ca from intracellular stores, stimulated the Na-K pump in isolated rat liver cells. This resulted in transient decreases in internal Na content and external K concentration.2. The effect of the hormones was observed in the presence of the f8-adrenergic antagonist propranolol and was blocked by the a-antagonist phenoxybenzamine. Prazosin appeared to be 1000 times more potent than yohimbine in suppressing the cell response to the hormone, suggesting that the effect is mediated by an activation of ac-adrenergic receptors.3. Externally applied ATP and the Ca ionophore A23187 which, in common with a-agonists, deplete internal Ca stores in this tissue, similarly stimulated the Na-K pump and transiently decreased internal Na and external K. 4. The effects of noradrenaline and ATP were not additive. Moreover, the cell response to ATP was observed in the presence ofthe a-antagonist phenoxybenzamine, indicating that though acting via separate receptors, noradrenaline and ATP use a common mechanism to alter the carrier.5. The effect of noradrenaline and A23187 on the Na-K pump was not dependent on the presence of extracellular Ca. In contrast, when the hepatocytes were incubated in Ca-free medium for long periods (cell Ca depletion) the activity of the Na-K pump was increased to a level corresponding to that induced by maximal doses of noradrenaline. In these conditions, noradrenaline and A23187 did not increase the pump activity further.6. In cells in which the Na content was raised, leading to a 3-fold increase in the Na-K pump activity, noradrenaline continued to be able to stimulate the pump. Again long-term incubations in Ca-free medium increased the pump activity and the effect of noradrenaline was greatly reduced.7. It is proposed that in isolated rat liver cells ac-agonists and applied ATP influence the Na-K pump by releasing Ca bound to plasma membranes, thus removing the inhibitory effect of this ion on the Na pump.

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Section: Discussioncontrasting

confidence: 52%

Mechanism of action of noradrenaline on the sodium‐potassium pump in isolated rat liver cells.

Berthon¹,

Burgess²,

Capiod³

et al. 1983

The Journal of Physiology

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“…These results are not consistent with those by Bihler et al (6), suggesting that A23187 may release Ca 2+ from intracellular storage and binding sites on the sarcoplasmic reticulum in rat dia phragm muscles (6). The complete inhibition by A23187 of insulin-stimulated glucose up take at 2.5 mM Ca 2+ were not due to Ca 2+ from the sarcoplasmic reticulum but due to extracellular Ca 2+, because A23187 did not inhibit insulin-stimulated glucose uptake in the absence of external Ca2+…”

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confidence: 55%

Intracellular Ca2+ and Mg2+ Regulation for Insulin-Stimulated Glucose Uptake into Mouse Diaphragm Muscles.

et al. 1991

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ABSTRACT-We investigated whether the changed levels of intracellular Ca 2+ and Mg2+ in mouse skeletal muscles affected insulin-stimulated glucose uptake. Insulin alone had no effect on 45Ca2+ efflux and uptake. A23187 at 20 ttM increased 45Ca2+influx and inhibited insulin-stimulated 14C-glucose uptake with normal external con centrations of Ca2+ and Mg2+ or in the absence of both cations. These results suggest that the increase in Ca 2+ influx into, and in Mg2+ efflux from, skeletal muscles may inhibit insulin-stimulated glucose uptake.

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“…The latter evidence is the most direct support for a role of Ca2+ in the activation process. The hypothesis has been refined by the suggestion [4] that the Ca2+ pool involved in glucose-transport activation is not cytoplasmic, but is membrane-bound, since contraction-stimulated glucose uptake does not return to basal levels for a considerable time after contraction has ceased. We have measured insulin-stimulated 2-deoxy-D-glucose uptake in isolated heart cells from the adult rat, and have found a response to insulin similar in magnitude and sensitivity to that of the whole heart.…”

Section: Introduction 2 Materials and Methodsmentioning

confidence: 99%

Insulin stimulates deoxyglucose transport in adult rat heart cells in the absence of Ca²⁺

Haworth¹,

Hunter²,

Berkoff³

1982

FEBS Letters

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Effects of the calcium ionophore A-23187 on the regulation of sugar transport in muscle

Cited by 29 publications

References 14 publications

Mechanism of action of noradrenaline on the sodium‐potassium pump in isolated rat liver cells.

Mechanism of action of noradrenaline on the sodium‐potassium pump in isolated rat liver cells.

Intracellular Ca2+ and Mg2+ Regulation for Insulin-Stimulated Glucose Uptake into Mouse Diaphragm Muscles.

Insulin stimulates deoxyglucose transport in adult rat heart cells in the absence of Ca²⁺

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Effects of the calcium ionophore A-23187 on the regulation of sugar transport in muscle

Cited by 29 publications

References 14 publications

Mechanism of action of noradrenaline on the sodium‐potassium pump in isolated rat liver cells.

Mechanism of action of noradrenaline on the sodium‐potassium pump in isolated rat liver cells.

Intracellular Ca2+ and Mg2+ Regulation for Insulin-Stimulated Glucose Uptake into Mouse Diaphragm Muscles.

Insulin stimulates deoxyglucose transport in adult rat heart cells in the absence of Ca2+

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Insulin stimulates deoxyglucose transport in adult rat heart cells in the absence of Ca²⁺