Comparison of isoproterenol with BRL37344 in activation of β3-adrenoceptors to inhibit the uptake of [14C]deoxy-D-glucose and translocation of glucose transporter (GLUT4) to membrane fraction in rat adipocytes

Chih-Jen Chang, Jau Tsuen Kao, Tzung Long Lee, Chih Wei Lai, Juei Tang Cheng

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Abstract

In an attempt to understand the role of β3-adrenoceptors in the regulation of glucose uptake, the effect of isoproterenol was compared with BRL37344 in isolated white adipocytes of the rat using [14C]deoxy-D-glucose as an indicator. In the presence of BRL37344, the specific agonist of β3-adrenoceptors, spontaneous uptake of [14C]deoxy-D-glucose (glucose uptake) into adipocytes was markedly attenuated. Similar concentration-dependent inhibition of glucose uptake was also observed in the samples treated with isoproterenol, an agonist for all kinds of β-adrenoceptors. Action of BRL37344 was blocked by propranolol at concentrations sufficient to abolish the activity of isoproterenol. Pindolol reversed BRL37344-induced inhibition more effectively than propranolol. Moreover, unlike the action of isoproterenol, BRL37344 did not modify the insulin-stimulated glucose uptake. Translocation of glucose transporter (GLUT4) from cytosol to membrane stimulated with insulin was reduced by isoproterenol but not by BRL37344. Combination with the findings that isoproterenol prolonged the time for insulin to reach maximum stimulation of glucose uptake, leads to the conclusion that delay of insulin action by isoproterenol can be considered as one of the mechanisms for this inhibition. The results obtained suggest that BRL37344 decreased the spontaneous uptake of glucose via an activation of β3-adrenoceptors while the insulin stimulated glucose uptake was inhibited by isoproterenol but not by BRL37344.

Original languageEnglish
Pages (from-to)191-194
Number of pages4
JournalJournal of the Autonomic Nervous System
Volume61
Issue number2
DOIs
Publication statusPublished - 1996 Nov 6

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Facilitative Glucose Transport Proteins
Isoproterenol
Adipocytes
Adrenergic Receptors
Glucose
Membranes
Insulin
Propranolol
White Adipocytes
Pindolol
Cytosol

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Physiology
  • Clinical Neurology

Cite this

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title = "Comparison of isoproterenol with BRL37344 in activation of β3-adrenoceptors to inhibit the uptake of [14C]deoxy-D-glucose and translocation of glucose transporter (GLUT4) to membrane fraction in rat adipocytes",
abstract = "In an attempt to understand the role of β3-adrenoceptors in the regulation of glucose uptake, the effect of isoproterenol was compared with BRL37344 in isolated white adipocytes of the rat using [14C]deoxy-D-glucose as an indicator. In the presence of BRL37344, the specific agonist of β3-adrenoceptors, spontaneous uptake of [14C]deoxy-D-glucose (glucose uptake) into adipocytes was markedly attenuated. Similar concentration-dependent inhibition of glucose uptake was also observed in the samples treated with isoproterenol, an agonist for all kinds of β-adrenoceptors. Action of BRL37344 was blocked by propranolol at concentrations sufficient to abolish the activity of isoproterenol. Pindolol reversed BRL37344-induced inhibition more effectively than propranolol. Moreover, unlike the action of isoproterenol, BRL37344 did not modify the insulin-stimulated glucose uptake. Translocation of glucose transporter (GLUT4) from cytosol to membrane stimulated with insulin was reduced by isoproterenol but not by BRL37344. Combination with the findings that isoproterenol prolonged the time for insulin to reach maximum stimulation of glucose uptake, leads to the conclusion that delay of insulin action by isoproterenol can be considered as one of the mechanisms for this inhibition. The results obtained suggest that BRL37344 decreased the spontaneous uptake of glucose via an activation of β3-adrenoceptors while the insulin stimulated glucose uptake was inhibited by isoproterenol but not by BRL37344.",
author = "Chih-Jen Chang and Kao, {Jau Tsuen} and Lee, {Tzung Long} and Lai, {Chih Wei} and Cheng, {Juei Tang}",
year = "1996",
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T1 - Comparison of isoproterenol with BRL37344 in activation of β3-adrenoceptors to inhibit the uptake of [14C]deoxy-D-glucose and translocation of glucose transporter (GLUT4) to membrane fraction in rat adipocytes

AU - Chang, Chih-Jen

AU - Kao, Jau Tsuen

AU - Lee, Tzung Long

AU - Lai, Chih Wei

AU - Cheng, Juei Tang

PY - 1996/11/6

Y1 - 1996/11/6

N2 - In an attempt to understand the role of β3-adrenoceptors in the regulation of glucose uptake, the effect of isoproterenol was compared with BRL37344 in isolated white adipocytes of the rat using [14C]deoxy-D-glucose as an indicator. In the presence of BRL37344, the specific agonist of β3-adrenoceptors, spontaneous uptake of [14C]deoxy-D-glucose (glucose uptake) into adipocytes was markedly attenuated. Similar concentration-dependent inhibition of glucose uptake was also observed in the samples treated with isoproterenol, an agonist for all kinds of β-adrenoceptors. Action of BRL37344 was blocked by propranolol at concentrations sufficient to abolish the activity of isoproterenol. Pindolol reversed BRL37344-induced inhibition more effectively than propranolol. Moreover, unlike the action of isoproterenol, BRL37344 did not modify the insulin-stimulated glucose uptake. Translocation of glucose transporter (GLUT4) from cytosol to membrane stimulated with insulin was reduced by isoproterenol but not by BRL37344. Combination with the findings that isoproterenol prolonged the time for insulin to reach maximum stimulation of glucose uptake, leads to the conclusion that delay of insulin action by isoproterenol can be considered as one of the mechanisms for this inhibition. The results obtained suggest that BRL37344 decreased the spontaneous uptake of glucose via an activation of β3-adrenoceptors while the insulin stimulated glucose uptake was inhibited by isoproterenol but not by BRL37344.

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