TY - JOUR
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
N1 - Funding Information:
We thank Dr. J. Hunter and Mr. S. Trowbridge (SmithKline Beecham Pharmaceuticals, Herts, UK) for the kindly supply of BRL37344. The present study was supported in part by a grant from the Hospital Research Foundation for C.J.C. (NCKH-FR-83-01) in addition to the main support from the National Science Council of the Republic of China (NSC84-233 l-B006-102-M 13).
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.
AB - 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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U2 - 10.1016/S0165-1838(96)00068-9
DO - 10.1016/S0165-1838(96)00068-9
M3 - Article
C2 - 8946341
AN - SCOPUS:0030572883
SN - 0165-1838
VL - 61
SP - 191
EP - 194
JO - Journal of the Autonomic Nervous System
JF - Journal of the Autonomic Nervous System
IS - 2
ER -