The beta3-adrenergic agonist BRL37344 increases glucose transport into L6 myocytes through a mechanism different from that of insulin.

The beta3-adrenergic agonist BRL37344 increases glucose transport into L6 myocytes through a mechanism different from that of insulin. Research Abstract Details 

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The beta3-adrenergic agonist BRL37344 increases glucose transport into L6 myocytes through a mechanism different from that of insulin. Abstract Text:

T Tanishita,Y Shimizu,Y Minokoshi,T Shimazu,

In the present study, we examined the effects of BRL37344, a selective beta3-adrenergic agonist, on glucose transport into L6 myocytes and the results were compared with the effects of insulin. Insulin increased 2-deoxyglucose (2-DG) uptake in a dose-dependent manner, with maximal stimulation at 10(-7)M. BRL37344 ranging from 10(-7) to 10(-5)M also enhanced 2-DG uptake in the absence of insulin. The effects of insulin and BRL37344 were completely additive, suggesting that these two agents enhance glucose uptake by L6 myocytes through different mechanisms. In fact, BRL37344 apparently did not increase tyrosine phosphorylation of cellular proteins in L6 myocytes, whereas insulin stimulated tyrosine phosphorylation of 180-190 and 95 kDa proteins. Furthermore, BRL37344-induced increase in glucose transport was not blocked by wortmannin, an inhibitor of phosphatidylinositol 3-kinase, whereas the insulin-induced effect was completely abolished. When L6 myocytes were incubated with insulin, the content of GLUT4 in the plasma membrane was increased. However, BRL37344 did not affect the GLUT4 content in the plasma membrane. BRL37344 did not increase the Vmax value for glucose uptake but decreased the Km value, although insulin increased the Vmax value. These results suggest that BRL37344 enhances glucose transport into L6 myocytes through a signaling pathway different from that of insulin and that the mechanism does not involve the translocation of GLUT4, but may be due to an increase in the intrinsic activity of GLUT present in the plasma membrane.

The beta3-adrenergic agonist BRL37344 increases glucose transport into L6 myocytes through a mechanism different from that of insulin. Publishing Authors By Initials

T Tanishita,Y Shimizu,Y Minokoshi,T Shimazu,

For similar amino acids, peptides, and proteins: amino acids: amino acids, cyclic: amino acids, aromatic: tyrosine research abstracts see: amino acids, peptides, and proteins: amino acids: amino acids, cyclic: amino acids, aromatic: tyrosine research

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The beta3-adrenergic agonist BRL37344 increases glucose transport into L6 myocytes through a mechanism different from that of insulin. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Journal of biochemistry

VOLUME: 122

Page Numbers: 90-5

Journal Abbreviation: J. Biochem.

ISSN: 0021-924X

DAY: 19

MONTH: Jul

YEAR: 1997

The beta3-adrenergic agonist BRL37344 increases glucose transport into L6 myocytes through a mechanism different from that of insulin. Information

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LANGUAGE: eng

NlmUniqueID: 376600

The beta3-adrenergic agonist BRL37344 increases glucose transport into L6 myocytes through a mechanism different from that of insulin. Keywords Mesh Terms:

KEYWORDS: Tyrosine

MESH TERMS: metabolism

Chemical & Substance for Abstract: The beta3-adrenergic agonist BRL37344 increases glucose transport into L6 myocytes through a mechanism different from that of insulin. Information

Substance Name: Tyrosine

Registry Number: 55520-40-6

Grant and Affiliation Information for The beta3-adrenergic agonist BRL37344 increases glucose transport into L6 myocytes through a mechanism different from that of insulin.

AFFILIATION: Department of Medical Biochemistry, Ehime University School of Medicine.

Country: JAPAN

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MEDLINETA: J Biochem

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