AMP-Activated protein kinase is activated by the stimulations of G(q)-coupled receptors

The AMP-activated protein kinase (AMPK) functions as a metabolic sensor that monitors cellular AMP and ATP levels. Platelet-activating factor (PAF) activates endogeneous AMPKalpha1 in Chinese hamster ovary cells expressing the PAF receptor coupled with both G(i) and G(q), but its activity was not in...

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Published in:Biochemical and biophysical research communications 2000-09, Vol.276 (1), p.16-22
Main Authors: Kishi, K, Yuasa, T, Minami, A, Yamada, M, Hagi, A, Hayashi, H, Kemp, B E, Witters, L A, Ebina, Y
Format: Article
Language:English
Subjects:
AMP-Activated Protein Kinases
Animals
Biological Transport
CHO Cells
Cricetinae
Enzyme Activation
Glucose - metabolism
Glucose Transporter Type 4
GTP-Binding Protein alpha Subunits, Gq-G11
Heterotrimeric GTP-Binding Proteins - metabolism
Monosaccharide Transport Proteins - metabolism
Multienzyme Complexes - metabolism
Muscle Proteins
Protein-Serine-Threonine Kinases - metabolism
Receptors, Adrenergic, alpha-1 - metabolism
Receptors, Bradykinin - metabolism
Signal Transduction
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Summary:The AMP-activated protein kinase (AMPK) functions as a metabolic sensor that monitors cellular AMP and ATP levels. Platelet-activating factor (PAF) activates endogeneous AMPKalpha1 in Chinese hamster ovary cells expressing the PAF receptor coupled with both G(i) and G(q), but its activity was not inhibited after treatment with islet-activating protein. Norepinephrine and bradykinin also activated AMPKalpha1 in cells expressing the G(q)-coupled alpha(1b)-adrenergic receptor and bradykinin receptor, respectively. Stimulations of the G(i)-coupled alpha(2A)-adrenergic receptor, fMet-Leu-Phe receptor, prostaglandin EP3alpha receptor, and G(s)-coupled beta(2)-adrenergic receptor did not activate AMPKalpha1. AMPKalpha1 thus is activated specifically by stimulation of G(q)-coupled receptors. G(q)-coupled receptors transmit the signal for GLUT4 translocation and glucose uptake through an insulin-independent pathway. However, direct activation of AMPKalpha1 with treatment of 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside did not trigger GLUT4 translocation nor stimulate glucose uptake in our cells. Thus, activation of AMPKalpha1 via G(q) is not sufficient to trigger GLUT4 translocation or stimulate glucose uptake.
ISSN:0006-291X
DOI:10.1006/bbrc.2000.3417