NDLI: Leptin regulates KATP channel trafficking in pancreatic ß-cells by a signaling mechanism involving AMP-activated protein kinase (AMPK) and cAMP-dependent protein kinase (PKA).

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Leptin regulates KATP channel trafficking in pancreatic ß-cells by a signaling mechanism involving AMP-activated protein kinase (AMPK) and cAMP-dependent protein kinase (PKA).

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Leptin regulates KATP channel trafficking in pancreatic ß-cells by a signaling mechanism involving AMP-activated protein kinase (AMPK) and cAMP-dependent protein kinase (PKA).

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Shyng, Show-ling Chen, Pei-chun Kryukova, Yelena N.
Description	Author Affiliation: Chen PC ( From the Department of Biochemistry and Molecular Biology, Oregon Health and Science University, Portland, Oregon 97239.)
Abstract	Pancreatic ß-cells secrete insulin in response to metabolic and hormonal signals to maintain glucose homeostasis. Insulin secretion is under the control of ATP-sensitive potassium (KATP) channels that play key roles in setting ß-cell membrane potential. Leptin, a hormone secreted by adipocytes, inhibits insulin secretion by increasing KATP channel conductance in ß-cells. We investigated the mechanism by which leptin increases KATP channel conductance. We show that leptin causes a transient increase in surface expression of KATP channels without affecting channel gating properties. This increase results primarily from increased channel trafficking to the plasma membrane rather than reduced endocytosis of surface channels. The effect of leptin on KATP channels is dependent on the protein kinases AMP-activated protein kinase (AMPK) and PKA. Activation of AMPK or PKA mimics and inhibition of AMPK or PKA abrogates the effect of leptin. Leptin activates AMPK directly by increasing AMPK phosphorylation at threonine 172. Activation of PKA leads to increased channel surface expression even in the presence of AMPK inhibitors, suggesting AMPK lies upstream of PKA in the leptin signaling pathway. Leptin signaling also leads to F-actin depolymerization. Stabilization of F-actin pharmacologically occludes, whereas destabilization of F-actin simulates, the effect of leptin on KATP channel trafficking, indicating that leptin-induced actin reorganization underlies enhanced channel trafficking to the plasma membrane. Our study uncovers the signaling and cellular mechanism by which leptin regulates KATP channel trafficking to modulate ß-cell function and insulin secretion.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	47
Volume Number	288
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2013-11-22
Publisher Place	United States
Access Restriction	Open
Subject Keyword	AMP-Activated Protein Kinases Metabolism Cyclic AMP-Dependent Protein Kinases Insulin-Secreting Cells Leptin Potassium Channels Signal Transduction Physiology Genetics Actins Animals Cell Line Cell Membrane Insulin Secretion Cytology Phosphorylation Protein Transport Research Support, N.I.H., Extramural Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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