RGD Reference Report - Glucose deprivation regulates KATP channel trafficking via AMP-activated protein kinase in pancreatic beta-cells. - Rat Genome Database

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Glucose deprivation regulates KATP channel trafficking via AMP-activated protein kinase in pancreatic beta-cells.

Authors: Lim, A  Park, SH  Sohn, JW  Jeon, JH  Park, JH  Song, DK  Lee, SH  Ho, WK 
Citation: Lim A, etal., Diabetes. 2009 Dec;58(12):2813-9. doi: 10.2337/db09-0600. Epub 2009 Aug 31.
RGD ID: 7296981
Pubmed: PMID:19720793   (View Abstract at PubMed)
PMCID: PMC2780861   (View Article at PubMed Central)
DOI: DOI:10.2337/db09-0600   (Journal Full-text)

OBJECTIVE: AMP-activated protein kinase (AMPK) and the ATP-sensitive K(+) (K(ATP)) channel are metabolic sensors that become activated during metabolic stress. AMPK is an important regulator of metabolism, whereas the K(ATP) channel is a regulator of cellular excitability. Cross talk between these systems is poorly understood. RESEARCH DESIGN AND METHODS: Rat pancreatic beta-cells or INS-1 cells were pretreated for 2 h at various concentrations of glucose. Maximum K(ATP) conductance (G(max)) was monitored by whole-cell measurements after intracellular ATP washout using ATP-free internal solutions. K(ATP) channel activity (NPo) was monitored by inside-out patch recordings in the presence of diazoxide. Distributions of K(ATP) channel proteins (Kir6.2 and SUR1) were examined using immunofluorescence imaging and surface biotinylation studies. Insulin secretion from rat pancreatic islets was measured using an enzyme immunoassay. RESULTS: G(max) and NPo in cells pretreated with glucose-free or 3 mmol/l glucose solutions were significantly higher than in cells pretreated in 11.1 mmol/l glucose solutions. Immunofluorescence imaging and biotinylation studies revealed that glucose deprivation induced an increase in the surface level of Kir6.2 without affecting the total cellular amount. Increases in G(max) and the surface level of Kir6.2 were inhibited by compound C, an AMPK inhibitor, and siAMPK transfection. The effects of glucose deprivation on K(ATP) channels were mimicked by an AMPK activator. Glucose deprivation reduced insulin secretion, but this response was attenuated by compound C. CONCLUSIONS: K(ATP) channel trafficking is regulated by energy status via AMPK, and this mechanism may play a key role in inhibiting insulin secretion under low energy status.

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
cellular response to glucose stimulus  IEP 7296981 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Kcnj11  (potassium inwardly-rectifying channel, subfamily J, member 11)


Additional Information