| A role for AMPK in increased insulin action after serum starvation. | |
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MedLine Citation:
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PMID: 20810907 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Serum starvation is a common cell culture procedure for increasing cellular response to insulin, though the mechanism for the serum starvation effect is not understood. We hypothesized that factors known to potentiate insulin action [e.g., AMP-activated protein kinase (AMPK) and p38] or to be involved in insulin signaling leading to glucose transport [e.g., Akt, PKCζ, AS160, and ataxia telangiectasia mutated (ATM)] would be phosphorylated during serum starvation and would be responsible for increased insulin action after serum starvation. L6 myotubes were incubated in serum-containing or serum-free medium for 3 h. Levels of phosphorylated AMPK, Akt, and ATM were greater in serum-starved cells than in control cells. Serum starvation did not affect p38, PKCζ, or AS160 phosphorylation or insulin-stimulated Akt or AS160 phosphorylation. Insulin had no effect on glucose transport in control cells but caused an increase in glucose uptake for serum-starved cells that was preventable by compound C (an AMPK inhibitor), by expression of dominant negative AMPK (AMPK-DN), and by KU55933 (an ATM inhibitor). ATM protein levels increased during serum starvation, and this increase in ATM was prevented by compound C and AMPK-DN. Thus, it appears that AMPK is required for the serum starvation-related increase in insulin-stimulated glucose transport, with ATM as a possible downstream effector. |
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Authors:
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James Kain Ching; Pooja Rajguru; Nandhini Marupudi; Sankha Banerjee; Jonathan S Fisher |
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Publication Detail:
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Type: Journal Article; Research Support, American Recovery and Reinvestment Act; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2010-09-01 |
Journal Detail:
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Title: American journal of physiology. Cell physiology Volume: 299 ISSN: 1522-1563 ISO Abbreviation: Am. J. Physiol., Cell Physiol. Publication Date: 2010 Nov |
Date Detail:
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Created Date: 2010-10-28 Completed Date: 2010-11-22 Revised Date: 2011-11-02 |
Medline Journal Info:
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Nlm Unique ID: 100901225 Medline TA: Am J Physiol Cell Physiol Country: United States |
Other Details:
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Languages: eng Pagination: C1171-9 Citation Subset: IM |
Affiliation:
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Department of Biology, Saint Louis University, St. Louis, Missouri 63103, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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AMP-Activated Protein Kinases
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antagonists & inhibitors,
metabolism* Animals Biological Transport / physiology Cell Culture Techniques* Cell Cycle Proteins / antagonists & inhibitors, genetics, metabolism Cell Line DNA-Binding Proteins / antagonists & inhibitors, genetics, metabolism Glucose / metabolism Insulin / metabolism* Isoenzymes / genetics, metabolism Mice Mice, Knockout Muscle Fibers, Skeletal / cytology, drug effects, metabolism Protein-Serine-Threonine Kinases / antagonists & inhibitors, genetics, metabolism Pyrazoles / pharmacology Pyrimidines / pharmacology Starvation / metabolism* Tumor Suppressor Proteins / antagonists & inhibitors, genetics, metabolism |
| Grant Support | |
ID/Acronym/Agency:
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K01 DK066330/DK/NIDDK NIH HHS; R15 DK080437/DK/NIDDK NIH HHS; R15 DK080437-01S2/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/(6-(4-(2-piperidin-1-ylethoxy)phenyl))-3-pyridin-4-ylpyrazolo(1,5-a)pyrimidine; 0/Cell Cycle Proteins; 0/DNA-Binding Proteins; 0/Isoenzymes; 0/Pyrazoles; 0/Pyrimidines; 0/Tumor Suppressor Proteins; 11061-68-0/Insulin; 50-99-7/Glucose; EC 2.7.11.1/AMP-Activated Protein Kinases; EC 2.7.11.1/Protein-Serine-Threonine Kinases; EC 2.7.11.1/ataxia telangiectasia mutated protein |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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