| Extracellular high dosages of adenosine triphosphate induce inflammatory response and insulin resistance in rat adipocytes. | |
| | |
MedLine Citation:
|
PMID: 20946888 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
Adenosine triphosphate (ATP), an important signaling molecule, participates in various pathophysiological processes via the activation of purinergic-receptors. Recent studies have shown that the expression and function of purinergic-receptors (P2-receptors) could be altered in diabetic or hyperinsulinemia conditions. To characterize the effect of ATP on insulin signaling, we treated primary rat adipocytes with varied concentrations of ATP. The pre-treatment led to impaired insulin signaling, i.e., blunted phosphorylation in Insulin Receptor Substrate-1 (IRS-1) tyrosine and Protein Kinase B (PKB) Ser473 in response to insulin treatment, when ATP concentration reached 1mM. We then observed that ATP dose-dependently reduced the level of IκB, a negative regulator of inflammatory response. Consistently, IRS-1 Ser307 phosphorylation in response to insulin treatment, a site for inflammatory pathway to interfere insulin signaling, was enhanced by ATP. Furthermore, effects of ATP on insulin signaling and IκB content were blocked by P2-receptor inhibition. Finally, insulin-stimulated glucose uptake was impaired by ATP in adipocytes but not in the L6 muscle cells. This study therefore shows for the first time the involvement of ATP-evoked P2-receptor activation in mediating the inflammatory response and the generation of insulin resistance in adipocytes. |
| | |
Authors:
|
Zhiwen Yu; Tianru Jin |
Related Documents
:
|
15889998 - Hyperglycemia potentiates h(2)o(2) production in adipocytes and enhances insulin signal... 12960228 - Insulin-dependent signaling regulates azurophil granule-selective macroautophagy in hum... 10216198 - Insulin induces tyrosine phosphorylation of the insulin receptor and shc, and shc/grb2 ... 7929278 - Potentiation of insulin stimulation of phosphatidylinositol 3-kinase by thiazolidinedio... 17316628 - Iron overload in hepc1(-/-) mice is not impairing glucose homeostasis. 10169538 - Resource utilization and work or school loss reported by patients with diabetes: experi... |
Publication Detail:
|
Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-10-12 |
Journal Detail:
|
Title: Biochemical and biophysical research communications Volume: 402 ISSN: 1090-2104 ISO Abbreviation: Biochem. Biophys. Res. Commun. Publication Date: 2010 Nov |
Date Detail:
|
Created Date: 2010-11-24 Completed Date: 2010-12-28 Revised Date: - |
Medline Journal Info:
|
Nlm Unique ID: 0372516 Medline TA: Biochem Biophys Res Commun Country: United States |
Other Details:
|
Languages: eng Pagination: 455-60 Citation Subset: IM |
Copyright Information:
|
Copyright © 2010 Elsevier Inc. All rights reserved. |
Affiliation:
|
Dept. of Nutrition, School of Public Health, Sun Yat-Sen University, Guangzhou, People's Republic of China. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Adenosine Triphosphate
/
metabolism,
pharmacology* Adipocytes / drug effects*, metabolism Animals Cells, Cultured Glucose / metabolism* Inflammation / chemically induced*, metabolism Insulin / metabolism* Insulin Receptor Substrate Proteins / metabolism Insulin Resistance* Male Phosphorylation Rats Rats, Sprague-Dawley Serine / metabolism Signal Transduction / drug effects |
| Chemical | |
Reg. No./Substance:
|
0/Insulin Receptor Substrate Proteins; 0/Irs1 protein, rat; 11061-68-0/Insulin; 50-99-7/Glucose; 56-45-1/Serine; 56-65-5/Adenosine Triphosphate |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Th1 cells promote neurite outgrowth from cortical neurons via a mechanism dependent on semaphorins.
Next Document: Malformation of the human superior olive in autistic spectrum disorders.