دورية أكاديمية

Neuropeptide Y impairs insulin-stimulated translocation of glucose transporter 4 in 3T3-L1 adipocytes through the Y1 receptor.

التفاصيل البيبلوغرافية
العنوان: Neuropeptide Y impairs insulin-stimulated translocation of glucose transporter 4 in 3T3-L1 adipocytes through the Y1 receptor.
المؤلفون: Gericke MT; Institute of Anatomy, University of Leipzig, D-04103 Leipzig, Germany. martin.gericke@medizin.uni-leipzig.de, Schröder T, Kosacka J, Nowicki M, Klöting N, Spanel-Borowski K
المصدر: Molecular and cellular endocrinology [Mol Cell Endocrinol] 2012 Jan 02; Vol. 348 (1), pp. 27-32. Date of Electronic Publication: 2011 Jul 27.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: North Holland Publishing Country of Publication: Ireland NLM ID: 7500844 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1872-8057 (Electronic) Linking ISSN: 03037207 NLM ISO Abbreviation: Mol Cell Endocrinol Subsets: MEDLINE
أسماء مطبوعة: Publication: Limerick : North Holland Publishing
Original Publication: Amsterdam, North-Holland.
مواضيع طبية MeSH: Protein Transport*, Adipocytes/*metabolism , Cell Membrane/*metabolism , Glucose Transporter Type 4/*metabolism , Insulin/*physiology , Neuropeptide Y/*physiology , Receptors, Neuropeptide Y/*metabolism, 3T3-L1 Cells ; Adipocytes/drug effects ; Animals ; Arginine/analogs & derivatives ; Arginine/pharmacology ; Glucose/metabolism ; Glucose Transporter Type 4/genetics ; Insulin/pharmacology ; Mice ; Neuropeptide Y/pharmacology ; Phosphorylation ; Proto-Oncogene Proteins c-akt/metabolism ; Receptors, Neuropeptide Y/agonists ; Receptors, Neuropeptide Y/antagonists & inhibitors ; Up-Regulation
مستخلص: Neuropeptide Y (NPY) is expressed in adipose tissue and is involved in adipocyte metabolism. Although NPY impacts on glucose utilization in vivo, the underlying cellular mechanism is yet to be fully elucidated. In this study we investigated the effect of NPY on the insulin-stimulated translocation of glucose transporter 4 (GLUT4) from intracellular stores to the cell surface in vitro. Using cellular fractionation and immunofluorescence we analyzed the cellular localization and content of GLUT4 in 3T3-L1 adipocytes. Additionally we investigated the effect of NPY on insulin action in adipocyte cultures by assessing the phosphorylation of Akt and [(3)H]-deoxyglucose uptake. Our data suggest that in 3T3-L1 adipocytes NPY inhibits insulin-stimulated glucose uptake in a GLUT4-dependent manner. The insulin induced translocation of GLUT4 was attenuated by the Y1 receptor agonist [Phe(7),Pro(34)] pNPY, demonstrating an essential role of the Y1 receptor in GLUT4 translocation. Additionally, we observed an NPY dose-dependent impairment of Akt phosphorylation. This study provides evidence that NPY impairs the insulin sensitivity of adipocytes and suggests that the Y1 receptor could be a potential therapeutic target for type 2 diabetes.
(Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)
المشرفين على المادة: 0 (BIBP 3226)
0 (Glucose Transporter Type 4)
0 (Insulin)
0 (Neuropeptide Y)
0 (Npy1r protein, mouse)
0 (Receptors, Neuropeptide Y)
94ZLA3W45F (Arginine)
EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
IY9XDZ35W2 (Glucose)
تواريخ الأحداث: Date Created: 20110802 Date Completed: 20120305 Latest Revision: 20131121
رمز التحديث: 20231215
DOI: 10.1016/j.mce.2011.07.028
PMID: 21801810
قاعدة البيانات: MEDLINE
الوصف
تدمد:1872-8057
DOI:10.1016/j.mce.2011.07.028