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Ordelheide, A.-M. ; Gerst, F.* ; Rothfuss, O.* ; Heni, M.* ; Haas, C. ; Thielker, I. ; Herzberg-Schäfer, S.* ; Böhm, A. ; Machicao, F. ; Ullrich, S. ; Stefan, N. ; Fritsche, A. ; Häring, H.-U. ; Staiger, H.

Nor-1, a novel incretin-responsive regulator of insulin genes and insulin secretion.

Mol. Metab. 2, 243-255 (2013)
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B-cell failure at the onset of type 2 diabetes is caused by a decline in β-cell function in the postprandial state and loss of pancreatic β-cell mass. Recently, we showed an association between increased insulin secretion and a single nucleotide polymorphism (SNP), SNP rs12686676, in the NR4A3 gene locus encoding the nuclear receptor Nor-1. Nor-1 is expressed in β-cells, however, not much is known about its function with regard to insulin gene expression and insulin secretion. Nor-1 is induced in a glucose-/incretin-dependent manner via the PKA pathway and directly induces insulin gene expression. Additionally, it stimulates insulin secretion possibly via regulation of potentially important genes in insulin exocytosis. Moreover, we show that the minor allele of NR4A3 SNP rs12686676 fully rescues incretin resistance provoked by a well-described polymorphism in TCF7L2. Thus, Nor-1 represents a promising new target for pharmacological intervention to fight diabetes.
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Publication type Article: Journal article
Document type Scientific Article
Keywords Nor-1; Insulin gene expression; Insulin secretion; Incretin resistance; TCF7L2
Language english
Publication Year 2013
HGF-reported in Year 0
ISSN (print) / ISBN 2212-8778
e-ISSN 2212-8778
Journal Molecular Metabolism
Quellenangaben Volume: 2, Issue: 3, Pages: 243-255 Article Number: , Supplement: ,
Publisher Elsevier
Publishing Place Amsterdam
Reviewing status Peer reviewed
Institute(s) Institute of Diabetes Research and Metabolic Diseases (IDM)
POF-Topic(s) 90000 - German Center for Diabetes Research
Research field(s) Helmholtz Diabetes Center
PSP Element(s) G-502400-002
G-502400-001
PubMed ID 24044104
DOI 10.1016/j.molmet.2013.06.003
Erfassungsdatum 2013-12-17
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