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Clinical Chemistry and Laboratory Medicine (CCLM)

Published in Association with the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM)

Editor-in-Chief: Plebani, Mario

Ed. by Gillery, Philippe / Greaves, Ronda / Lackner, Karl J. / Lippi, Giuseppe / Melichar, Bohuslav / Payne, Deborah A. / Schlattmann, Peter


IMPACT FACTOR 2018: 3.638

CiteScore 2018: 2.44

SCImago Journal Rank (SJR) 2018: 1.191
Source Normalized Impact per Paper (SNIP) 2018: 1.205

Online
ISSN
1437-4331
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Volume 47, Issue 4

Issues

Risk loci for type 2 diabetes – Quo vadis?

Rob N.M. Weijers
Published Online: 2009-02-09 | DOI: https://doi.org/10.1515/CCLM.2009.077

Abstract

Reduced insulin sensitivity plays a role in the early pathogenesis of type 2 diabetes, and defects in insulin secretion by pancreatic β-cells are instrumental in hyperglycemic progression. There is strong evidence that genetic factors play an important role in both of these components. Several of the single nucleotide polymorphisms (SNPs) of genes associated with an increased risk of type 2 diabetes are hypothesized to influence β-cell function. The aim of the present study was to describe the function of the latter genes, to analyze the implications of the SNP positions within or near these genes, and to evaluate the suggested primary role of pancreatic β-cells in the etiology of type 2 diabetes.

Clin Chem Lab Med 2009;47:383–6.

Keywords: genome-wide association study; mitochondrion; pancreatic β-cell function; single nucleotide polymorphism; type 2 diabetes

About the article

Corresponding author: R.N.M. Weijers, PhD, Teaching Hospital OLVG, Onze Lieve Vrouwe Gasthuis, Oosterpark 9, PO Box 95500, 1090 HM Amsterdam, The Netherlands


Received: 2008-10-21

Accepted: 2008-12-09

Published Online: 2009-02-09

Published in Print: 2009-04-01


Citation Information: Clinical Chemistry and Laboratory Medicine, Volume 47, Issue 4, Pages 383–386, ISSN (Online) 1437-4331, ISSN (Print) 1434-6621, DOI: https://doi.org/10.1515/CCLM.2009.077.

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