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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 / Lackner, Karl J. / Lippi, Giuseppe / Melichar, Bohuslav / Payne, Deborah A. / Schlattmann, Peter / Tate, Jillian R.

IMPACT FACTOR increased in 2015: 3.017
Rank 5 out of 30 in category Medical Laboratory Technology in the 2014 Thomson Reuters Journal Citation Report/Science Edition

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Impact per Publication (IPP) 2015: 2.238

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Risk loci for type 2 diabetes – Quo vadis?

Rob N.M. Weijers1

1Teaching Hospital OLVG, Onze Lieve Vrouwe Gasthuis, Amsterdam, The Netherlands

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

Citation Information: Clinical Chemistry and Laboratory Medicine. Volume 47, Issue 4, Pages 383–386, ISSN (Online) 1437-4331, ISSN (Print) 1434-6621, DOI: 10.1515/CCLM.2009.077, February 2009

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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

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