Susceptibility to type 1 diabetes is associated with ApoCIII gene haplotypes

Diabetes
John E HokansonMarian Rewers

Abstract

Type 1 diabetes is a disease of beta-cell destruction leading to insulin deficiency. Genes for type 1 diabetes have been identified; however, much of the genetic risk remains unexplained. Genetic variation within the apolipoprotein CIII (apoCIII) gene alters apoCIII levels, which are increased in type 1 diabetes and induce beta-cell apoptosis. We therefore hypothesize haplotypes within the apoCIII gene are associated with type 1 diabetes. DNA from 584 type 1 diabetic patients and 591 control subjects were genotyped for six single nucleotide polymorphisms (SNPs) in the apoCIII gene (C-641A, C-482T, T-455C, C1100T, C3175G, and T3206G). Two alleles of a haplotype block (promoter SNPs + C3175G) were associated with type 1 diabetes. The A-T-C-C allele frequency was higher in type 1 diabetes (0.19 vs. 0.16, P = 0.05), and the C-C-T-C allele was reduced in type 1 diabetes (0.60 vs. 0.65, P = 0.04). The odds ratio (OR) for A-T-C-C allele increased with 0, 1, and 2 copies (OR of 1.00, 1.24, and 1.60, respectively; P = 0.05) and decreased for the C-C-T-C allele (1.00, 0.97, and 0.73, respectively; P = 0.03). This haplotype block contains an insulin response element. Screening for this haplotype may identify at-risk individuals, and this ...Continue Reading

References

Apr 1, 1988·Southern Medical Journal·P BlackettP Alaupovic
May 15, 1993·Proceedings of the National Academy of Sciences of the United States of America·M DammermanJ L Breslow
Aug 1, 1996·Arteriosclerosis, Thrombosis, and Vascular Biology·A P SurguchovE Boerwinkle
Jun 28, 2001·Atherosclerosis·M GroenendijkG M Dallinga-Thie
Aug 20, 2002·Immunogenetics·William KlitzHenry A Erlich
Jun 24, 2004·Proceedings of the National Academy of Sciences of the United States of America·Lisa Juntti-BerggrenPer-Olof Berggren
Sep 18, 2004·Metabolism: Clinical and Experimental·Richard L KleinUNKNOWN DCCT/EDIC Research Group
Jul 28, 2005·Diabetes·Andrea K SteckMarian J Rewers

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Citations

Jun 15, 2011·Proceedings of the National Academy of Sciences of the United States of America·Rebecka HolmbergLisa Juntti-Berggren
Mar 1, 2009·Proteomics. Clinical Applications·Jakob AlbrethsenHenrik Bindesbøl Mortensen
Sep 18, 2013·Diabetes, Obesity & Metabolism·M H Abdulreda, P-O Berggren
Nov 1, 2006·The International Journal of Biochemistry & Cell Biology·Shao Chin Lee, Shazib Pervaiz
Feb 19, 2015·Current Opinion in Endocrinology, Diabetes, and Obesity·Alison B Kohan
Dec 18, 2018·Diabetes/metabolism Research and Reviews·Eliza ChristopoulouMoses Elisaf
Feb 29, 2020·Scandinavian Journal of Clinical and Laboratory Investigation·Åsa SandinGösta Eggertsen
Oct 12, 2018·Evidence-based Complementary and Alternative Medicine : ECAM·Xin QiuFuer Lu
Oct 13, 2018·Laboratory animal research·Karin ÅvallLisa Juntti-Berggren
Nov 23, 2019·Nutrition, Metabolism, and Cardiovascular Diseases : NMCD·Lutgarda BozzettoKirsi H Pietiläinen
Jan 23, 2021·International Journal of Molecular Sciences·Ismael Valladolid-AcebesLisa Juntti-Berggren
Nov 23, 2016·Current Opinion in Lipidology·Lisa Juntti-Berggren, Per-Olof Berggren

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