No linkage of P187S polymorphism in NAD(P)H: quinone oxidoreductase (NQO1/DIA4) and type 1 diabetes in the Danish population. DIEGG and DSGD. Danish IDDM Epidemiology and Genetics Group and The Danish Study Group of Diabetes in Childhood

Recent genome screening studies have identified novel regions of possible interest for susceptibility to type 1 diabetes. One of these is a 30-35 cM region mapping to 16q22-q24 (D16S515-D16S520), where also the gene encoding NAD(P)H: quinone oxidoreductase (NQO1) maps. Data has suggested association...

Full description

Saved in:
Bibliographic Details
Published in:Human mutation 1999, Vol.14 (1), p.67-70
Main Authors: Kristiansen, O P, Larsen, Z M, Johannesen, J, Nerup, J, Mandrup-Poulsen, T, Pociot, F
Format: Article
Language:English
Subjects:
Chromosomes, Human, Pair 16
Denmark
Diabetes Mellitus, Type 1 - enzymology
Diabetes Mellitus, Type 1 - genetics
Female
Genetic Linkage
Genetic Predisposition to Disease
Heterozygote
Humans
Linkage Disequilibrium
Male
NAD(P)H Dehydrogenase (Quinone) - genetics
Polymorphism, Genetic
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Recent genome screening studies have identified novel regions of possible interest for susceptibility to type 1 diabetes. One of these is a 30-35 cM region mapping to 16q22-q24 (D16S515-D16S520), where also the gene encoding NAD(P)H: quinone oxidoreductase (NQO1) maps. Data has suggested association of a polymorphism (P187S) in the NQO1 gene and type 1 diabetes. NQO1 is involved in protection against oxidative stress, which is likely to be involved in beta-cell destruction. By use of the transmission disequilibrium test (TDT), we analyzed the P187S polymorphism for association to type 1 diabetes in a population-based sample of 247 Danish nuclear type 1 diabetic families. Random transmission patterns were observed to all affected offspring (p(tdt) = 0.82), to index cases (P(tdt) = 0.77), as well as to unaffected offspring (P(tdt) = 0.93). Hence, the NQO1 polymorphism is not likely to be an etiological mutation underlying the reported linkage of the 16q22-q24 region.
ISSN:1059-7794