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Analysis of three glucose transporter genes in a Caucasian population: no associations with non‐insulin‐dependent diabetes and obesity
Author(s) -
Oelbaum R. S.
Publication year - 1992
Publication title -
clinical genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.543
H-Index - 102
eISSN - 1399-0004
pISSN - 0009-9163
DOI - 10.1111/j.1399-0004.1992.tb03252.x
Subject(s) - glut2 , linkage disequilibrium , glucose transporter , endocrinology , biology , medicine , genetics , genotype , locus (genetics) , diabetes mellitus , population , allele , insulin , gene , haplotype , environmental health
The significance of variation within the genes coding for three glucose transporter proteins in the aetiology of non‐insulin dependent diabetes mellitus was assessed by analysing restriction fragment length polymorphisms in an English Caucasian population. Two polymorphisms at the HepG2/erythrocyte glucose transporter (GLUT1) locus, four at the liver/ pancreatic glucose transporter (GLUT2) locus and one at the muscle/ adipocyte glucose transporter (GLUT4) were analysed in a sample of diabetic and non‐diabetic subjects. No significant differences in the allelic, genotypic or haplotypic frequencies of the polymorphisms at these three loci were observed between the diabetic or non‐diabetic populations. No significant linkage disequilibrium was observed between the two GLUT1 polymorphic sites, whereas the four polymorphic sites at the GLUT2 locus, one of which appears to be due to a 100–200 base pair DNA insertion/deletion, were found to be in significant linkage disequilibrium. In order to study the possible role of glucose transporter gene variants contributing to the development of obesity, the body mass indexes were compared in the different genotypic groups of diabetic and non‐diabetic subjects. No differences in body mass index between genotype groups were found at the p < 0.005 level of significance.