Analysis of the HepG2/erythrocyte glucose transporter locus in a family with Type 2 (non-insulin-dependent) diabetes and obesity
- 1 April 1989
- journal article
- research article
- Published by Springer Nature in Diabetologia
- Vol. 32 (4) , 266-269
- https://doi.org/10.1007/bf00285296
Abstract
A recent report has shown an association between a specific Xba1 restriction fragment of the human HepG2-Erythrocyte glucose transporter gene and Type 2 (non-insulin dependent) diabetes. To further examine the significance of this finding we have studied Type 2 diabetic pedigrees for linkage between the Xba1 alleles of this glucose transporter gene and diabetes. One large pedigree, in which the diabetic phenotype was associated with obesity and insulin resistance, was informative. In this family the disease did not co-segregate with the glucose transporter locus. Formal linkage analysis was performed assuming autosomal dominant inheritance with age-dependent penetrance. At putative gene frequencies of 0.01 and 0.001 the logarithin of the odds for linkage versus non-linkage at a recombination fraction of 0.001 was −1.84 and −3.32 respectively (a value of <-2 indicates definite non-linkage). Genetic variations in the HepG2-Erythrocyte glucose transporter gene are unlikely to be responsible for the development of diabetes in this pedigree.Keywords
This publication has 10 references indexed in Scilit:
- Linkage analysis of the human insulin receptor gene in Type 2 (non-insulin-dependent) diabetic families and a family with maturity onset diabetes of the youngDiabetologia, 1988
- ASSOCIATION OF GENETIC VARIANT OF THE GLUCOSE TRANSPORTER WITH NON-INSULIN-DEPENDENT DIABETES MELLITUSThe Lancet, 1988
- Type 2 (non-insulin-dependent) diabetes mellitus new genetics for old nightmaresDiabetologia, 1988
- Insulin-regulatable tissues express a unique insulin-sensitive glucose transport proteinNature, 1988
- Role of glucose transporters in the cellular insulin resistance of type II non-insulin-dependent diabetes mellitus.Journal of Clinical Investigation, 1988
- BETA-CELL DYSFUNCTION, RATHER THAN INSULIN INSENSITIVITY, IS THE PRIMARY DEFECT IN FAMILIAL TYPE 2 DIABETESThe Lancet, 1986
- Easy calculations of lod scores and genetic risks on small computers.1984
- Lilly Lecture 1980: Insulin Resistance and Insulin Action: An In Vitro and In Vivo PerspectiveDiabetes, 1981