Association of a microsatellite in FASL to type II diabetes and of the FAS-670G > A genotype to insulin resistance
(2006) In Genes and Immunity 7(4). p.316-321- Abstract
- Type II diabetes is caused by a failure of the pancreatic beta-cells to compensate for insulin resistance leading to hyperglycaemia. There is evidence for an essential role of an increased beta-cell apoptosis in type II diabetes. High glucose concentrations induce IL-1 beta production in human beta-cells, Fas expression and concomitant apoptosis owing to a constitutive expression of FasL. FASL and FAS map to loci linked to type II diabetes and estimates of insulin resistance, respectively. We have tested two functional promoter polymorphisms, FAS-670 G > A and FASL-844C > T as well as a microsatellite in the 3' UTR of FASL for association to type II diabetes in 549 type II diabetic patients and 525 normal-glucose-tolerant (NGT)... (More)
- Type II diabetes is caused by a failure of the pancreatic beta-cells to compensate for insulin resistance leading to hyperglycaemia. There is evidence for an essential role of an increased beta-cell apoptosis in type II diabetes. High glucose concentrations induce IL-1 beta production in human beta-cells, Fas expression and concomitant apoptosis owing to a constitutive expression of FasL. FASL and FAS map to loci linked to type II diabetes and estimates of insulin resistance, respectively. We have tested two functional promoter polymorphisms, FAS-670 G > A and FASL-844C > T as well as a microsatellite in the 3' UTR of FASL for association to type II diabetes in 549 type II diabetic patients and 525 normal-glucose-tolerant (NGT) control subjects. Furthermore, we have tested these polymorphisms for association to estimates of beta-cell function and insulin resistance in NGT subjects. We found significant association to type II diabetes for the allele distribution of the FASL microsatellite (P-value 0.02, Bonferroni corrected). The FAS-670G > A was associated with homeostasis model assessment insulin resistance index and body mass index (P-values 0.02 and 0.02). We conclude that polymorphisms of FASL and FAS associate with type II diabetes and estimates of insulin resistance in Danish white subjects. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/406822
- author
- Nolsoe, RL ; Hamid, YH ; Pociot, Flemming LU ; Paulsen, S ; Andersen, KM ; Borch-Johnsen, K ; Drivsholm, T ; Hansen, T ; Pedersen, O and Mandrup-Poulsen, T
- organization
- publishing date
- 2006
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- insulin, resistance, functional variants, FASL, type II diabetes, FAS, genetics
- in
- Genes and Immunity
- volume
- 7
- issue
- 4
- pages
- 316 - 321
- publisher
- Nature Publishing Group
- external identifiers
-
- wos:000238122400006
- pmid:16691186
- scopus:33745054115
- ISSN
- 1476-5470
- DOI
- 10.1038/sj.gene.6364300
- language
- English
- LU publication?
- yes
- id
- 3bd23a24-53eb-4b58-beb5-5ac7b334732e (old id 406822)
- date added to LUP
- 2016-04-01 12:10:10
- date last changed
- 2022-05-19 01:59:40
@article{3bd23a24-53eb-4b58-beb5-5ac7b334732e,
abstract = {{Type II diabetes is caused by a failure of the pancreatic beta-cells to compensate for insulin resistance leading to hyperglycaemia. There is evidence for an essential role of an increased beta-cell apoptosis in type II diabetes. High glucose concentrations induce IL-1 beta production in human beta-cells, Fas expression and concomitant apoptosis owing to a constitutive expression of FasL. FASL and FAS map to loci linked to type II diabetes and estimates of insulin resistance, respectively. We have tested two functional promoter polymorphisms, FAS-670 G > A and FASL-844C > T as well as a microsatellite in the 3' UTR of FASL for association to type II diabetes in 549 type II diabetic patients and 525 normal-glucose-tolerant (NGT) control subjects. Furthermore, we have tested these polymorphisms for association to estimates of beta-cell function and insulin resistance in NGT subjects. We found significant association to type II diabetes for the allele distribution of the FASL microsatellite (P-value 0.02, Bonferroni corrected). The FAS-670G > A was associated with homeostasis model assessment insulin resistance index and body mass index (P-values 0.02 and 0.02). We conclude that polymorphisms of FASL and FAS associate with type II diabetes and estimates of insulin resistance in Danish white subjects.}},
author = {{Nolsoe, RL and Hamid, YH and Pociot, Flemming and Paulsen, S and Andersen, KM and Borch-Johnsen, K and Drivsholm, T and Hansen, T and Pedersen, O and Mandrup-Poulsen, T}},
issn = {{1476-5470}},
keywords = {{insulin; resistance; functional variants; FASL; type II diabetes; FAS; genetics}},
language = {{eng}},
number = {{4}},
pages = {{316--321}},
publisher = {{Nature Publishing Group}},
series = {{Genes and Immunity}},
title = {{Association of a microsatellite in FASL to type II diabetes and of the FAS-670G > A genotype to insulin resistance}},
url = {{http://dx.doi.org/10.1038/sj.gene.6364300}},
doi = {{10.1038/sj.gene.6364300}},
volume = {{7}},
year = {{2006}},
}