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Association of a microsatellite in FASL to type II diabetes and of the FAS-670G > A genotype to insulin resistance

Nolsoe, RL ; Hamid, YH ; Pociot, Flemming ; Paulsen, S ; Andersen, KM ; Borch-Johnsen, K ; Drivsholm, T ; Hansen, T ; Pedersen, O and Mandrup-Poulsen, T (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)
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author
; ; ; ; ; ; ; ; and
organization
publishing date
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
2021-09-22 02:12:18
@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},
  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},
}