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

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Standard

Association of a microsatellite in FASL to type II diabetes and of the FAS-670G>A genotype to insulin resistance. / Nolsøe, R L; Hamid, Y H; Pociot, F; Paulsen, S; Andersen, K M; Borch-Johnsen, K; Drivsholm, T; Hansen, T; Pedersen, O; Mandrup-Poulsen, T.

In: Genes and Immunity, Vol. 7, No. 4, 01.06.2006, p. 316-21.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Nolsøe, RL, Hamid, YH, Pociot, F, Paulsen, S, Andersen, KM, Borch-Johnsen, K, Drivsholm, T, Hansen, T, Pedersen, O & Mandrup-Poulsen, T 2006, 'Association of a microsatellite in FASL to type II diabetes and of the FAS-670G>A genotype to insulin resistance', Genes and Immunity, vol. 7, no. 4, pp. 316-21. https://doi.org/10.1038/sj.gene.6364300

APA

Nolsøe, R. L., Hamid, Y. H., Pociot, F., Paulsen, S., Andersen, K. M., Borch-Johnsen, K., ... Mandrup-Poulsen, T. (2006). Association of a microsatellite in FASL to type II diabetes and of the FAS-670G>A genotype to insulin resistance. Genes and Immunity, 7(4), 316-21. https://doi.org/10.1038/sj.gene.6364300

Vancouver

Nolsøe RL, Hamid YH, Pociot F, Paulsen S, Andersen KM, Borch-Johnsen K et al. Association of a microsatellite in FASL to type II diabetes and of the FAS-670G>A genotype to insulin resistance. Genes and Immunity. 2006 Jun 1;7(4):316-21. https://doi.org/10.1038/sj.gene.6364300

Author

Nolsøe, R L ; Hamid, Y H ; Pociot, F ; Paulsen, S ; Andersen, K M ; Borch-Johnsen, K ; Drivsholm, T ; Hansen, T ; Pedersen, O ; Mandrup-Poulsen, T. / Association of a microsatellite in FASL to type II diabetes and of the FAS-670G>A genotype to insulin resistance. In: Genes and Immunity. 2006 ; Vol. 7, No. 4. pp. 316-21.

Bibtex

@article{e83f339e971b436e9b30dda1a6afc09a,
title = "Association of a microsatellite in FASL to type II diabetes and of the FAS-670G>A genotype to insulin resistance",
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-1beta 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.",
keywords = "3' Untranslated Regions, Adult, Aged, Antigens, CD95, Apoptosis, Denmark, Diabetes Mellitus, Type 2, Fas Ligand Protein, Female, Humans, Insulin Resistance, Insulin-Secreting Cells, Male, Membrane Glycoproteins, Microsatellite Repeats, Middle Aged, Polymorphism, Genetic, Promoter Regions, Genetic, Quantitative Trait, Heritable, Receptors, Tumor Necrosis Factor, Tumor Necrosis Factors",
author = "Nols{\o}e, {R L} and Hamid, {Y H} and F Pociot and S Paulsen and Andersen, {K M} and K Borch-Johnsen and T Drivsholm and T Hansen and O Pedersen and T Mandrup-Poulsen",
year = "2006",
month = "6",
day = "1",
doi = "10.1038/sj.gene.6364300",
language = "English",
volume = "7",
pages = "316--21",
journal = "Genes and Immunity",
issn = "1466-4879",
publisher = "nature publishing group",
number = "4",

}

RIS

TY - JOUR

T1 - Association of a microsatellite in FASL to type II diabetes and of the FAS-670G>A genotype to insulin resistance

AU - Nolsøe, R L

AU - Hamid, Y H

AU - Pociot, F

AU - Paulsen, S

AU - Andersen, K M

AU - Borch-Johnsen, K

AU - Drivsholm, T

AU - Hansen, T

AU - Pedersen, O

AU - Mandrup-Poulsen, T

PY - 2006/6/1

Y1 - 2006/6/1

N2 - 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-1beta 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.

AB - 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-1beta 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.

KW - 3' Untranslated Regions

KW - Adult

KW - Aged

KW - Antigens, CD95

KW - Apoptosis

KW - Denmark

KW - Diabetes Mellitus, Type 2

KW - Fas Ligand Protein

KW - Female

KW - Humans

KW - Insulin Resistance

KW - Insulin-Secreting Cells

KW - Male

KW - Membrane Glycoproteins

KW - Microsatellite Repeats

KW - Middle Aged

KW - Polymorphism, Genetic

KW - Promoter Regions, Genetic

KW - Quantitative Trait, Heritable

KW - Receptors, Tumor Necrosis Factor

KW - Tumor Necrosis Factors

U2 - 10.1038/sj.gene.6364300

DO - 10.1038/sj.gene.6364300

M3 - Journal article

C2 - 16691186

VL - 7

SP - 316

EP - 321

JO - Genes and Immunity

JF - Genes and Immunity

SN - 1466-4879

IS - 4

ER -

ID: 33030373