Family history of Type 1 diabetes affects insulin secretion in patients with 'Type 2' diabetes

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Family history of Type 1 diabetes affects insulin secretion in patients with 'Type 2' diabetes. / Lundgren, V. M.; Andersen, M. K.; Isomaa, B.; Tuomi, T.

In: Diabetic Medicine, Vol. 30, No. 5, 01.05.2013.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Lundgren, VM, Andersen, MK, Isomaa, B & Tuomi, T 2013, 'Family history of Type 1 diabetes affects insulin secretion in patients with 'Type 2' diabetes', Diabetic Medicine, vol. 30, no. 5. https://doi.org/10.1111/dme.12069

APA

Lundgren, V. M., Andersen, M. K., Isomaa, B., & Tuomi, T. (2013). Family history of Type 1 diabetes affects insulin secretion in patients with 'Type 2' diabetes. Diabetic Medicine, 30(5). https://doi.org/10.1111/dme.12069

Vancouver

Lundgren VM, Andersen MK, Isomaa B, Tuomi T. Family history of Type 1 diabetes affects insulin secretion in patients with 'Type 2' diabetes. Diabetic Medicine. 2013 May 1;30(5). https://doi.org/10.1111/dme.12069

Author

Lundgren, V. M. ; Andersen, M. K. ; Isomaa, B. ; Tuomi, T. / Family history of Type 1 diabetes affects insulin secretion in patients with 'Type 2' diabetes. In: Diabetic Medicine. 2013 ; Vol. 30, No. 5.

Bibtex

@article{f79478078e724e72a7c6a3bc7313592a,
title = "Family history of Type 1 diabetes affects insulin secretion in patients with 'Type 2' diabetes",
abstract = "Aims: The aim was to evaluate the impact of family history of diabetes on the phenotype of patients diagnosed with Type 2 diabetes and the frequency of susceptibility genotypes. Methods: Patients with Type 2 diabetes with family history for both Type 1 and Type 2 diabetes (FHMIX, n = 196) or Type 2 diabetes only (FHT2, n = 139) matched for age, sex, BMI and age at diagnosis, underwent an oral glucose tolerance test and a combined glucagon test and insulin tolerance test. Glutamic acid decarboxylase (GAD) antibodies and major Type 1 and Type 2 diabetes susceptibility gene variants were analysed. Patients were stratified into groups according to family history or GAD antibody positivity (GADA+, GADA-) or a combination of these (GADA+/FHMIX, GADA+/FHT2, GADA-/FHMIX, GADA-/FHT2). Results: Compared with other patients, those with FHMIX more often had GAD antibodies (14.3 vs. 4.3%, P = 0.003), and those with both FHMIX and GAD antibodies had the highest frequency of insulin deficiency (stimulated serum C-peptide < 0.7 nmol/l, GADA+/FHMIX 46.4% vs. GADA-/FHMIX 9.5% (P < 0.00001), GADA-/FHT2 4.5% (P < 0.00001), GADA+/FHT2 0%). Patients with GADA+/FHMIX more often had HLA-DQB1 risk genotypes compared with patients with GADA-/FHMIX or GADA-/FHT2D (47 vs. 23 or 14%, P = 0.05 and P < 0.00001, respectively). In logistic regression analyses, FHMIX, GAD antibody positivity and HLA risk genotypes were independently associated with insulin deficiency. Conclusion: A family history for both type 1 and type 2 diabetes was associated with higher prevalence of GAD antibodies and HLA-DQB1 risk genotypes than a family history of type 2 diabetes only, and was associated with earlier and more severe development of insulin deficiency, which was only partially explained by GAD antibodies and HLA.",
author = "Lundgren, {V. M.} and Andersen, {M. K.} and B. Isomaa and T. Tuomi",
year = "2013",
month = may,
day = "1",
doi = "10.1111/dme.12069",
language = "English",
volume = "30",
journal = "Diabetic Medicine Online",
issn = "1464-5491",
publisher = "Wiley-Blackwell",
number = "5",

}

RIS

TY - JOUR

T1 - Family history of Type 1 diabetes affects insulin secretion in patients with 'Type 2' diabetes

AU - Lundgren, V. M.

AU - Andersen, M. K.

AU - Isomaa, B.

AU - Tuomi, T.

PY - 2013/5/1

Y1 - 2013/5/1

N2 - Aims: The aim was to evaluate the impact of family history of diabetes on the phenotype of patients diagnosed with Type 2 diabetes and the frequency of susceptibility genotypes. Methods: Patients with Type 2 diabetes with family history for both Type 1 and Type 2 diabetes (FHMIX, n = 196) or Type 2 diabetes only (FHT2, n = 139) matched for age, sex, BMI and age at diagnosis, underwent an oral glucose tolerance test and a combined glucagon test and insulin tolerance test. Glutamic acid decarboxylase (GAD) antibodies and major Type 1 and Type 2 diabetes susceptibility gene variants were analysed. Patients were stratified into groups according to family history or GAD antibody positivity (GADA+, GADA-) or a combination of these (GADA+/FHMIX, GADA+/FHT2, GADA-/FHMIX, GADA-/FHT2). Results: Compared with other patients, those with FHMIX more often had GAD antibodies (14.3 vs. 4.3%, P = 0.003), and those with both FHMIX and GAD antibodies had the highest frequency of insulin deficiency (stimulated serum C-peptide < 0.7 nmol/l, GADA+/FHMIX 46.4% vs. GADA-/FHMIX 9.5% (P < 0.00001), GADA-/FHT2 4.5% (P < 0.00001), GADA+/FHT2 0%). Patients with GADA+/FHMIX more often had HLA-DQB1 risk genotypes compared with patients with GADA-/FHMIX or GADA-/FHT2D (47 vs. 23 or 14%, P = 0.05 and P < 0.00001, respectively). In logistic regression analyses, FHMIX, GAD antibody positivity and HLA risk genotypes were independently associated with insulin deficiency. Conclusion: A family history for both type 1 and type 2 diabetes was associated with higher prevalence of GAD antibodies and HLA-DQB1 risk genotypes than a family history of type 2 diabetes only, and was associated with earlier and more severe development of insulin deficiency, which was only partially explained by GAD antibodies and HLA.

AB - Aims: The aim was to evaluate the impact of family history of diabetes on the phenotype of patients diagnosed with Type 2 diabetes and the frequency of susceptibility genotypes. Methods: Patients with Type 2 diabetes with family history for both Type 1 and Type 2 diabetes (FHMIX, n = 196) or Type 2 diabetes only (FHT2, n = 139) matched for age, sex, BMI and age at diagnosis, underwent an oral glucose tolerance test and a combined glucagon test and insulin tolerance test. Glutamic acid decarboxylase (GAD) antibodies and major Type 1 and Type 2 diabetes susceptibility gene variants were analysed. Patients were stratified into groups according to family history or GAD antibody positivity (GADA+, GADA-) or a combination of these (GADA+/FHMIX, GADA+/FHT2, GADA-/FHMIX, GADA-/FHT2). Results: Compared with other patients, those with FHMIX more often had GAD antibodies (14.3 vs. 4.3%, P = 0.003), and those with both FHMIX and GAD antibodies had the highest frequency of insulin deficiency (stimulated serum C-peptide < 0.7 nmol/l, GADA+/FHMIX 46.4% vs. GADA-/FHMIX 9.5% (P < 0.00001), GADA-/FHT2 4.5% (P < 0.00001), GADA+/FHT2 0%). Patients with GADA+/FHMIX more often had HLA-DQB1 risk genotypes compared with patients with GADA-/FHMIX or GADA-/FHT2D (47 vs. 23 or 14%, P = 0.05 and P < 0.00001, respectively). In logistic regression analyses, FHMIX, GAD antibody positivity and HLA risk genotypes were independently associated with insulin deficiency. Conclusion: A family history for both type 1 and type 2 diabetes was associated with higher prevalence of GAD antibodies and HLA-DQB1 risk genotypes than a family history of type 2 diabetes only, and was associated with earlier and more severe development of insulin deficiency, which was only partially explained by GAD antibodies and HLA.

UR - http://www.scopus.com/inward/record.url?scp=84876349276&partnerID=8YFLogxK

U2 - 10.1111/dme.12069

DO - 10.1111/dme.12069

M3 - Journal article

C2 - 23157220

AN - SCOPUS:84876349276

VL - 30

JO - Diabetic Medicine Online

JF - Diabetic Medicine Online

SN - 1464-5491

IS - 5

ER -

ID: 200858406