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Screening for MODY mutations, GAD antibodies, and type 1 diabetes--associated HLA genotypes in women with gestational diabetes mellitus.

Weng, Jianping ; Ekelund, Magnus ; Lehto, Markku ; Li, Haiyan LU ; Ekberg, Göran ; Frid, Anders LU ; Åberg, Anders E LU ; Groop, Leif LU and Berntorp, Kerstin LU (2002) In Diabetes Care 25(1). p.68-71
Abstract
OBJECTIVE: To investigate whether genetic susceptibility to type 1 diabetes or maturity-onset diabetes of the young (MODY) increases susceptibility to gestational diabetes mellitus (GDM). RESEARCH DESIGN AND METHODS: We studied mutations in MODY1-4 genes, the presence of GAD antibodies, and HLA DQB1 risk genotypes in 66 Swedish women with GDM and a family history of diabetes. An oral glucose tolerance test was repeated in 46 women at 1 year postpartum. RESULTS: There was no increase in type 1 diabetes-associated HLA-DQB1 alleles or GAD antibodies when compared with a group of type 2 diabetic patients (n = 82) or healthy control subjects (n = 86). Mutations in known MODY genes were identified in 3 of the 66 subjects (1 MODY2, 1 MODY3, and 1... (More)
OBJECTIVE: To investigate whether genetic susceptibility to type 1 diabetes or maturity-onset diabetes of the young (MODY) increases susceptibility to gestational diabetes mellitus (GDM). RESEARCH DESIGN AND METHODS: We studied mutations in MODY1-4 genes, the presence of GAD antibodies, and HLA DQB1 risk genotypes in 66 Swedish women with GDM and a family history of diabetes. An oral glucose tolerance test was repeated in 46 women at 1 year postpartum. RESULTS: There was no increase in type 1 diabetes-associated HLA-DQB1 alleles or GAD antibodies when compared with a group of type 2 diabetic patients (n = 82) or healthy control subjects (n = 86). Mutations in known MODY genes were identified in 3 of the 66 subjects (1 MODY2, 1 MODY3, and 1 MODY4). Of the 46 GDM subjects, 2 had diabetes (4%) and 17 had impaired glucose tolerance (IGT) (37%) at 1 year postpartum. Of the two subjects who developed manifest diabetes, one carried a MODY3 mutation (A203H in the hepatocyte nuclear factor-1alpha gene). There was no increase in high-risk HLA alleles or GAD antibodies in the women who had manifest diabetes or IGT at 1 year postpartum. CONCLUSIONS: MODY mutations but not autoimmunity contribute to GDM in Swedish women with a family history of diabetes and increase the risk of subsequent diabetes. (Less)
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organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Diabetes Mellitus Non-Insulin-Dependent : genetics, Diabetes Gestational : genetics : immunology, Female, Support Non-U.S. Gov't, Sweden, Risk Assessment, Pregnancy, Patient Selection, Mutation, Middle Age, Human, HLA Antigens : genetics, HLA-DQ Antigens : genetics, Genotype, Glucose Intolerance : genetics : immunology, Adult, Diabetes Mellitus Insulin-Dependent : genetics : immunology
in
Diabetes Care
volume
25
issue
1
pages
68 - 71
publisher
American Diabetes Association
external identifiers
  • pmid:11772903
  • wos:000173036900012
  • scopus:0036364915
ISSN
1935-5548
DOI
10.2337/diacare.25.1.68
language
English
LU publication?
yes
additional info
The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Endocrinology (013241500), Department of Obstetrics and Gynaecology (Lund) (013018000), Diabetes and Endocrinology (013241530), Pediatrics/Urology/Gynecology/Endocrinology (013240400)
id
1f69e3ba-4ed3-4f25-887f-8600366afec8 (old id 106886)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11772903&dopt=Abstract
date added to LUP
2016-04-01 17:09:49
date last changed
2024-04-12 14:37:52
@article{1f69e3ba-4ed3-4f25-887f-8600366afec8,
  abstract     = {{OBJECTIVE: To investigate whether genetic susceptibility to type 1 diabetes or maturity-onset diabetes of the young (MODY) increases susceptibility to gestational diabetes mellitus (GDM). RESEARCH DESIGN AND METHODS: We studied mutations in MODY1-4 genes, the presence of GAD antibodies, and HLA DQB1 risk genotypes in 66 Swedish women with GDM and a family history of diabetes. An oral glucose tolerance test was repeated in 46 women at 1 year postpartum. RESULTS: There was no increase in type 1 diabetes-associated HLA-DQB1 alleles or GAD antibodies when compared with a group of type 2 diabetic patients (n = 82) or healthy control subjects (n = 86). Mutations in known MODY genes were identified in 3 of the 66 subjects (1 MODY2, 1 MODY3, and 1 MODY4). Of the 46 GDM subjects, 2 had diabetes (4%) and 17 had impaired glucose tolerance (IGT) (37%) at 1 year postpartum. Of the two subjects who developed manifest diabetes, one carried a MODY3 mutation (A203H in the hepatocyte nuclear factor-1alpha gene). There was no increase in high-risk HLA alleles or GAD antibodies in the women who had manifest diabetes or IGT at 1 year postpartum. CONCLUSIONS: MODY mutations but not autoimmunity contribute to GDM in Swedish women with a family history of diabetes and increase the risk of subsequent diabetes.}},
  author       = {{Weng, Jianping and Ekelund, Magnus and Lehto, Markku and Li, Haiyan and Ekberg, Göran and Frid, Anders and Åberg, Anders E and Groop, Leif and Berntorp, Kerstin}},
  issn         = {{1935-5548}},
  keywords     = {{Diabetes Mellitus Non-Insulin-Dependent : genetics; Diabetes Gestational : genetics : immunology; Female; Support Non-U.S. Gov't; Sweden; Risk Assessment; Pregnancy; Patient Selection; Mutation; Middle Age; Human; HLA Antigens : genetics; HLA-DQ Antigens : genetics; Genotype; Glucose Intolerance : genetics : immunology; Adult; Diabetes Mellitus Insulin-Dependent : genetics : immunology}},
  language     = {{eng}},
  number       = {{1}},
  pages        = {{68--71}},
  publisher    = {{American Diabetes Association}},
  series       = {{Diabetes Care}},
  title        = {{Screening for MODY mutations, GAD antibodies, and type 1 diabetes--associated HLA genotypes in women with gestational diabetes mellitus.}},
  url          = {{http://dx.doi.org/10.2337/diacare.25.1.68}},
  doi          = {{10.2337/diacare.25.1.68}},
  volume       = {{25}},
  year         = {{2002}},
}