The variation of pancreatic beta-cell specific glucokinase gene promoter at the position of -30 bp in Koreans with gestational diabetes mellitus.
- Author:
Jin Woo KIM
1
;
In Myung YANG
;
Sung Woon KIM
;
Young Seol KIM
;
Young Kil CHOI
;
Jung Taek WOO
;
Se Yoon KIM
;
Seung Joon OH
;
Jeon Ryung PAENG
;
Hak Chul CHANG
Author Information
1. Department of Internal Medicine, Kyung-Hee University School of Medicine, Korea.
- Publication Type:Original Article
- MeSH:
Diabetes Mellitus, Type 2;
Diabetes, Gestational*;
DNA;
Female;
Genotype;
Glucokinase*;
Glucose;
Glucose Intolerance;
Humans;
Insulin;
Insulin-Secreting Cells;
Korea;
Leukocytes;
Liver;
Metabolism;
Pregnancy
- From:Korean Journal of Medicine
1999;57(5):916-924
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Glucokinase is expressed only in both liver and pancreatic beta cells and has a key role in the regulation of glucose metabolism in these tissues. A number of gene defects associated with glucokinase gene and the cause of non-insulin-dependent diabetes mellitus are known, and the defects along the -30bp promoter site in particular are thought to be related to diabetes and glucose intolerance. To research on gene study related to diabetes, we looked into the relationship between the variation at -30bp of pancreatic beta cell specific glucokinase gene promoter and gestational diabetes mellitus(GDM) in Korea. METHODS: Forty patients with GDM and 62 normal controls were studied. Genomic DNA was extracted from peripheral leukocyte of patients with GDM and normal controls. The nucleotide variation at -30 bp of pancreatic beta cell specific glucokinase gene promoter was analyzed by PCR-SSCP methods. The sequences of amplified DNA were confirmed with direct sequencing method. The clinical features and the response of insulin secretion to oral glucose were analyzed between patients with GDM according to genotypes. RESULTS: Allelic frequency of position -30 bp of pancreatic beta cell specific glucokinase gene promoter did not differ between patients with GDM and normal subjects. However the frequency of G/A and A/A genotypes seemed to show a higher tendency in patients with GDM compare to the normal subjects. Clinical features, insulin response to oral glucose did not differ according to the type of variation at -30bp of pancreatic beta cell specific glucokinase gene promoter. CONCLUSION: These data suggested that the variation at -30 bp of pancreatic beta cell specific glucokinase gene promoter in patients with GDM are unlikely to be one of the possibilities of the genetic factors in the development of GDM. Therefore more sophisticated studies will be needed to elucidate the role of variation at -30bp of pancreatic beta cell specific glucokinase gene promoter in the insulin secretion to oral glucose.
