Korean J Med.
1999 Nov;57(5):916-924.
The variation of pancreatic beta-cell specific glucokinase gene promoter at the position of -30 bp in Koreans with gestational diabetes mellitus
- Affiliations
-
- 1Department of Internal Medicine, Kyung-Hee University School of Medicine, Korea.
- 2Endocrine Research Institute, Kyung-Hee University School of Medicine, Korea.
- 3Department of Internal Medicine, Samsung Jaeil Hospital, Korea.
Abstract
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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.
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