No abstract available.
Apolipoproteins* ; Genotype* ; Humans ; Myocardial Infarction*

BACKGROUND: Peroxisome proliferator activated receptor-gamma (PPAR-gamma) is a nuclear receptor that regulate adipocyte differentiation and modulate intracellular insulin-signaling events. As such, PPARgamma is a candidate gene for several human disorders including obesity and type 2 diabetes mellitus. The objective of our study was to examine the relationship between genetic variation of PPARgamma2 and diabetes and obesity in Korean subjects. METHODS: We studied 99 subjects with type 2 diabetes mellitus, 128 obesity patients and 97 controls. Screening for mutation at codon 12 and 115 of PPARgamma2 were carried out by PCR-RFLP analyses. Statistical significance was evaluated by Chi-square test. RESULTS: The allele frequency of the Pro12Ala PPARgamma2 variant were 0.05 in controls, 0.06 in type 2 diabetes group, and 0.07 in obesity group (p=0.47). Pro115Gln variant were only proline homozygote in all groups. Genotype frequencies were also similar and conformed to expectations of the Hardy-Weinberg rule. The presence of PPARgamma2 gene variant was no associated with concentrations of total cholesterol, triglyceride, HDL-cholesterol, and also with fasting glucose. CONCLUSION: We concluded that the Pro12Ala and Pro115Gln PPARgamma2 missense mutation may not be associated with type 2 diabetes mellitus and obesity in Korean patients.
Adipocytes ; Cholesterol ; Codon ; Diabetes Mellitus, Type 2* ; Enzyme-Linked Immunosorbent Assay ; Fasting ; Gene Frequency ; Genetic Variation ; Genotype ; Glucose ; Homozygote ; Humans ; Liver Cirrhosis ; Mass Screening ; Mutation, Missense ; Obesity* ; Peroxisomes ; PPAR gamma* ; Proline ; Triglycerides

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.
Diabetes Mellitus, Type 2 ; Diabetes, Gestational* ; DNA ; Female ; Genotype ; Glucokinase* ; Glucose ; Glucose Intolerance ; Humans ; Insulin ; Insulin-Secreting Cells ; Korea ; Leukocytes ; Liver ; Metabolism ; Pregnancy

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.
Diabetes Mellitus, Type 2 ; Diabetes, Gestational* ; DNA ; Female ; Genotype ; Glucokinase* ; Glucose ; Glucose Intolerance ; Humans ; Insulin ; Insulin-Secreting Cells ; Korea ; Leukocytes ; Liver ; Metabolism ; Pregnancy