OBJECTIVE: To assess the frequency of 2 different forms of hemochromatosis HFE gene mutations (C282Y and H63D mutations) in a normal population in comparison with type 2 diabetic patients. METHODS: This case control study was undertaken in Zanjan Diabetic Care Center, Zanjan, western Tehran, in 2005. Two hundred and two individuals were included in this study: 101 type 2 diabetes mellitus (T2DM) patients, and 101 age, and gender-matched controls. The patients were examined for mutations in the HFE gene. Nucleotide 845 (C282Y) and 187 (H63D) alleles were amplified by polymerase chain reaction PCR with lymphocyte deoxy-ribonucleic acid. The PCR products were analyzed by restriction enzyme digestion. Chi-square, student's t test, and Fisher's exact tests were used for comparison, and odds' ratio was calculated. RESULTS: Two hundred and two individuals were studied. The frequency of wild/C282Y alleles was 98/2% in T2DM patients, and 99/1% in controls p=0.6. The frequency of wild/H63D alleles was 68.3/31.7% in diabetics p=0.08, and 73.4/26.3% in control subjects p=0.08. The distribution of genotypes was not statistically different. CONCLUSION: Based on our data, HFE mutations were not found in excess in patients with T2DM, and there was no evidence that a population-based search for an excess of these alleles in type 2 diabetes was indicated.
OBJECTIVE: To assess the frequency of 2 different forms of hemochromatosisHFE gene mutations (C282Y and H63D mutations) in a normal population in comparison with type 2 diabeticpatients. METHODS: This case control study was undertaken in Zanjan Diabetic Care Center, Zanjan, western Tehran, in 2005. Two hundred and two individuals were included in this study: 101 type 2 diabetes mellitus (T2DM) patients, and 101 age, and gender-matched controls. The patients were examined for mutations in the HFE gene. Nucleotide 845 (C282Y) and 187 (H63D) alleles were amplified by polymerase chain reaction PCR with lymphocyte deoxy-ribonucleic acid. The PCR products were analyzed by restriction enzyme digestion. Chi-square, student's t test, and Fisher's exact tests were used for comparison, and odds' ratio was calculated. RESULTS: Two hundred and two individuals were studied. The frequency of wild/C282Y alleles was 98/2% in T2DM patients, and 99/1% in controls p=0.6. The frequency of wild/H63D alleles was 68.3/31.7% in diabetics p=0.08, and 73.4/26.3% in control subjects p=0.08. The distribution of genotypes was not statistically different. CONCLUSION: Based on our data, HFE mutations were not found in excess in patients with T2DM, and there was no evidence that a population-based search for an excess of these alleles in type 2 diabetes was indicated.