Connecting peptide (c-peptide) and the duration of diabetes mellitus amongst patients, at the Federal Medical Centre (FMC), Owerri, southeast, Nigeria

Objective: C-peptide is derived from proinsulin and it is secreted in equimolar concentration with insulin. Plasma C-peptide is more stable than insulin and it provides an indirect measure of insulin secretory reserve and beta cell function. To determine relationship between C-peptide and duration of diabetes mellitus, age, body mass index, systolic blood pressure and diastolic blood pressure.Methods: This is a cross-sectional study of type 2 diabetes mellitus patients attending Endocrine Clinic. Information such as age, sex, height, weight, blood pressure and duration of diabetes were obtained. Blood samples were taken for fasting serum C-peptide. Data was analysed using SPSS version 16.Results: Out of the 46 subjects recruited 23 (50%) were females and 23 (50%) were males. The mean age was 55.63 ± 14.7 years. Mean duration of diabetes for both sexes was 8 years with a range of 1 to 32 years. The mean BMI was 26.87 ± 5.00 kg/m2for males and 30.09 ± 4.32 Kg/m2 for females. The mean fasting serum C-peptide was 2.16 ± 1.41 ng/ml and there was no significant difference between males and females. There is statistically significant inverse correlation between C-peptide and duration of diabetes (r= -0.356, p= 0.015). Conversely there is a direct relationship between C-peptide and BMI (r=0.307, p=0.038).Conclusion: Increasing duration of diabetes is associated with decreasing level of C-peptide and decreased beta cell secretory reserv

Expression of UDP Glucuronosyltransferases 2B15 and 2B17 is associated with methylation status in prostate cancer cells

Studies have suggested that abrogated expression of detoxification enzymes, UGT2B15 and UGT2B17, are associated with prostate tumour risk and progression. We investigated the role of EGF on the expression of these enzymes since it interacts with signalling pathways to also affect prostate tumour progression and is additionally associated with decreased DNA methylation. The expression of UGT2B15, UGT2B17, de novo methyltransferases, DNMT3A and DNMT3B was assessed in prostate cancer cells (LNCaP) treated with EGF, an EGFR inhibitor PD16893, and the methyltransferase inhibitor, 5-azacytidine, respectively. The results showed that EGF treatment decreased levels of expression of all four genes and that their expression was reversed by PD16893. Treatment with 5-azacytidine, markedly decreased expression of UGT2B15 and UGT2B17 over 85% as well as significantly decreased expression of DNMT3B, but not the expression of DNMT3A. DNMT3B siRNA treated LNCaP cells had decreased expression of UGT2B15 and UGT2B17, while DNMT3A siRNA treated cells had only moderately decreased UGT2B15 expression. Treatment with DNMT methyltransferase inhibitor, RG108, significantly decreased UGT2B17 expression. Additionally, methylation differences between prostate cancer samples and benign prostate samples from an Illumina 450K Methylation Array study were assessed. The results taken together suggest that hypomethylation of the UGT2B15 and UGT2B17 genes contributes to increased risk of prostate cancer and may provide a putative biomarker or epigenetic target for chemotherapeutics. Mechanistic studies are warranted to determine the role of the methylation marks in prostate cancer