RESUMO
(1) Background: Type 2 diabetes mellitus (T2DM) is one of the rapidly growing healthcare problems, and several vitamin D receptor (VDR) polymorphisms seem to modulate the risk of T2DM. Our research was designed to investigate the allelic discrimination of VDR polymorphisms and T2DM occurrence risk. (2) Methods: This case-control research included 156 patients with T2DM and 145 healthy control subjects. Most of the study population were males 56.6% vs. 62.8% in the case and control groups, respectively. Genotyping for VDR single nucleotide polymorphisms (SNPs), rs228570 (Fok1), rs7975232 (Apa1), and rs1544410 (Bsm1) was compared between both groups. (3) Results: There was a negative link between vitamin D levels and insulin sensitivity. A significant difference was noted in the allelic discrimination of VDR polymorphism rs228570 and rs1544410 between the study groups (p < 0.001). No difference was observed in the allelic discrimination of VDR polymorphism rs7975232 between the groups (p = 0.063). Moreover, T2DM patients had significantly higher levels of fasting blood sugar (FBS), glycated hemoglobin HbA1c, 2-h post-prandial blood sugar (PP), serum glutamic oxaloacetic transaminase (SGOT), serum glutamic-pyruvic transaminase (SGPT), total cholesterol, and triglycerides (p < 0.001), while High-Density Lipoprotein (HDL) Cholesterol (HDL-C) was significantly decreased (p = 0.006). (4) Conclusions: VDR polymorphisms had a positive association with T2DM risk among the Egyptian population. Further large-scale research using deep sequencing of samples is strongly urged to investigate different vitamin D gene variants and interactions, as well as the influence of vitamin D on T2DM.
RESUMO
BACKGROUND: Hepatitis C viral infection (HCV) and hepatocellular carcinoma (HCC) are potential health problems. New directly acting antivirals (DAAs) changed HCV treatment strategies. Selenoprotein P1 (SEPP1) is a hepatokine implicated in HCC pathogenesis. High mobility group box1 (HMGB1), a nuclear DNA-binding protein, involved in immune and inflammatory responses in HCV and HCC. Therefore, the aim of current study was to investigate HMGB1 and SEPP1 levels in HCV and HCVâ¯+â¯HCC patients and exploring DAAs effect on them. METHODS: 15 healthy volunteers, 25 HCV and 25 HCVâ¯+â¯HCC patients were included. Liver function tests, alpha fetoprotein (AFP), SEPP1 and HMGB1 serum levels were evaluated. For HCV group blood samples before and after treatment with sofosbuvir/daclatasvir combination were collected. RESULTS: HMGB1 was significantly higher in HCVâ¯+â¯HCC group than in control and HCV groups (pâ¯<â¯.05). SEPP1 decreased significantly in HCV and HCVâ¯+â¯HCC groups compared to control group (pâ¯<â¯.001). SEPP1 significantly elevated after treatment with DAAs (pâ¯=â¯.001). HMGB1 and SEPP1 were negatively correlated with each other in HCV group (pâ¯=â¯.047). Logistic regression analysis showed that HMGB1 and SEPP1 could be used as predictors for HCC in HCV infected patients (pâ¯=â¯.02,pâ¯=â¯.002) respectively. Receiver operating characteristic curve (ROC) revealed HMGB1 had 32% sensitivity and 100% specificity in differentiating HCV from HCVâ¯+â¯HCC patients, both SEPP1 and HMGB1 had high sensitivity (92%,60%) and 93% specificity in differentiating healthy from HCVâ¯+â¯HCC group. CONCLUSION: HMGB1 and SEPP1 are involved in pathogenesis of HCV and HCV induced HCC. Both of them could serve as predictive biomarkers for HCC in HCV patients.