Process of Glucose Increases Rather Than Constant High Glucose Was the Main Cause of Abnormal Glucose Induced Glomerulus Epithelial Cells Inflammatory Response.

Abnormal glycemia is frequently along with nephritis, whose pathogenesis is unexplicit. Here, we investigated the effects of abnormal glucose on the renal glomerulus epithelial cells by stimulating immortalized bovine renal glomerulus epithelial (MDBK) cells with five different levels of glucose, including low glucose (2.5 mM for 48 h, LG), normal glucose (5 mM for 48 h, NG), high glucose (25 mM for 48 h, HG), increasing glucose (24 h of 2.5 mM glucose followed by 24 h of 25 mM, IG), and reducing glucose (24 h of 25 mM glucose followed by 24 h of 2.5 mM, RG). The results showed that LG and RG treatments had nonsignificant effects (p > 0.05) on the viability of MDBK cells. HG treatment decreased the viabilities of cells (p < 0.01) without triggering an apparent inflammatory response by activating the nox4/ROS/p53/caspase-3-mediated apoptosis pathway. IG treatment decreased the viabilities of cells significantly (p < 0.01) with high levels of pro-inflammatory cytokines IL-1ß and IL-18 in the supernatant (p < 0.05) by triggering the txnip/nlrp3/gsdmd-mediated pyroptosis pathway. These results indicated that the process of glucose increase rather than the constant high glucose was the main cause of abnormal glucose-induced MDBK cell inflammatory death, prompting that the process of glycemia increases might be mainly responsible for the nephritis in diabetic nephropathy, underlining the importance of glycemic control in diabetes patients.

Identifying adolescents with high fasting glucose: the importance of adding grandparents' data when assessing family history of diabetes.

OBJECTIVE: To evaluate the role of adding grandparents' data to parental information to the assessment of a family history of diabetes, in order to identify adolescents with high fasting glucose. METHOD: In 2003 we evaluated 1276 population-based 13-year-olds, from Porto, Portugal. The history of diabetes in parents and grandparents was collected using self-reported questionnaires and a clinical evaluation was performed, including a fasting blood sample. The 75th percentile of fasting plasma glucose (FPG=91 mg/dl) was used to create two groups of participants (high vs. low fasting glucose). RESULTS: No association was found between family history of diabetes (with or without grandparental data) and a high FPG. The sensitivity to identify individuals with high FPG increased from 7.8% to 47.9% when grandparental history was combined with parental data. The positive predictive value was slightly increased (25.2% vs. 27.8%) but the specificity dropped (91.8% vs. 56.4%). CONCLUSION: Combining parental with grandparental history increased the number of adolescents with a positive family history of diabetes and also increased the sensitivity to identify adolescents with high FPG. So, even if it determines a decrease in specificity, grandparental data is relevant when screening for high fasting glucose in adolescents.