PDF(Pubmed)
Abstract：
Diabetes is a metabolic disorder associated with chronic inflammation; pre-diabetes phase promotes to inflammatory mechanism then finally progress to diabetes and its associated complications. Therefore, it is of interest to investigate the changes in inflammatory biomarkers Evidence that inflammatory markers play a role in the development as well as severity of Type 2 diabetes mellitus (T2DM). This study has been designed to decipher the involvement of Tumor Necrosis Factor (TNFα), Interleukin-6 (IL-6), Nesfatin-1 and Blood sugar in the etiopathogenesis of T2DM. This retrospective observational study analyzed patient records from our hospital, focusing on those with diabetes or pre-diabetes. Glycosylated hemoglobin, inflammatory biomarkers, Fasting Blood Glucose, and Post-Prandial Blood Glucose were assessed. SPSS 28 facilitated statistical analysis; utilizing Bivariate Correlation assessed the relationship between inflammatory biomarkers and diabetes status (glycosylated hemoglobin). In the pre-diabetic vs. diabetic groups, significant differences exist in IL-6 (p=0.0344), TNF-α (p=0.041), Nesfatin-1 (p=0.0485), fasting blood glucose (p=0.036), and 2h post-prandial blood glucose (p=0.048). IL6 (AUC=0.729, p<0.001), TNF (AUC=0.761, p<0.001), and Nesfatin1 (AUC=0.892, p<0.001) show moderate discriminative power. PP (AUC=0.992, p<0.001) and hbA1c (AUC=0.993, p<0.001) exhibit excellent discriminatory ability. Correlations: IL6 with TNF (r=0.672, p<0.001) and Nesfatin1 (r=0.542, p<0.001); TNF with Nesfatin1 (r=0.591, p<0.001), hbA1c (r=0.683, p<0.001), and PP (r=0.367, p<0.001); Nesfatin1 with PP (r=0.594, p<0.001) and hbA1c (r=0.800, p<0.001). Age has a negative correlation with hbA1c (r=-0.119, p=0.086). Thus, data shows a significant association between inflammatory markers, blood glucose levels, and the progression from pre-diabetes to diabetes.
摘要：
糖尿病是与慢性炎症相关的代谢紊乱;糖尿病前期促进炎症机制,然后最终发展为糖尿病及其相关并发症。因此,研究炎症生物标志物的变化是有意义的。证据表明炎症标志物在2型糖尿病（T2DM）的发展和严重程度中起作用。本研究旨在破译肿瘤坏死因子（TNFα）的参与，白细胞介素-6(IL-6),Nesfatin-1和血糖在T2DM发病机制中的作用.这项回顾性观察研究分析了我们医院的患者记录，专注于糖尿病或糖尿病前期患者。糖化血红蛋白,炎症生物标志物，空腹血糖,和餐后血糖进行评估。SPSS28有助于统计分析;利用双变量相关性评估炎症生物标志物和糖尿病状态(糖基化血红蛋白)之间的关系。在糖尿病前期与糖尿病组，IL-6存在显著差异(p=0.0344)，TNF-α（p=0.041），Nesfatin-1（p=0.0485），空腹血糖（p=0.036），和餐后2h血糖(p=0.048)。IL6（AUC=0.729，p<0.001），TNF（AUC=0.761，p<0.001），和Nesfatin1(AUC=0.892,p<0.001)显示中等判别力。PP(AUC=0.992,p<0.001)和hbA1c(AUC=0.993,p<0.001)表现出优异的辨别能力。相关性：IL6与TNF（r=0.672，p<0.001）和Nesfatin1（r=0.542，p<0.001）；TNF与Nesfatin1（r=0.591，p<0.001），hbA1c（r=0.683，p<0.001），和PP（r=0.367，p<0.001）；Nesfatin1与PP（r=0.594，p<0.001）和hbA1c（r=0.800，p<0.001）。年龄与hbA1c呈负相关(r=-0.119,p=0.086)。因此，数据显示炎症标志物之间存在显著关联，血糖水平，以及从糖尿病前期到糖尿病的进展。
