Predictive value of biliverdin reductase-A and homeostasis model assessment of insulin resistance on mild cognitive impairment in patients with type 2 diabetes

胆绿素还原酶A和胰岛素抵抗稳态模型评估对2型糖尿病患者轻度认知障碍的预测价值

阅读:1

Abstract

AIMS/INTRODUCTION: To investigate the predictive value of the biliverdin reductase-A (BVR-A) and the homeostasis model assessment for insulin resistance (HOMA-IR) on mild cognitive impairment (MCI) in patients with type 2 diabetes mellitus, and to establish a nomogram model. MATERIALS AND METHODS: This study included 140 patients with type 2 diabetes mellitus. Based on Montreal Cognitive Assessment (MoCA) scores, participants were categorized into the normal cognitive function (T2DM-NCF) group (65 cases) and the mild cognitive impairment (T2DM-MCI) group (75 cases). Multivariate logistic regression analysis was performed to identify the factors associated with MCI in patients with type 2 diabetes mellitus. A nomogram prediction model was developed using R software for the selected factors, and its predictability and accuracy were verified. RESULTS: Compared with the T2DM-NCF group, subjects with MCI were older, had a longer duration of diabetes, higher HOMA-IR, lower BVR-A, lower cognitive scores, and lower education levels (all P < 0.05). Multivariate logistic regression analysis showed that duration of diabetes (OR = 1.407, 95% CI: 1.163-1.701), HOMA-IR (OR = 1.741, 95% CI: 1.197-2.53), and BVR-A (OR = 0.528, 95% CI: 0.392-0.712) were significantly associated with the development of MCI in patients with type 2 diabetes mellitus. The C-index of the nomogram was 0.863 (95% CI: 0.752-0.937). CONCLUSIONS: Our findings suggest that BVR-A and HOMA-IR are significantly associated with the development of MCI in patients with type 2 diabetes mellitus. The nomogram incorporating BVR-A and HOMA-IR aids in predicting the risk of developing MCI in these patients.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。