Relationship Between a Novel Model of Insulin Sensitivity and Arterial Stiffness in Non-Obese Patients with Type 2 Diabetes: A Cross-Sectional Study

一种新型胰岛素敏感性模型与非肥胖2型糖尿病患者动脉硬化的关系:一项横断面研究

阅读:1

Abstract

AIM: Insulin resistance (IR) is closely associated with arterial stiffness (AS) and cardiovascular diseases (CVDs). Recently, several non-insulin-based IR surrogate markers have been demonstrated to be related to AS. The natural log transformation of the glucose disposal rate (log(e) GDR) is a novel indicator of insulin sensitivity (IS) developed in patients with type 2 diabetes (T2D). We aim to investigate the relationship between the log(e) GDR and AS in non-obese patients with T2D. METHODS: A cross-sectional study of 790 non-obese patients with T2D were included. Clinical and biochemical characteristics were collected. AS was assessed by brachial-ankle pulse wave velocity (baPWV), and according to the baPWV levels, patients were divided into two groups: AS group (baPWV ≥ 1800 cm/s) and non-AS group (baPWV < 1800 cm/s). The correlation between AS and log(e) GDR was analyzed. RESULTS: Compared with the non-AS group, the log(e) GDR decreased in the AS group (P < 0.001). With the tertiles of log(e) GDR increased, the bapWV and the prevalence of AS were decreased (both P < 0.001). Univariate analysis showed that the log(e) GDR was negatively correlated with the baPWV and AS (both P < 0.001). Furthermore, multivariate regression analyses demonstrated that the log(e) GDR was independently associated with bapWV (β: -0.162; P < 0.001) and AS (OR: 0.286; 95% CI: 0.110-0.743). Integrating log(e) GDR modestly improved the ability of the model to identify AS (Net reclassification improvement (NRI): 0.043, 95% CI 0.009-0.079, P = 0.011). CONCLUSION: The log(e) GDR is independently correlated with AS in non-obese patients with T2D, and its utility for risk stratification requires further validation.

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。