Association between angiopoietin-1 and metabolic dysfunction-associated steatotic liver disease: a cross‑sectional study

血管生成素-1与代谢功能障碍相关脂肪肝疾病的关联:一项横断面研究

阅读:1

Abstract

BACKGROUND AND AIM: Angiogenesis is considered a vital mechanism of metabolic dysfunction-associated steatotic liver disease (MASLD), while angiopoietin-1 (ANGPT1) is a crucial regulatory factor of angiogenesis. However, whether circulating ANGPT1 level is related to MASLD remains unclear. METHODS: To conduct this cross-sectional study, adults who underwent their annual health examinations at the First Affiliated Hospital of Zhejiang University during January, 2024 to March, 2024 were enrolled. Anthropometric and biochemical parameters were measured. Mann-Whitney U test, chi-squared (χ2) test, Spearman's analysis, step-wise univariate and multivariate logistic regression were used to analyze the role of ANGPT1 in MASLD. RESULTS: A total of 169 MASLD patients and 204 non-MASLD controls were enrolled. MASLD patients had significantly higher serum level of ANGPT1 than non-MASLD controls (44.37(36.86-50.43) versus 35.17(26.10-43.89), ng/ml, P < 0.001). Serum ANGPT1 levels were positively related to the prevalence of MASLD (from 5.71% in the first quartile, to 37.32%, 53.71%, 95.24% in the second, third, and fourth quartiles, respectively, P(trend) < 0.001). Both univariate and multivariate stepwise logistic regression show positive correlation between ANGPT1 and MASLD (odds ratio (OR) 1.088, 95% confidence interval (CI) 1.063-1.113, P < 0.001; adjusted OR 1.084, 95% CI 1.038-1.133, P < 0.001, respectively). These positive correlations remain significant in different subgroups of age, gender, w/o obese or hyperglycemia (adjusted OR 1.031-1.172, all P < 0.01). CONCLUSIONS: This study revealed a positive association between serum ANGPT1 and MASLD, suggesting its potential as both a diagnostic and a therapeutic target.

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。