1591-P: Circulating Levels of ELABELA is Inversely Associated with Hepatic Fibrosis of Nonalcoholic Fatty Liver Disease in Patients with Type 2 Diabetes Mellitus
Diabetes(2024)
摘要
Background: Non-alcoholic steatohepatitis is closely associated with the progression of diabetic kidney disease (DKD) in type 2 diabetes mellitus (T2DM). We aimed to investigate whether plasma ELABELA, recently identified as a latent biomarker for DKD, is related to the severity of NAFLD. Methods: A total of 362 patients with T2DM were enrolled in this study. Noninvasive clinical markers of hepatic fibrosis including fibrosis-4 (FIB-4) index, NAFLD fibrosis score (NFS) and aspartate aminotransferase-to-platelet ratio index (APRI) were determined. The levels of plasma ELABELA, UACR, creatinine and glucometabolic parameters were measured. The relationships between plasma ELABELA and the clinical markers were statistically evaluated. Results: Based on the median value of the plasma ELABELA, subjects were divided into low and high ELABELA groups. The low ELABELA group showed a significantly longer duration of diabetes, worsened nephropathic indices, and a more enhanced hepatic fibrosis index. A lower ELABELA was associated with a greater odds ratio for the risk of higher hepatic fibrosis stage (OR, 0.98; 95% CI, 0.966 to 0.994). Multiple regression analysis including confounding factors showed that ELABELA independently contributed to decreases in FIB-4 index (P=0.044), NFS (P=0.012). In addition, logistic regression analysis for the prevalence of advanced hepatic fibrosis defined by the cutoff points of the clinical scores showed that ELABELA was the sole and common negative factor for prevalence of advanced hepatic fibrosis (FIB-4 index: P=0.016, NFS: P=0.005). Conclusion: The decline of plasma ELABELA was independently associated with a higher degree of hepatic fibrosis in patients with T2DM. Considering the common metabolic milieu of renal and hepatic fibrosis in T2DM, the potential use of plasma ELABELA as an effective biomarker reflecting hepatic fibrosis in T2DM needs to be validated in the future. M. Shi: None. H. Cao: None. Y. Liu: None. W. Gu: None. H. Zhang: None. Jiangsu Province Science and Technology Plan Special Funds (BE2023745); Jiangsu Health Commission Medical Scientific Research Project (H2023137)
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