Background: Inflammation is key in the pathogenesis of Nonalcoholic Fatty Liver Disease (NAFLD) – a common progressive liver disease. The soluble receptor for advanced glycation end products (sRAGE) attenuates inflammatory signaling; low levels of sRAGE are correlated with increased inflammation. Aim: We sought to describe associations between sRAGE and NAFLD. Methods: We conducted a cross-sectional analysis of 1088 Atherosclerosis Risk in Communities (ARIC) Study participants and used logistic regression to investigate the associations between sRAGE and NAFLD defined by elevated liver enzymes and fibrosis score. Results: In this community-based sample (n = 1,088, mean age 56 years, 61% female, 78% Caucasian), persons in the lowest vs. highest quartile of sRAGE had significantly higher odds of elevated ALT (OR 2.82, 95% CI 1.18-6.76) but not elevated AST (OR 1.16, 95% CI 0.45-2.99); persons in the lowest vs. highest quartile had significantly lower odds of elevated FIB-4 index (OR 0.56, 95% CI 0.37-0.84). Conclusions: We found an inverse cross-sectional association between sRAGE and liver inflammation; this is consistent with prior studies linking low sRAGE to inflammatory states. However, we observed a direct association between sRAGE and fibrosis. Our findings suggest that sRAGE is dynamic in NAFLD and patterns may vary with different stages of disease.
Bibliographical noteFunding Information:
This work was supported in part by federal funds from the National Institutes of Health ( NIH 5T32HL007180-44 ). The Atherosclerosis Risk in Communities study has been funded in whole or in part with Federal funds from the National Heart, Lung, and Blood Institute , National Institutes of Health, Department of Health and Human Services, under Contract nos. ( HHSN268201700001I , HHSN268201700002I , HHSN268201700003I , HHSN268201700005I , HHSN268201700004I ).
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- Receptor for advanced glycation end products