Lipocalin-2 is a biomarker in rat fatty liver induced by fructose-enriched diet

Alwahsh, SM; Xu, Mengyi; Ramadori, G; Schultze, FC

doi:10.1055/s-0032-1331996

Cited by 2 publications

(2 citation statements)

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“…Previous studies have indicated that the serum LCN2 level may be used as a diagnostic marker for various diseases, including colorectal cancer and cholangiocarcinoma [ 37 , 38 ]. However, based on a rat model that was induced via a fructose-enriched diet, an elevated LCN2 level was suggested to be a biomarker for fructose-induced fatty liver [ 39 ], which is supported by the fact that LCN2 expression is indicative of pathological conditions, including hepatic steatosis and inflammation [ 40 ]. Largely in consistence, our animal model of well-characterized NASH with fibrosis progression indicates that the liver LCN2 was increased along with the transition from NAFL to NASH and further fibrotic progression.…”

Section: Discussionmentioning

confidence: 99%

“…Previous studies have indicated that the serum LCN2 level may be used as a diagnostic marker for various diseases, including colorectal cancer and cholangiocarcinoma (37,38). However, based on a rat model that was induced via a fructose-enriched diet, an elevated LCN2 level was suggested to be a biomarker for fructose-induced fatty liver (39), which is supported by the fact that LCN2 expression is indicative of pathological conditions, including hepatic steatosis and inflammation (40).…”

Section: Discussionmentioning

confidence: 99%

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Serum lipocalin-2 is a potential biomarker for the clinical diagnosis of nonalcoholic steatohepatitis

Wang

Ying

et al. 2021

Clin Mol Hepatol

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Background/Aims: Nonalcoholic steatohepatitis (NASH) is a progressive form of nonalcoholic fatty liver disease (NAFLD) characterized by hepatic steatosis, inflammation, hepatocellular injury, and fibrosis. We aimed to investigate the usefulness of a key biomarker, lipocalin-2 (LCN2), for the detection of NASH progression.Methods: A mouse NASH model was established using a high-fat diet and a high-sugar drinking water. Gene expression profile of the NASH model was analyzed using RNA sequencing. Moreover, 360 NAFLD patients (steatosis, 83; NASH, 277), 40 healthy individuals, and 87 patients with alcoholic fatty liver disease were recruited.Results: Inflammatory infiltration, focal necrosis in the leaflets, steatosis, and fibrosis were documented in the mouse liver. In total, 504 genes were differentially expressed in the livers of NASH mice, and showed significant functional enrichment in the inflammation-related category. Upregulated liver LCN2 was found to be significantly interactive with various interleukins and toll-like receptors. Serum LCN2 levels were significantly increased in NAFLD patients. Serum LCN2 levels were correlated with steatosis, intralobular inflammation, semiquantitative fibrosis score, and nonalcoholic fatty liver disease activity score. The area under the curve of serum LCN2 was 0.987 with a specificity of 100% and a sensitivity of 93.5% for NASH diagnosis, and 0.977 with almost the same specificity and sensitivity for steatosis.Conclusions: LCN2 might be involved in the transition from NAFL to NASH by mediating inflammation. Serum LCN2 levels might be a novel biomarker for the diagnosis of NASH.

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