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Evaluation of Serum Lipocalin 13 Levels and Its Association with Insulin Resistance in Patients with Non-Alcoholic Fatty Liver Disease compared to control group: A Case-Control Study
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Nariman Moradi1    , Riyadh Alhaideri2 , Zakaria Vahabzadeh3 , Somaieh Fatahi2 , Farshad Sheikhesmaili4 , Bijan Nouri5 |
1- Liver and Digestive Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran , narimanmoradi8463@gmail.com
2- Student Research Committee, Kurdistan University of Medical Sciences, Sanandaj, Iran
3- Cellular and Molecular Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran
4- Liver and Digestive Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran
5- Social Determinants of Health Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran |
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Abstract: (20 Views) |
Background and Aim: Non-alcoholic fatty liver disease (NAFLD) is a prevalent metabolic disorder globally. Lipocalin 13 (LCN13) is a hepatokine involved in lipid metabolism and insulin sensitivity via the farnesoid X receptor (FXR) pathway, but its serum levels and association with insulin resistance (IR) in human NAFLD remain unclear.
Materials and Methods: This case-control study included 89 participants: 72 patients with NAFLD diagnosed by clinical, biochemical, and FibroScan criteria (fibrosis grades F0-F3) and 17 healthy controls. Serum LCN13 levels were measured by ELISA. Lipid profile, liver enzymes (ALT, AST), fasting blood glucose, and insulin were assessed. IR was calculated using HOMA-IR. Statistical analyses included Mann-Whitney U, Kruskal-Wallis, Spearman correlation, and ROC curve (STATA v.17). P<0.05 was considered significant.
Results: Serum LCN13 levels were significantly lower in NAFLD patients compared to controls. No significant differences were observed across fibrosis grades or NAFLD severity grades. NAFLD patients showed significantly higher triglycerides, total cholesterol, ALT, and AST, and lower HDL. Insulin resistance did not differ between groups. No significant correlation was found between LCN13 and insulin resistance or lipid parameters. ROC analysis revealed an AUC of 0.76 (sensitivity 70%, specificity 73%) for LCN13 in NAFLD diagnosis.
Conclusion: Reduced serum LCN13 levels are associated with NAFLD, suggesting a potential early diagnostic biomarker. However, the lack of correlation with insulin resistanceand fibrosis limits its utility in advanced disease stages. Further studies are warranted to explore the therapeutic modulation of LCN13 via the FXR pathway. |
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| Keywords: Lipocalin 13, Non-alcoholic fatty liver disease, Insulin resistance, Hepatokine, Lipid metabolism |
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Type of Study: Original Research |
Subject:
Biochemistry and Clinical Laboratory
Received: 2026/06/23 | Accepted: 2026/10/20
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