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Does Lipocalin-2 Affect Metabolic Syndrome in Hepatic Infections?

Background and objective Lipocalin-2 (LCN-2) is an adipokine that plays a protective role in various inflammatory disorders and regulates innate immune response to acute and chronic infections. However, scant information is available regarding the relationship between serum LCN-2 levels and type 2 d...

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Detalles Bibliográficos
Autores principales: Shahnawaz, Waqas, Suhail, Nawal, Siddiqui, Muhammad Ahsan Iqbal, Yasmeen, Saira, Fatima, Syeda Sadia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cureus 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7515810/
https://www.ncbi.nlm.nih.gov/pubmed/32983730
http://dx.doi.org/10.7759/cureus.10040
Descripción
Sumario:Background and objective Lipocalin-2 (LCN-2) is an adipokine that plays a protective role in various inflammatory disorders and regulates innate immune response to acute and chronic infections. However, scant information is available regarding the relationship between serum LCN-2 levels and type 2 diabetes mellitus (T2DM) occurring concurrently with chronic hepatic infections. The present study sought to investigate the association of LCN-2 with T2DM patients with hepatic infections. Methods The association of LCN-2 with T2DM, hepatic steatosis, and inflammation was tested in 37 non-T2DM noninfectious individuals (group A, control group) and 55 age-matched patients with T2DM and chronic infection (group B). Anthropometric data were measured and the body-fat percentage was calculated using bioelectrical impedance analysis (BIA). Hemoglobin (Hb), fasting plasma glucose (FPG), hemoglobin A1c (HbA1c), liver function enzymes (LFEs), lipid profile, and total leukocyte count (TLC) were measured. Serum LCN-2 levels were measured using a commercially available sandwich enzyme-linked immunosorbent assay method. Results Levels of LCN-2 were significantly elevated in group B (1896.90 ± 73.13 ng/ml) versus control group A (263.58 ± 15.66 ng/mL; p<0.001). LCN-2 correlated moderately with alanine aminotransferase (ALT) (r=0.369), alkaline phosphatase ALP (r=0.419), and HbA1c (r=0.341) (p<0.01). All correlations were lost when adjusted for the presence of hepatitis, indicating that liver infection exacerbates insulin resistance. Conclusion Based on our findings, circulating LCN-2 is elevated in T2DM subjects with hepatitis B co-infection and may contribute towards deranged inflammatory response.