PMID- 32983730
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201001
IS  - 2168-8184 (Print)
IS  - 2168-8184 (Electronic)
IS  - 2168-8184 (Linking)
VI  - 12
IP  - 8
DP  - 2020 Aug 26
TI  - Does Lipocalin-2 Affect Metabolic Syndrome in Hepatic Infections?
PG  - e10040
LID - 10.7759/cureus.10040 [doi]
LID - e10040
AB  - 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.
CI  - Copyright (c) 2020, Shahnawaz et al.
FAU - Shahnawaz, Waqas
AU  - Shahnawaz W
AD  - Biological and Biomedical Sciences, Aga Khan University Medical College, Karachi, 
      PAK.
FAU - Suhail, Nawal
AU  - Suhail N
AD  - Biological and Biomedical Sciences, Aga Khan University Medical College, Karachi, 
      PAK.
FAU - Siddiqui, Muhammad Ahsan Iqbal
AU  - Siddiqui MAI
AD  - Biological and Biomedical Sciences, Aga Khan University Medical College, Karachi, 
      PAK.
FAU - Yasmeen, Saira
AU  - Yasmeen S
AD  - Physiology, Jinnah Postgraduate Medical Centre, Karachi, PAK.
FAU - Fatima, Syeda Sadia
AU  - Fatima SS
AD  - Biological and Biomedical Sciences, Aga Khan University, Karachi, PAK.
LA  - eng
PT  - Journal Article
DEP - 20200826
PL  - United States
TA  - Cureus
JT  - Cureus
JID - 101596737
PMC - PMC7515810
OTO - NOTNLM
OT  - diabetes
OT  - hepatitis
OT  - lipocalin
OT  - obesity
COIS- The authors have declared that no competing interests exist.
EDAT- 2020/09/29 06:00
MHDA- 2020/09/29 06:01
PMCR- 2020/08/26
CRDT- 2020/09/28 05:43
PHST- 2020/09/28 05:43 [entrez]
PHST- 2020/09/29 06:00 [pubmed]
PHST- 2020/09/29 06:01 [medline]
PHST- 2020/08/26 00:00 [pmc-release]
AID - 10.7759/cureus.10040 [doi]
PST - epublish
SO  - Cureus. 2020 Aug 26;12(8):e10040. doi: 10.7759/cureus.10040.