Evidence-Based Medicine
Copyright ©2014 Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jun 14, 2014; 20(22): 6912-6917
Published online Jun 14, 2014. doi: 10.3748/wjg.v20.i22.6912
Serum adipokines in inflammatory bowel disease
Marek Waluga, Marek Hartleb, Grzegorz Boryczka, Michał Kukla, Krystyna Żwirska-Korczala
Marek Waluga, Marek Hartleb, Grzegorz Boryczka, Department of Gastroenterology and Hepatology, Medical University of Silesia, 40-752 Katowice, Poland
Michał Kukla, Krystyna Żwirska-Korczala, Department of Physiology Zabrze, Medical University of Silesia, 40-055 Katowice, Poland
Author contributions: Waluga M conceived the study, analyzed the data and drafted the manuscript; Hartleb M participated in the study design and helped prepare the manuscript; Boryczka G assisted with blood samples and data collection; Kukla M and Żwirska-Korczala K assisted with technical issues and statistical analysis; all authors read and approved the final version of the manuscript.
Supported by A grant from the Medical University of Silesia, No. KNW-1-119/P/1/0
Correspondence to: Marek Waluga, MD, PhD, Department of Gastroenterology and Hepatology, Medical University of Silesia, ul. Medyków 14, 40-752 Katowice, Poland. mwaluga@sum.edu.pl
Telephone: +48-32-7894401 Fax: +48-32-7894402
Received: December 12, 2013
Revised: February 18, 2014
Accepted: March 8, 2014
Published online: June 14, 2014
Processing time: 186 Days and 15.7 Hours
Abstract

AIM: To investigate serum adipokine levels in inflammatory bowel disease (IBD) patients before treatment and after achieving clinical remission.

METHODS: Serum concentrations of six adipokines (tissue growth factor-β1, adiponectin, leptin, chemerin, resistin, and visfatin) were studied in 40 subjects with active IBD [24 subjects with Crohn’s disease (CD) and in 16 subjects with ulcerative colitis (UC)] before and after three months of therapy with corticosteroids and/or azathioprine. Clinical diagnoses were based on ileocolonoscopy, computed tomography or magnetic resonance enterography and histological examination of mucosal biopsies sampled during endoscopy. Serum levels of adipokines were assessed by an indirect enzyme-linked immunosorbent assay. The control group was comprised of 16 age- and sex-matched healthy volunteers.

RESULTS: Baseline leptin concentrations were significantly decreased in both types of IBD compared to controls (8.0 ± 9.1 in CD and 8.6 ± 6.3 in UC vs 16.5 ± 10.1 ng/mL in controls; P < 0.05), and significantly increased after treatment only in subjects with CD (14.9 ± 15.1 ng/mL; P < 0.05). Baseline serum resistin concentrations were significantly higher in CD (19.3 ± 12.5 ng/mL; P < 0.05) and UC subjects (23.2 ± 11.0 ng/mL; P < 0.05) than in healthy controls (10.7 ± 1.1 ng/mL). Treatment induced a decrease in the serum resistin concentration only in UC subjects (14.5 ± 4.0 ng/mL; P < 0.05). Baseline serum concentrations of visfatin were significantly higher in subjects with CD (23.2 ± 3.2 ng/mL; P < 0.05) and UC (18.8 ± 5.3 ng/mL; P < 0.05) than in healthy controls (14.1 ± 5.3 ng/mL). Treatment induced a decrease in the serum visfatin concentrations only in CD subjects (20.4 ± 4.8 ng/mL; P < 0.05). Serum levels of adiponectin, chemerin and tissue growth factor-β1 did not differ between CD and UC subjects compared to healthy controls and also were not altered by anti-inflammatory therapy. Clinical indices of IBD activity did not correlate with adipokine levels.

CONCLUSION: IBD modulates serum adipokine levels by increasing resistin and visfatin release and suppressing leptin production.

Keywords: Adipokines; Tumor growth factor-β1; Crohn’s disease; Ulcerative colitis; Inflammatory bowel disease

Core tip: Recently, many adipokines with varying metabolic effects have been discovered. A bidirectional interaction between inflammation of the gut and visceral fat may exist in cases of inflammatory bowel disease (IBD). In this work, plasma levels of selected adipokines were studied in subjects with Crohn’s disease and ulcerative colitis before treatment and after achieving clinical remission. The results of this study indicate that IBD modulates serum adipokine levels by stimulating resistin and visfatin release and suppressing leptin production.