Serum adipokines in inflammatory bowel disease

World J Gastroenterol. 2014 Jun 14;20(22):6912-7. doi: 10.3748/wjg.v20.i22.6912.

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; Crohn’s disease; Inflammatory bowel disease; Tumor growth factor-β1; Ulcerative colitis.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipokines / blood*
  • Adrenal Cortex Hormones / therapeutic use
  • Adult
  • Anti-Inflammatory Agents / therapeutic use
  • Azathioprine / therapeutic use
  • Biopsy
  • Case-Control Studies
  • Colitis, Ulcerative / blood*
  • Colitis, Ulcerative / diagnosis
  • Colitis, Ulcerative / drug therapy
  • Colitis, Ulcerative / immunology
  • Colonoscopy
  • Crohn Disease / blood*
  • Crohn Disease / diagnosis
  • Crohn Disease / drug therapy
  • Crohn Disease / immunology
  • Cytokines / blood
  • Drug Therapy, Combination
  • Enzyme-Linked Immunosorbent Assay
  • Female
  • Gastrointestinal Agents / therapeutic use
  • Humans
  • Leptin / blood
  • Magnetic Resonance Imaging
  • Male
  • Middle Aged
  • Nicotinamide Phosphoribosyltransferase / blood
  • Resistin / blood
  • Time Factors
  • Tomography, X-Ray Computed
  • Treatment Outcome
  • Young Adult

Substances

  • Adipokines
  • Adrenal Cortex Hormones
  • Anti-Inflammatory Agents
  • Cytokines
  • Gastrointestinal Agents
  • Leptin
  • RETN protein, human
  • Resistin
  • Nicotinamide Phosphoribosyltransferase
  • nicotinamide phosphoribosyltransferase, human
  • Azathioprine