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Gut 54:789-796 doi:10.1136/gut.2004.046516
  • Inflammatory bowel disease

Production of adiponectin, an anti-inflammatory protein, in mesenteric adipose tissue in Crohn’s disease

  1. K Yamamoto1,
  2. T Kiyohara1,
  3. Y Murayama1,
  4. S Kihara1,
  5. Y Okamoto1,
  6. T Funahashi1,
  7. T Ito2,
  8. R Nezu3,
  9. S Tsutsui1,
  10. J-I Miyagawa1,
  11. S Tamura1,
  12. Y Matsuzawa4,
  13. I Shimomura1,
  14. Y Shinomura1
  1. 1Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, Osaka, Japan
  2. 2Department of Surgery, Graduate School of Medicine, Osaka University, Osaka, Japan
  3. 3Department of Surgery, Osaka Rosai Hospital, Osaka, Japan
  4. 4Department of Internal Medicine, Sumitomo Hospital, Osaka, Japan
  1. Correspondence to:
    Dr T Kiyohara
    Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, 2-2 B-5, Yamadaoka, Suita, 565-0871, Japan; kiyohara{at}imed2.med.osaka-u.ac.jp
  • Accepted 1 November 2004
  • Revised 28 October 2004

Abstract

Background and aims: A characteristic feature of Crohn’s disease (CD) is mesenteric adipose tissue hypertrophy. Mesenteric adipocytes or specific proteins secreted by them may play a role in the pathogenesis of CD. We recently identified adiponectin as an adipocyte specific protein with anti-inflammatory properties. Here we report on expression of adiponectin in mesenteric adipose tissue of CD patients.

Methods and results: Mesenteric adipose tissue specimens were obtained from patients with CD (n = 22), ulcerative colitis (UC) (n = 8) and, for controls, colon carcinoma patients (n = 28) who underwent intestinal resection. Adiponectin concentrations were determined by enzyme linked immunosorbent assay, and adiponectin mRNA levels were determined by real time quantitative reverse transcription-polymerase chain reaction. Tissue concentrations and release of adiponectin were significantly increased in hypertrophied mesenteric adipose tissue of CD patients compared with normal mesenteric adipose tissue of CD patients (p = 0.002, p = 0.040, respectively), UC patients (p = 0.002, p = 0.003), and controls (p<0.0001, p<0.0001). Adiponectin mRNA levels were significantly higher in hypertrophied mesenteric adipose tissue of CD patients than in paired normal mesenteric adipose tissue from the same subjects (p = 0.024). Adiponectin concentrations in hypertrophied mesenteric adipose tissue of CD patients with an internal fistula were significantly lower than those of CD patients without an internal fistula (p = 0.003).

Conclusions: Our results suggest that adipocytes in hypertrophied mesenteric adipose tissue produce and secrete significant amounts of adiponectin, which could be involved in the regulation of intestinal inflammation associated with CD.

Footnotes

  • Conflict of interest: None declared.