Yamamoto, K. et al. Production of adiponectin, an anti-inflammatory protein, in mesenteric adipose tissue in Crohn's disease. Gut 54, 789-796

Department of Internal Medicine and Molecular Science, Graduate School of Medicine, Osaka University, 2-2 B-5, Yamadaoka, Suita 565-0871, Japan.
Gut (Impact Factor: 14.66). 07/2005; 54(6):789-96. DOI: 10.1136/gut.2004.046516
Source: PubMed


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.
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).
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.

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    • "This alteration extends from the mesentery, partially covers the circumference, presents an outer layer of intestinal fat and may involve the small and large bowel. [4] Differential expression of adipocytokines and pro-inflammatory cytokines, as well as, histological alterations have been previously described in the MAT of CD individuals. [5]–[8] However, no studies regarding apoptosis pathways in this tissue have been yet reported. "
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    ABSTRACT: BackgroundCrohn’s disease (CD) is associated with complex pathogenic pathways involving defects in apoptosis mechanisms. Recently, mesenteric adipose tissue (MAT) has been associated with CD ethiopathology, since adipose thickening is detected close to the affected intestinal area. However, the potential role of altered apoptosis in MAT of CD has not been addressed.AimsTo evaluate apoptosis in the intestinal mucosa and MAT of patients with CD.MethodsSamples of intestinal mucosa and MAT from patients with ileocecal CD and from non-inflammatory bowel diseases patients (controls) were studied. Apoptosis was assessed by TUNEL assay and correlated with the adipocytes histological morphometric analysis. The transcriptional and protein analysis of selected genes and proteins related to apoptosis were determined.ResultsTUNEL assay showed fewer apoptotic cells in CD, when compared to the control groups, both in the intestinal mucosa and in MAT. In addition, the number of apoptotic cells (TUNEL) correlated significantly with the area and perimeter of the adipose cells in MAT. Transcriptomic and proteomic analysis reveal a significantly lower transcript and protein levels of Bax in the intestinal mucosa of CD, compared to the controls; low protein levels of Bax were found localized in the lamina propria and not in the epithelium of this tissue. Furthermore, higher level of Bcl-2 and low level of Caspase 3 were seen in the MAT of CD patients.ConclusionThe defective apoptosis in MAT may explain the singular morphological characteristics of this tissue in CD, which may be implicated in the pathophysiology of the disease.
    Full-text · Article · Jun 2014 · PLoS ONE
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    • "Diffuse, symmetric and continuous wall thickening [29] Young patients p-ANCA Crohn disease [29] Halo and target signs [48] Infectious colitis Comb sign [49] Radiation colitis [50] [51] Pylephlebitis [52] [53] Crohn disease Right colon ± ileum [29] Marked wall thickening eccentric [2] [9] [16] [54] [55] Young patients ASCA Tuberculosis [23] [27] Asymmetric and segmental [6] Actinomycosis [56] Halo and target signs [48] Typhlitis [46] [47] Comb sign [49] Proliferation of mesenteric fat [57] [58] Lymph nodes [18] Pericolic phlegmon and abscess [59] Sinus tract, fistula or perforation [56] [60] Ischemic colitis Left colon [61] ''Wet'' form [62] Vascular disease Metabolic acidosis and septic shock [63] Halo or target sign Rectal bleeding [61] ''Dry'' form [62] Thin and unenhancing colonic wall ± dilatation Arterial thrombus Pneumatosis [42] [43] Phlebosclerotic colitis Right colon [64] Marked edematous thickening Chronic diarrhea with melena [64] Ischemic colitis 65—67 Dilated collaterals veins with calcifications ± obstructions [68] [69] Pericolic stranding [68] [69] "
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    ABSTRACT: Acute colitis is often diagnosed on multidetector row computed tomography (MDCT) because patients with this condition present with abdominal pain and a variety of nonspecific symptoms. Acute colitis has multiple causes with varying degrees of severity. Analysis of the extent of colonic involvement, presence of specific MDCT imaging features and associated signs should help radiologist narrow the diagnosis. Integrating the results of clinical examination and biological tests is mandatory, and in case of ambiguous or nonspecific MDCT findings, endoscopy and colon biopsy should always be considered for a definite diagnosis. The purpose of this review is to discuss and illustrate MDCT features that are helpful for characterizing acute colitis in adults and to provide an update in current MDCT features.
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    • "Experimental colitis in rats resulted in elevated circulating leptin levels which correlate with the degree of inflammation and the development of anorexia [77] and leptin antagonist ameliorated the development of chronic experimental colitis [78]. Another adipokine, adiponectin, which is considered anti-inflammatory, has a structure similar to TNF-α but antagonizes its effects by reducing secretion and attenuating the biological actions by competing for the receptor [79–81]. Divergent data have been presented about circulating levels of adiponectin in patients with IBD [72, 74, 80, 82–86]. "
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    ABSTRACT: We reviewed and analyzed the relationship between physical exercise and inflammatory bowel disease (IBD) which covers a group of chronic, relapsing, and remitting intestinal disorders including Crohn's disease (CD) and ulcerative colitis. The etiology of IBD likely involves a combination of genetic predisposition and environmental risk factors. Physical training has been suggested to be protective against the onset of IBD, but there are inconsistencies in the findings of the published literature. Hypertrophy of the mesenteric white adipose tissue (mWAT) is recognized as a characteristic feature of CD, but its importance for the perpetuation of onset of this intestinal disease is unknown. Adipocytes synthesize proinflammatory and anti-inflammatory cytokines. Hypertrophy of mWAT could play a role as a barrier to the inflammatory process, but recent data suggest that deregulation of adipokine secretion is involved in the pathogenesis of CD. Adipocytokines and macrophage mediators perpetuate the intestinal inflammatory process, leading to mucosal ulcerations along the mesenteric border, a typical feature of CD. Contracting skeletal muscles release biologically active myokines, known to exert the direct anti-inflammatory effects, and inhibit the release of proinflammatory mediators from visceral fat. Further research is required to confirm these observations and establish exercise regimes for IBD patients.
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