Abnormalities of adipose tissue in the mesentery, including adipose tissue hypertrophy and fat wrapping, have been long recognized on surgical specimens as characteristic features of Crohn's disease. However, the importance, origin, and significance of the mesenteric fat hypertrophy in this chronic inflammatory disease are unknown. Desreumaux and colleagues evaluated this phenomenon and quantified intra-abdominal fat in patients with CD vs UC by using magnetic resonance imaging (51). By applying this technique they were able to demonstrate a significant accumulation of intraabdominal fat in patients with CD. This mesenteric obesity, present from the onset of disease, is associated with overexpression of PPARy as well as TNF-a mRNA, as evaluated by RT-PCR studies (51). In a subsequent study, the same group could demonstrate an overexpression of leptin mRNA in the mesenteric adipose tissue in inflammatory bowel disease, whereas no difference could be detected between UC and CD. The increase in leptin went in parallel with an increase in TNF-a mRNA expression (27).
Comparable with other cytokines known to play a local role, reports about alterations in leptin plasma levels in IBD are inconsistent so far. Whereas some authors could detect no increase in circulating leptin levels in IBD (52,53), one group noted a significant increase in patients with acute UC, an observation supported by a further study where, in patients with active CD, a nonsignificant increase of serum leptin was detected (54,55). However, as leptin exerts stimulatory effects on a variety of cells involved in the induction and persistence of IBD (summarized in Fig. 1) a closer characterization of leptin levels during stages of IBD might be crucial to understanding its contribution to these inflammatory diseases.
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