There is evidence that adipocytokines play an important role in metabolism and in inflammation. Because human metabolism dramatically changes in inflammatory bowel disease (IBD) and chronic inflammation is the hallmark of the disease, we studied serum levels of leptin, adiponectin, resistin, and ghrelin in patients with ulcerative colitis (UC) and Crohn's disease (CD) in comparison with healthy controls (HC).
Leptin, adiponectin, resistin, and active ghrelin serum levels were measured in 100 IBD patients (46 UC and 54 CD) and in 60 matched HC using commercially available enzyme-linked immunosorbent assays. Leptin, adiponectin, resistin, and ghrelin levels were correlated with disease activity, type, localization, and treatment.
Mean serum leptin levels were 10.6 ± 2.0 ng/mL in UC patients, 12.5 ± 2.6 ng/mL in CD patients, and 15.0 ± 1.8 ng/mL in HC (P = .01). Mean serum adiponectin levels were 9514.8 ± 787.8 ng/mL in UC patients, 7651.1 ± 613 ng/mL in CD patients, and 7270.6 ± 559.4 ng/mL in HC (P = .05). Mean serum resistin levels were 21.2 ± 2.2 ng/mL in UC patients, 18.7 ± 1.6 ng/mL in CD patients and 11.8 ± 0.6 ng/mL in HC (P = .0002). Mean serum ghrelin levels were 48.2 ± 4.2 pg/mL in UC patients, 49.4 ± 4.6 pg/mL in CD patients and 14.8 ± 3.0 pg/mL in HC (P < .0001). Serum levels of these adipocytokines were not correlated with either C-reactive protein levels or the clinical indices of activity. No association between serum adipocytokines levels and disease localization in both UC and CD patients was found. Only serum ghrelin was significantly higher in ileal compared with colonic CD (P = .04).
Serum levels of adiponectin, resistin, and active ghrelin are increased whereas serum levels of leptin are decreased in patients with IBD. Further studies are needed to elucidate the role of adipocytokines in IBD.
1 Department of Gastroenterology, University Hospital, Heraklion, Crete, Greece
*Reprints: Department of Gastroenterology, University Hospital Heraklion, PO Box 1352, 71110 Heraklion, Crete, Greece
Received 1 September 2005; Accepted 1 December 2005