Research Article Favorable Effect of Anti-TNF Therapy on Insulin Sensitivity in Nonobese, Nondiabetic Patients with Inflammatory Bowel Disease Stavroula A. Paschou , 1 Fotios Kothonas, 2 Apostolos Lafkas, 1 Alexandros Myroforidis, 2 Vasiliki Loi, 1 Thomais Terzi, 1 Olympia Karagianni, 1 Androniki Poulou, 2 Konstantinos Goumas, 2 and Andromachi Vryonidou 1 1 Department of Endocrinology and Diabetes, Hellenic Red Cross Hospital, Athens, Greece 2 Department of Gastroenterology, Hellenic Red Cross Hospital, Athens, Greece Correspondence should be addressed to Stavroula A. Paschou; s.a.paschou@gmail.com Received 11 August 2017; Accepted 17 January 2018; Published 5 March 2018 Academic Editor: Claudio Casella Copyright © 2018 Stavroula A. Paschou et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background. The aim of this study was to investigate the effect of anti-TNF therapy on glucose and lipid metabolism in nondiabetic, nonobese patients with inflammatory bowel disease (IBD). Patients and Methods. We studied 44 patients with IBD, without a known history of diabetes. Three of the patients were diagnosed with overt diabetes and were excluded. Eighteen of the remaining patients (9 M/9 F, 33.6 ± 8.8 years) were on anti-TNF therapy for longer than 1 year, while 23 patients (16 M/7 F, 38.7 ± 12.5 years) were treated with aminosalicylates (AMSs). Twelve of the patients from the second group were then treated with anti-TNF and reassessed 6 months later. Fasting glucose, insulin, c-peptide, HbA1c, lipid, CRP, and fibrinogen levels were determined, and HOMA-IR index was calculated in all patients. Results. Patients from the two therapy groups were matched for age and BMI and were not obese. We did not find any differences between patients from the two therapy groups regarding fasting glucose, c-peptide, HbA1c, total cholesterol, HDL, LDL, triglycerides, CRP, and HOMA-IR index. In patients who were treated for 6 months with anti-TNF, a statistically significant decrease in insulin (before 15.5 ± 5.9 versus after 9.9 ± 2.9 μIU/ml, p =0 042) and c-peptide (before 2.4 ± 1 versus after 1.3 ± 0.4 ng/ml, p =0 030) levels as well as the HOMA-IR index (before 4.2 ± 1.9 versus after 2.2 ± 0.9, p =0 045) was observed, without any changes in weight, BMI, glucose, HbA1c, lipid, CRP, and fibrinogen levels. Conclusion. Anti-TNF therapy exerts a favorable effect on insulin sensitivity, while it has no effect on lipid levels in nondiabetic, nonobese patients with inflammatory bowel disease. 1. Introduction Inflammatory bowel disease (IBD) is an immune-mediated disorder of the intestine, encompassing two different clinical entities, Crohn’s disease and ulcerative colitis. These diseases share some clinical features but also present distinct charac- teristics regarding both histopathology and topography [1]. As tumor necrosis factor alpha (TNFα) plays a central role in the inflammatory process of IBD, many of these patients with active disease are treated with anti-TNF agents [2, 3]. Patients with autoimmune diseases often present insulin resistance, dyslipidemia, type 2 diabetes, and increased cardiovascular risk. This has been reported in rheumatoid arthritis and psoriasis [4, 5]. In patients with IBD, insulin resistance is also present, but the presence of increased risk for type 2 diabetes and cardiovascular disease has not been documented yet [6, 7]. Inflammation and insulin resistance are closely linked, and inflammatory cytokines such as tumor necrosis factor alpha (TNFα) may inhibit insulin signaling and promote insulin resistance [8]. Specifically, TNFα induces phosphorylation of insulin receptor substrate proteins at serine residues instead of tyrosine ones. As phosphorylation at tyrosine residues is essential for the initiation of intracellular signaling cascade and normal insulin action, TNFα leads to insulin resistance [9–11]. Anti-TNF therapy reduces activity and severity of inflamma- tory autoimmune diseases. Furthermore, such therapy has resulted in the reduction of cardiovascular disease events. Hindawi International Journal of Endocrinology Volume 2018, Article ID 6712901, 5 pages https://doi.org/10.1155/2018/6712901