1 Address for Correspondence: Cumali KARATOPRAK, Bezmialem Vakıf Üniversitesi Tıp Fakültesi, İstanbul, Türkiye E-mail: ckaratoprak@hotmail.com This study was presented at the “75. American Diabetes Association Congress ”, “June 5-9, 2015, Boston, Massachusetts, USA”. Bezmialem Science 2018; 6: 1-5 DOI: 10.14235/bs.2018.1050 Original Article ©Copyright 2018 by Bezmialem Vakif University - Available online at www.bezmialemscience.org Vildagliptin Treatment on the Portal Venous Pressure and Hepatosteatosis in Patients with Type 2 Diabetes Mellitus Received : 27.05.2016 Accepted : 31.10.2016 ABSTRACT Objective: Tis study investigated how vildagliptin (a di-peptidyl peptidase 4 inhibitor) afects portal vein pressure and hepatosteatosis in patients with type 2 diabetes mellitus. Methods: Tis cross-sectional study evaluated the use of specifc drugs for at least 3 months on two groups of type 2 diabetes mel- litus cases. Group 1 used metformin and gliclazide, Group 2 used the same amounts of metformin and gliclazide, with the addition of vildagliptin. Using Doppler ultrasound, all cases were measured for portal vein fow velocity, portal vein fow and portal vein diameter. Degree of hepatosteatosis was also recorded. Results: A total of 97 patients completed the study. Te study fnished with 49 type 2 DM patients in Group1 (20 men, 29 women) and 48 patients in Group2 (20 men, 28 women. No signifcant diference was found in term of age, gender, BMI, HbA1c, mean arte- rial pressure, LDL-C, HDL-C or triglyceride levels in two groups.Portal vein fow velocity, portal vein fow volume, and portal vein diameter of all cases were measured by Doppler ultrasound in both groups. No signifcant diference was found between the groups (respectively p=0.92, p=0.60, p=0.92). Tere was no signifcant diference between groups regarding to ultrasonographic grading of hepatosteatosis. Conclusion: Treating type 2 diabetes mellitus patients with vildagliptin for had no efect on portal vein hemodynamics and hepatos- teatosis as assessed with Doppler ultrasound. Further long-term studies with better evaluation methods are needed to demonstrate any expected benefcial efect of vildagliptin on portal hemodynamics and hepatosteatosis. Keywords: Di-Peptidyl peptidase 4 inhibitors, vildagliptin, portal vein pressure, hepatosteatosis, type 2 diabetes mellitus Cumali KARATOPRAK 1 , Rukiye KILIÇARSLAN 2 , Mustafa CAKIRCA 1 , Sinem AYDIN 3 , Tuba ÖZKAN 1 , Orhan KOCAMAN 4 , Servet YOLBAŞ 5 , Mehmet ZORLU 1 , Muharrem KISKAÇ 1 , Mehmet Ali ÇIKRIKCIOĞLU 6 , Reha ERKOÇ 7 1 Department of Internal Disease, Bezmialem Vakif University School of Medicine, İstanbul, Turkey 2 Department of Radyology, Medipol University School of Medicine, İstanbul, Turkey 3 Department of Radyology, Bezmialem Vakif University School of Medicine, İstanbul, Turkey 4 Clinic of Gastroenterology, Medical Park Hospital, İstanbul, Turkey 5 Department of Rheumatology, İnönü University School of Medicine, Malatya, Turkey 6 Private Practice, İstanbul, Turkey 7 Private Saygı Hospital, İstanbul, Turkey Cite this article as: Karatoprak C, Kılıçarslan R, Cakırca M, Aydın S, Özkan T, Kocaman O, et al. Vildagliptin Treatment on the Portal Venous Pressure and Hepatosteatosis in Patients with Type 2 Diabetes Mellitus. Bezmialem Science 2018; 6: 1-5. Introduction Recent years have seen the development of drugs that increase plasma incretins for treatment of type 2 diabetes mellitus (DM). Incretins are secreted as an intestinal hormone by entero-endocrine cells immediately after meals for the purpose of regulating glucose. Te two known incretins are glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide-1 (GLP-1). Both of the incretins are rapidly inactivated by the enzyme named dipeptil peptidase 4 (DPP-4). Developed DPP-4 inhibitor drugs increase the plasma concentrations of GIP and GLP-1 by preventing their degradation by inhibiting the pertinent enzyme (1, 2). Although DPP-4 inhibitors mainly afect the pancreatic gland, they also afect the gastrointestinal tract, central nervous system, bone, adipose tissue, and the cardiovascular system (1, 2). Tey both incretins reduce intestinal motility, extend the