Uncorrected Proof Iran J Pediatr. In Press(In Press):e117353. Published online 2021 October 13. doi: 10.5812/ijp.117353. Research Article Omentin-1 Levels and Non-alcoholic Fatty Liver Disease in Obese Adolescents Emine Turkkan 1 , Huseyin Dag 1, * , Okan Dikker 2 , Nevin Cetin Dag 1 , Alper Kacar 1 and Soner Sazak 1 1 Department of Pediatrics, Istanbul Prof. Dr. Cemil Ta¸ scıo ˘ glu City Hospital, University of Health Sciences, Istanbul, Turkey 2 Department of Medical Biochemistry, Istanbul Prof. Dr. Cemil Ta¸ scıo ˘ glu City Hospital, University of Health Sciences, Istanbul, Turkey * Corresponding author: Department of Pediatrics, Istanbul Prof. Dr. Cemil Ta¸ scıo ˘ glu City Hospital, University of Health Sciences, Istanbul, Turkey. Email: huseyindag2003@gmail.com Received 2021 June 26; Revised 2021 August 21; Accepted 2021 September 04. Abstract Background: Omentin-1 is an adipocytokine secreted from visceral adipose tissue that is thought to increase insulin sensitivity. Non-alcoholic fatty liver disease (NAFLD) is a comparatively extensive problem in obese adolescents. Decreased omentin-1 levels have been reported in obese patients, but the relationship between NAFLD and omentin-1 is contradictory. Objectives: We aimed to evaluate the omentin-1 levels in the sera of obese adolescents with and without NAFLD and compare them with each other. Methods: In this study, a total of 88 adolescents (56 obese and 32 normal-weight) were enrolled. Abdominal ultrasonography (US) identified 28 obese adolescents with grade 2-3 hepatosteatosis constituting the NAFLD group and 28 without hepatosteatosis on US constituting the non-NAFLD group. The control group included 32 age- and gender-matched cases without hepatosteatosis and with normal percentile body mass index (BMI). Serum omentin-1 levels were evaluated and compared. Results: The mean age of the research group was 12.72 ± 1.91 years. Unsurprisingly, BMI, glycated hemoglobin (HbA1c), liver transam- inases (AST, ALT), total cholesterol, triglyceride, low-density lipoprotein cholesterol (LDL), homeostatic model assessment for insulin resistance (HOMA-IR), and insulin rates were noticeably elevated in obese adolescents compared to controls (P < 0.05). However, omentin-1 and high-density lipoprotein cholesterol (HDL) levels were remarkably lower in the obese group (P < 0.05). No signifi- cant difference was found between the NAFLD and non-NAFLD groups regarding omentin-1, HbA1c, glucose, urea, creatinine, AST, C-reactive protein (CRP), total cholesterol, triglyceride, HDL, LDL, thyroid stimulating hormone, 25-hydroxyvitamin D3, HOMA-IR, and insulin. The BMI and ALT grades of the non-NAFLD group were notably lower than the NAFLD group (P < 0.05). While there was no significant difference between omentin-1 and other parameters in obese adolescents without NAFLD (P > 0.05), we found a significant difference between omentin-1 and BMI, AST, ALT, HOMA-IR, and insulin values in obese adolescents with NAFLD (P < 0.05). Conclusions: Omentin-1 levels were decreased in obese adolescents regardless of the presence of NAFLD. However, in obese patients with NAFLD, there was a significant difference between omentin-1 and several markers of obesity and insulin resistance. Keywords: Omentin-1, Obesity, Non-alcoholic Fatty Liver Disease, Adolescents 1. Background Obesity is a complex multifactorial condition charac- terized by excessive fat accumulation. It may play a role in pathophysiological changes such as inflammation, oxida- tive stress, endothelial dysfunction, and energy homeosta- sis disorder. Increased fat accumulation is associated with negative health consequences (1). Childhood obesity is an important public health problem of the 21st century with an increasing frequency. It affects approximately 25 - 30% of children globally (2). Non-alcoholic fatty liver disease (NAFLD), one of the problems caused by obesity, is seen in 22 - 52% of obese children (3). NAFLD is described as the col- lection of liver fat in excess of 5% in the lack of major alco- hol consumption, viral infection, or any obvious etiology of the liver. Although there are many causes of fatty liver, an increase in the total of fatty acid coming to the liver and an increase in hepatic fatty acid synthesis are the main rea- sons (4). Adipose tissue is considered to be an endocrine organ that secretes cytokines called adipokine (5). Dysregulation of adipokines stimulates systemic inflammation and con- tributes to obesity-related metabolic complications such as NAFLD, metabolic syndrome, insulin resistance, and cardiovascular disease (6). Omentin-1, also known as int- Copyright © 2021, Author(s). This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International License (http://creativecommons.org/licenses/by-nc/4.0/) which permits copy and redistribute the material just in noncommercial usages, provided the original work is properly cited.