Research Article Follistatin-Like 1 Is Downregulated in Morbidly and Super Obese Central-European Population Martin Horak , 1,2 Daniela Kuruczova, 1,2 Filip Zlamal, 1,2 Josef Tomandl , 3 and Julie Bienertova-Vasku 1,2 1 Department of Pathological Physiology, Faculty of Medicine, Masaryk University, Kamenice 5, Brno 625 00, Czech Republic 2 Research Centre for Toxic Compounds in the Environment, Faculty of Science, Masaryk University, Kamenice 5, Brno 625 00, Czech Republic 3 Department of Biochemistry, Faculty of Medicine, Masaryk University, Kamenice 5, Brno 625 00, Czech Republic Correspondence should be addressed to Martin Horak; horak@mail.com Received 12 June 2018; Revised 29 August 2018; Accepted 1 November 2018; Published 22 November 2018 Academic Editor: Claudio Letizia Copyright © 2018 Martin Horak 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. Follistatin-like 1 (FSTL1) is a secreted adipomyokine with a possible link to obesity; however, its connection to extreme obesity currently remains unknown. In order to analyze such association for the very first time, we employed a unique cohort of morbidly and super obese individuals with a mean BMI of 44.77 kg/m 2 and measured the levels of circulating FSTL1. We explored the 3′ UTR of FSTL1 to locate a genetic variant which impairs microRNA binding. We located and investigated such SNP (rs1057231) in relation to the FSTL1 protein level, obesity status, and other body composition parameters. We observed a significant decline in FSTL1 level in obese subjects in comparison to nonobese ones. The evaluated SNP was found to correlate with FSTL1 only in nonobese subjects. The presented results were not affected by sex since both males and females expressed FSTL1 equally. We suggest that the FSTL1 decrease observed in extremely obese subjects is a result of adipogenesis reduction accompanied by a senescence of preadipocytes which otherwise willingly express FSTL1, increased adipocyte apoptosis, and epigenetic FSTL1 silencing. 1. Introduction According to the latest WHO estimates for the European Union region, approximately 40–70% of adults are over- weight and 10–30% are affected by obesity, i.e., an abnormal or excessive fat accumulation which constitutes a health risk. Obesity prevalence has tripled in many EU countries since the 1980s and this alarming number continues to rise. As a result, obesity is considered to be one of the greatest public health challenges of the 21st century, which is also evident from the fact that it consumes 4–7% of the total EU health- care costs. It is responsible for increased morbidity and mor- tality and enhances the risk of developing metabolic and nonmetabolic disorders such as type 2 diabetes mellitus, glu- cose intolerance, or chronic low-grade inflammation and cardiovascular disease, cancer, glomerulopathy, or bone fra- gility, respectively. It is a well-known fact that, far from being an inert fat deposit, adipose tissue constitutes an important and meta- bolically active endocrine organ which secretes proteins known as adipokines. To date, hundreds of adipokines have been identified and the vast majority of them, if not all, are linked to obesity [1]. Unfortunately, since current proteomic methodologies are not capable of describing pathophysio- logical pathways of obesity development on the level of indi- vidual adipokines, molecular approaches based on the study of a candidate molecule remain relevant. Although some adipokines, including, e.g., leptin, adiponectin, ghrelin, resistin, or interleukins have been studied extensively, the role of many others, including follistatin-like 1 (FSTL1), which has also been suggested as linked to obesity, remains unclear [2, 3]. FSTL1 was first described in 1993 as TSC-36 (TGFB- stimulated clone 36) in a study designed to identify genes Hindawi Disease Markers Volume 2018, Article ID 4140815, 7 pages https://doi.org/10.1155/2018/4140815