Detailed Information on Publication Record
2018
Follistatin-Like 1 Is Downregulated in Morbidly and Super Obese Central-European Population
HOŘÁK, Martin, Daniela KURUCZOVÁ, Filip ZLÁMAL, Josef TOMANDL, Julie DOBROVOLNÁ et. al.Basic information
Original name
Follistatin-Like 1 Is Downregulated in Morbidly and Super Obese Central-European Population
Authors
HOŘÁK, Martin (203 Czech Republic, guarantor, belonging to the institution), Daniela KURUCZOVÁ (703 Slovakia, belonging to the institution), Filip ZLÁMAL (203 Czech Republic, belonging to the institution), Josef TOMANDL (203 Czech Republic, belonging to the institution) and Julie DOBROVOLNÁ (203 Czech Republic)
Edition
Disease Markers, London, Hindawi Publishing Corporation, 2018, 0278-0240
Other information
Language
English
Type of outcome
Článek v odborném periodiku
Field of Study
30109 Pathology
Country of publisher
United Kingdom of Great Britain and Northern Ireland
Confidentiality degree
není předmětem státního či obchodního tajemství
Impact factor
Impact factor: 2.761
RIV identification code
RIV/00216224:14110/18:00106292
Organization unit
Faculty of Medicine
UT WoS
000451854900001
Keywords in English
Follistatin-like 1
Tags
International impact, Reviewed
Změněno: 26/3/2019 10:31, Soňa Böhmová
Abstract
V originále
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.
Links
EF15_003/0000469, research and development project |
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LM2015051, research and development project |
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