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Follistatin-Like 1 Is Downregulated in Morbidly and Super Obese Central-European Population
M. Horak, D. Kuruczova, F. Zlamal, J. Tomandl, J. Bienertova-Vasku,
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články
NLK
Free Medical Journals
od 1998
PubMed Central
od 1998
Europe PubMed Central
od 1998
Open Access Digital Library
od 1993-01-01 do 2024-05-30
Open Access Digital Library
od 1993-01-01 do 2024-05-30
Open Access Digital Library
od 1998-01-01 do 2024-05-30
Wiley-Blackwell Open Access Titles
od 1993
ROAD: Directory of Open Access Scholarly Resources
od 1983
PubMed
30595761
DOI
10.1155/2018/4140815
Knihovny.cz E-zdroje
- MeSH
- 3' nepřekládaná oblast MeSH
- adipogeneze genetika MeSH
- běloši MeSH
- biologické markery krev MeSH
- dospělí MeSH
- down regulace MeSH
- jednonukleotidový polymorfismus * MeSH
- lidé středního věku MeSH
- lidé MeSH
- mikro RNA metabolismus MeSH
- mladiství MeSH
- morbidní obezita krev genetika MeSH
- obezita krev genetika MeSH
- proteiny související s folistatinem krev genetika MeSH
- senioři MeSH
- vazebná místa MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mladiství MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- Geografické názvy
- Česká republika MeSH
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/m2 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.
Citace poskytuje Crossref.org
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