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Adipose tissue-specific ablation of PGC-1 beta impairs thermogenesis in brown fat
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SYSNO ASEP 0557788 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Adipose tissue-specific ablation of PGC-1 beta impairs thermogenesis in brown fat Author(s) Funda, Jiří (FGU-C) ORCID
Villena, J. A. (ES)
Bardová, Kristina (FGU-C) RID, ORCID, SAI
Adamcová, Kateřina (FGU-C) ORCID, RID
Irodenko, Ilaria (FGU-C)
Flachs, Pavel (FGU-C) RID
Jedličková, I. (CZ)
Haasová, Eliška (FGU-C)
Rossmeisl, Martin (FGU-C) RID, ORCID
Kopecký, Jan (FGU-C) RID, ORCID
Janovská, Petra (FGU-C) RID, ORCIDArticle number dmm049223 Source Title Disease Models & Mechanisms. - : Company of Biologists - ISSN 1754-8403
Roč. 15, č. 4 (2022)Number of pages 11 s. Language eng - English Country GB - United Kingdom Keywords lipid metabolism ; OPA1 ; mice ; adrenergic control OECD category Endocrinology and metabolism (including diabetes, hormones) R&D Projects LM2018129 GA MŠMT - Ministry of Education, Youth and Sports (MEYS) EF16_013/0001775 GA MŠMT - Ministry of Education, Youth and Sports (MEYS) GA18-04483S GA ČR - Czech Science Foundation (CSF) Method of publishing Open access Institutional support FGU-C - RVO:67985823 UT WOS 000796546700007 EID SCOPUS 85128801831 DOI 10.1242/dmm.049223 Annotation Impaired thermogenesis observed in mice with whole-body ablation of peroxisome proliferator-activated receptor-gamma coactivator-1 beta (PGC-1 beta, officially known as PPARGC1B) may result from impaired brown fat (brown adipose tissue, BAT) function, but other mechanism(s) could be involved. Here, using adipose-specific PGC-1 beta knockout mice (PGC-1 beta-AT-KO mice) we aimed to learn whether specific PGC-1 beta ablation in adipocytes is sufficient to drive cold sensitivity. Indeed, we found that warm-adapted (30 degrees C) mutant mice were relatively sensitive to acute cold exposure (6 degrees C). When these mice were subjected to cold exposure for 7 days (7-day-CE), adrenergic stimulation of their metabolism was impaired, despite similar levels of thermogenic uncoupling protein 1 in BAT in PGC-1 beta-AT-KO and wild-type mice. Gene expression in BAT of mutant mice suggested a compensatory increase in lipid metabolism to counteract the thermogenic defect. Interestingly, a reduced number of contacts between mitochondria and lipid droplets associated with low levels of L-form of optic atrophy 1 was found in BAT of PGC-1 beta-AT-KO mice. These genotypic differences were observed in warm-adapted mutant mice, but they were partially masked by 7-day-CE. Collectively, our results suggest a role for PGC-1 beta in controlling BAT lipid metabolism and thermogenesis. Workplace Institute of Physiology Contact Lucie Trajhanová, lucie.trajhanova@fgu.cas.cz, Tel.: 241 062 400 Year of Publishing 2023 Electronic address https://doi.org/10.1242/dmm.049223
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