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001-es BibID:	BIBFORM079713
035-os BibID:	(WoS)000486972404107
Első szerző:	Arianti, Rini (biokémikus)
Cím:	Identification of unique molecular signature ofbrowning in human primary adipocytes fromdeep and subcutaneous neck fat / Arianti Rini, Shaw Abhirup, Vámos Attila, Bartáné Tóth Beáta, Győry Ferenc, Póliska Szilárd, Kristóf Endre Károly, Fésüs László
Dátum:	2019
ISSN:	2211-5463
Megjegyzések:	There are two types of thermogenic adipocytes, classical brown and beige (BAT) which are UCP1-positive dissipating energy as heat. BAT markers have been well studied in rodents but detailed molecular studies are still lacking in humans where BAT is interspersed at several sites and may serve as a target of anti-obesity therapies. Our study aims to identify the unique signature of browning in human primary adipocytes from the different anatomical location by analyzing global gene expression patterns. Preadipocytes were obtained from subcutaneous (SC) and deep neck (DN) and differentiated to white and brown adipocytes. We analyzed differential gene expressions by total RNA sequencing, molecular pathways by KEGG Mapper, genetic constraint by ExAC and verified several genes of interest associated with adipocytes browning. We identified 37 genes which are closely clustered to UCP1. Out of those 13 genes have been already described to play a role in thermogenesis (CIDEA, CKMT1A/B), while the roles of the others are still unclear (ANO5, FAM151a). Several pathways were represented, such as retinoic acid biosynthesis which was upregulated (CPT1, CYP261B), while extracellular matrix organization pathways were among the downregulated ones (COL, ITGF). Mitochondrial creatine kinases, CKMT1a/b, are reported to play role in UCP1-independent thermogenesis; UCP1 and CKMT1a were expressed higher in DN, as compared to SC adipocytes and this was verified by RT-qPCR. Several transporters were expressed higher in DN, such as transporter of amino acids (SLC7A10), glutamate (SLC25A18) and pyruvate (SLC16A7). Our data proves that progenitors from DN fat can be differentiated to browning adipocytes at a greater extent than SC ones. We have started to investigate revealed molecular elements not linked yet to browning by deleting, inhibiting or overexpressing them.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok poszter folyóiratcikk
Megjelenés:	FEBS Open Bio. - 9 : S1 (2019), p. 289-290. -
További szerzők:	Shaw, Abhirup (1992-) Vámos Attila (1991-) (gyógyszer-biotechnológus) Bartáné Tóth Beáta (1970-) (molekuláris biológus) Győry Ferenc (1969-) (kardiológus) Póliska Szilárd (1978-) (biológus) Kristóf Endre (1987-) (általános orvos) Fésüs László (1947-) (orvos biokémikus)
Pályázati támogatás:	GINOP-2.3.2-15-2016-00006 GINOP
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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001-es BibID:	BIBFORM131954
Első szerző:	Kristóf Endre (általános orvos)
Cím:	LAT1-mediated amino acid transport supports thermogenesis of human brown adipocytes / Kristóf Endre, Arianti Rini, Enyedi Nóra, Vinnai Boglárka Ágnes, Alrifai Rahaf, Karadsheh Gyath, Póliska Szilárd, Csősz Éva, Fésüs László
Dátum:	2025
ISSN:	2211-5463
Megjegyzések:	Thermogenically active adipocytes utilize high amounts of metabolic substrates, such as glucose, fatty acids, and amino acids (AAs), which provide sufficient energy for heat generation via UCP1-mediated proton leak in the inner membrane of mitochondria. However, the mechanism of how brown adipocytes can uptake distinct types of AAs remains unclear. Our preliminary data showed that the consumption of branched-chain and other AAs as well as the expression of L-amino acid transporter (LAT) 1 (encoded by SLC7A5) and its heterodimer protein 4F2hc (encoded by SLC3A2) was upregulated during adrenergic stimulation [Previously published in: Arianti R et al. (2024) Sci Rep 14, 28272]. Therefore, we aimed to investigate the role of LAT1 in the thermogenesis of human brown adipocytes. Stromal vascular fraction was isolated from cervical adipose tissue biopsies and differentiated into brown adipocytes for 14?days. The expression of LAT1 was silenced by siRNA-mediated interference and then dibutyryl-cAMP was administered to mimic in vivo thermogenesis. We found that LAT1 deficiency in adrenergic stimulated matured adipocytes inhibited AA influx and led to reduced proton leak respiration which is associated with UCP1-dependent heat generation. Dibutyryl-cAMP-stimulated elevation of Etomoxir-resistant respiration, which correlates with glucose and amino acid utilization, was also abrogated in LAT1 knock-down adipocytes. LAT1 silencing also resulted in decreased expression of thermogenic markers, such as UCP1 and PPARGC1a during adrenergic stimulation, as well as genes which were involved in various biological pathways, such as the TGF-?, MAPK, or PI3K-Akt signaling. Our data suggest that LAT1 regulates human brown adipocyte thermogenesis by mediating the uptake of several AAs to support the high metabolic activity and by controlling the transcriptional program of thermogenesis-related genes.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok poszter folyóiratcikk
Megjelenés:	FEBS Open Bio. - 15 : Suppl. 2 (2025), p. 70-71. -
További szerzők:	Arianti, Rini (1991-) (biokémikus) Enyedi Nóra Vinnai Boglárka Ágnes (1996-) (molekuláris biológus) Alrifai, Rahaf Karadsheh, Gyath (1997-) (biokémia) Póliska Szilárd (1978-) (biológus) Csősz Éva (1977-) (biokémikus, molekuláris biológus) Fésüs László (1947-) (orvos biokémikus)
Internet cím:	Szerző által megadott URL DOI Intézményi repozitóriumban (DEA) tárolt változat
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