Detail
Článek
Článek online
FT
Medvik - BMČ
  • Je něco špatně v tomto záznamu ?

Control of Adipocyte Thermogenesis and Lipogenesis through β3-Adrenergic and Thyroid Hormone Signal Integration

A. Guilherme, B. Yenilmez, AH. Bedard, F. Henriques, D. Liu, A. Lee, L. Goldstein, M. Kelly, SM. Nicoloro, M. Chen, L. Weinstein, S. Collins, MP. Czech

. 2020 ; 31 (5) : 107598. [pub] 20200505

Jazyk angličtina Země Spojené státy americké

Typ dokumentu časopisecké články, Research Support, N.I.H., Extramural, práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/bmc21020561

Grantová podpora
R01 DK116056 NIDDK NIH HHS - United States
P30 DK058404 NIDDK NIH HHS - United States
R01 DK116625 NIDDK NIH HHS - United States
R37 DK030898 NIDDK NIH HHS - United States
R01 DK030898 NIDDK NIH HHS - United States

Here, we show that β adrenergic signaling coordinately upregulates de novo lipogenesis (DNL) and thermogenesis in subcutaneous white adipose tissue (sWAT), and both effects are blocked in mice lacking the cAMP-generating G protein-coupled receptor Gs (Adipo-GsαKO) in adipocytes. However, UCP1 expression but not DNL activation requires rapamycin-sensitive mTORC1. Furthermore, β3-adrenergic agonist CL316243 readily upregulates thermogenic but not lipogenic genes in cultured adipocytes, indicating that additional regulators must operate on DNL in sWAT in vivo. We identify one such factor as thyroid hormone T3, which is elevated locally by adrenergic signaling. T3 administration to wild-type mice enhances both thermogenesis and DNL in sWAT. Mechanistically, T3 action on UCP1 expression in sWAT depends upon cAMP and is blocked in Adipo-GsαKO mice even as elevated DNL persists. Thus, T3 enhances sWAT thermogenesis by amplifying cAMP signaling, while its control of adipocyte DNL can be mediated independently of both cAMP and rapamycin-sensitive mTORC1.

Citace poskytuje Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc21020561
003      
CZ-PrNML
005      
20210830102217.0
007      
ta
008      
210728s2020 xxu f 000 0|eng||
009      
AR
024    7_
$a 10.1016/j.celrep.2020.107598 $2 doi
035    __
$a (PubMed)32375048
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a xxu
100    1_
$a Guilherme, Adilson $u Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA. Electronic address: adilson.guilherme@umassmed.edu
245    10
$a Control of Adipocyte Thermogenesis and Lipogenesis through β3-Adrenergic and Thyroid Hormone Signal Integration / $c A. Guilherme, B. Yenilmez, AH. Bedard, F. Henriques, D. Liu, A. Lee, L. Goldstein, M. Kelly, SM. Nicoloro, M. Chen, L. Weinstein, S. Collins, MP. Czech
520    9_
$a Here, we show that β adrenergic signaling coordinately upregulates de novo lipogenesis (DNL) and thermogenesis in subcutaneous white adipose tissue (sWAT), and both effects are blocked in mice lacking the cAMP-generating G protein-coupled receptor Gs (Adipo-GsαKO) in adipocytes. However, UCP1 expression but not DNL activation requires rapamycin-sensitive mTORC1. Furthermore, β3-adrenergic agonist CL316243 readily upregulates thermogenic but not lipogenic genes in cultured adipocytes, indicating that additional regulators must operate on DNL in sWAT in vivo. We identify one such factor as thyroid hormone T3, which is elevated locally by adrenergic signaling. T3 administration to wild-type mice enhances both thermogenesis and DNL in sWAT. Mechanistically, T3 action on UCP1 expression in sWAT depends upon cAMP and is blocked in Adipo-GsαKO mice even as elevated DNL persists. Thus, T3 enhances sWAT thermogenesis by amplifying cAMP signaling, while its control of adipocyte DNL can be mediated independently of both cAMP and rapamycin-sensitive mTORC1.
650    _2
$a tukové buňky $x metabolismus $7 D017667
650    _2
$a hnědá tuková tkáň $x metabolismus $7 D002001
650    _2
$a bílá tuková tkáň $x metabolismus $7 D052436
650    _2
$a adrenergní látky $x metabolismus $7 D018663
650    _2
$a zvířata $7 D000818
650    _2
$a lipogeneze $x fyziologie $7 D050155
650    _2
$a myši transgenní $7 D008822
650    _2
$a signální transdukce $x fyziologie $7 D015398
650    _2
$a termogeneze $x genetika $7 D022722
650    _2
$a hormony štítné žlázy $x metabolismus $7 D013963
655    _2
$a časopisecké články $7 D016428
655    _2
$a Research Support, N.I.H., Extramural $7 D052061
655    _2
$a práce podpořená grantem $7 D013485
700    1_
$a Yenilmez, Batuhan $u Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA
700    1_
$a Bedard, Alexander H $u Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA
700    1_
$a Henriques, Felipe $u Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA
700    1_
$a Liu, Dianxin $u Departments of Medicine, Cardiovascular Medicine, and Molecular Physiology & Biophysics, Vanderbilt University Medical Center, Nashville, TN 37232, USA
700    1_
$a Lee, Alexandra $u Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA
700    1_
$a Goldstein, Lauren $u Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA
700    1_
$a Kelly, Mark $u Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA
700    1_
$a Nicoloro, Sarah M $u Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA
700    1_
$a Chen, Min $u Metabolic Diseases Branch, NIDDK, NIH, Bethesda, MD 20892-1752, USA
700    1_
$a Weinstein, Lee $u Metabolic Diseases Branch, NIDDK, NIH, Bethesda, MD 20892-1752, USA
700    1_
$a Collins, Sheila $u Departments of Medicine, Cardiovascular Medicine, and Molecular Physiology & Biophysics, Vanderbilt University Medical Center, Nashville, TN 37232, USA
700    1_
$a Czech, Michael P $u Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA. Electronic address: michael.czech@umassmed.edu
773    0_
$w MED00188029 $t Cell reports $x 2211-1247 $g Roč. 31, č. 5 (2020), s. 107598
856    41
$u https://pubmed.ncbi.nlm.nih.gov/32375048 $y Pubmed
910    __
$a ABA008 $b sig $c sign $y p $z 0
990    __
$a 20210728 $b ABA008
991    __
$a 20210830102217 $b ABA008
999    __
$a ok $b bmc $g 1691185 $s 1141007
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2020 $b 31 $c 5 $d 107598 $e 20200505 $i 2211-1247 $m Cell reports $n Cell Rep $x MED00188029
GRA    __
$a R01 DK116056 $p NIDDK NIH HHS $2 United States
GRA    __
$a P30 DK058404 $p NIDDK NIH HHS $2 United States
GRA    __
$a R01 DK116625 $p NIDDK NIH HHS $2 United States
GRA    __
$a R37 DK030898 $p NIDDK NIH HHS $2 United States
GRA    __
$a R01 DK030898 $p NIDDK NIH HHS $2 United States
LZP    __
$a Pubmed-20210728

Najít záznam

Citační ukazatele

Možnosti archivace