ADRA1A–Gαq signalling potentiates adipocyte thermogenesis through CKB and TNAP

Noradrenaline (NA) regulates cold-stimulated adipocyte thermogenesis 1 . Aside from cAMP signalling downstream of β-adrenergic receptor activation, how NA promotes thermogenic output is still not fully understood. Here, we show that coordinated α 1 -adrenergic receptor (AR) and β 3 -AR signalling in...

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Published inNature metabolism Vol. 4; no. 11; pp. 1459 - 1473
Main Authors Rahbani, Janane F., Scholtes, Charlotte, Lagarde, Damien M., Hussain, Mohammed F., Roesler, Anna, Dykstra, Christien B., Bunk, Jakub, Samborska, Bozena, O’Brien, Shannon L., Tripp, Emma, Pacis, Alain, Angueira, Anthony R., Johansen, Olivia S., Cinkornpumin, Jessica, Hossain, Ishtiaque, Lynes, Matthew D., Zhang, Yang, White, Andrew P., Pastor, William A., Chondronikola, Maria, Sidossis, Labros, Klein, Samuel, Kralli, Anastasia, Cypess, Aaron M., Pedersen, Steen B., Jessen, Niels, Tseng, Yu-Hua, Gerhart-Hines, Zachary, Seale, Patrick, Calebiro, Davide, Giguère, Vincent, Kazak, Lawrence
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.11.2022
Subjects
45/77
59/57
631/443/319/2723
631/45
631/80/304
64/110
64/60
82/80
Adipocytes - metabolism
Biomedical and Life Sciences
Creatine - metabolism
Creatine Kinase - metabolism
Energy Metabolism - genetics
Letter
Life Sciences
Thermogenesis - genetics
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Abstract Noradrenaline (NA) regulates cold-stimulated adipocyte thermogenesis 1 . Aside from cAMP signalling downstream of β-adrenergic receptor activation, how NA promotes thermogenic output is still not fully understood. Here, we show that coordinated α 1 -adrenergic receptor (AR) and β 3 -AR signalling induces the expression of thermogenic genes of the futile creatine cycle 2 , 3 , and that early B cell factors, oestrogen-related receptors and PGC1α are required for this response in vivo. NA triggers physical and functional coupling between the α 1 -AR subtype (ADRA1A) and Gα q to promote adipocyte thermogenesis in a manner that is dependent on the effector proteins of the futile creatine cycle, creatine kinase B and tissue-non-specific alkaline phosphatase. Combined Gα q and Gα s signalling selectively in adipocytes promotes a continual rise in whole-body energy expenditure, and creatine kinase B is required for this effect. Thus, the ADRA1A–Gα q –futile creatine cycle axis is a key regulator of facultative and adaptive thermogenesis. Rahbani et al. show that the α 1 -adrenergic receptor potentiates thermogenesis in thermogenic adipocytes, acting via Gα q signalling, creatine kinase B and tissue-non-specific alkaline phosphatase.
AbstractList Noradrenaline (NA) regulates cold-stimulated adipocyte thermogenesis 1 . Aside from cAMP signalling downstream of β-adrenergic receptor activation, how NA promotes thermogenic output is still not fully understood. Here, we show that coordinated α 1 -adrenergic receptor (AR) and β 3 -AR signalling induces the expression of thermogenic genes of the futile creatine cycle 2 , 3 , and that early B cell factors, oestrogen-related receptors and PGC1α are required for this response in vivo. NA triggers physical and functional coupling between the α 1 -AR subtype (ADRA1A) and Gα q to promote adipocyte thermogenesis in a manner that is dependent on the effector proteins of the futile creatine cycle, creatine kinase B and tissue-non-specific alkaline phosphatase. Combined Gα q and Gα s signalling selectively in adipocytes promotes a continual rise in whole-body energy expenditure, and creatine kinase B is required for this effect. Thus, the ADRA1A–Gα q –futile creatine cycle axis is a key regulator of facultative and adaptive thermogenesis. Rahbani et al. show that the α 1 -adrenergic receptor potentiates thermogenesis in thermogenic adipocytes, acting via Gα q signalling, creatine kinase B and tissue-non-specific alkaline phosphatase.
Noradrenaline (NA) regulates cold-stimulated adipocyte thermogenesis . Aside from cAMP signalling downstream of β-adrenergic receptor activation, how NA promotes thermogenic output is still not fully understood. Here, we show that coordinated α -adrenergic receptor (AR) and β -AR signalling induces the expression of thermogenic genes of the futile creatine cycle , and that early B cell factors, oestrogen-related receptors and PGC1α are required for this response in vivo. NA triggers physical and functional coupling between the α -AR subtype (ADRA1A) and Gα to promote adipocyte thermogenesis in a manner that is dependent on the effector proteins of the futile creatine cycle, creatine kinase B and tissue-non-specific alkaline phosphatase. Combined Gα and Gα signalling selectively in adipocytes promotes a continual rise in whole-body energy expenditure, and creatine kinase B is required for this effect. Thus, the ADRA1A-Gα -futile creatine cycle axis is a key regulator of facultative and adaptive thermogenesis.
Author Samborska, Bozena
O’Brien, Shannon L.
Jessen, Niels
Angueira, Anthony R.
Scholtes, Charlotte
Roesler, Anna
Johansen, Olivia S.
White, Andrew P.
Cinkornpumin, Jessica
Pedersen, Steen B.
Seale, Patrick
Calebiro, Davide
Pastor, William A.
Gerhart-Hines, Zachary
Hossain, Ishtiaque
Sidossis, Labros
Tripp, Emma
Lagarde, Damien M.
Cypess, Aaron M.
Kralli, Anastasia
Bunk, Jakub
Lynes, Matthew D.
Klein, Samuel
Hussain, Mohammed F.
Tseng, Yu-Hua
Giguère, Vincent
Kazak, Lawrence
Zhang, Yang
Rahbani, Janane F.
Dykstra, Christien B.
Pacis, Alain
Chondronikola, Maria
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Snippet Noradrenaline (NA) regulates cold-stimulated adipocyte thermogenesis 1 . Aside from cAMP signalling downstream of β-adrenergic receptor activation, how NA...
Noradrenaline (NA) regulates cold-stimulated adipocyte thermogenesis . Aside from cAMP signalling downstream of β-adrenergic receptor activation, how NA...
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Adipocytes - metabolism
Biomedical and Life Sciences
Creatine - metabolism
Creatine Kinase - metabolism
Energy Metabolism - genetics
Letter
Life Sciences
Thermogenesis - genetics
Title ADRA1A–Gαq signalling potentiates adipocyte thermogenesis through CKB and TNAP
URI https://link.springer.com/article/10.1038/s42255-022-00667-w
https://www.ncbi.nlm.nih.gov/pubmed/36344764
Volume 4
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