ADRA1A–Gαq signalling potentiates adipocyte thermogenesis through CKB and TNAP

• DOI: 10.1038/s42255-022-00667-w
• Publication Date: 2022-11-07T17:03:57Z
• Authors: Janane F. Rahbani; Charlotte Scholtes; Damien M. Lagarde; Mohammed F. Hussain; Anna Roesler; Christien B. Dykstra; Jakub Bunk; Bozena Samborska; Shannon L. O’Brien; Emma Tripp; Alain Pacis; Anthony R. Angueira; Olivia S. Johansen; Jessica Cinkornpumin; Ishtiaque Hossain; Matthew D. Lynes; Yang Zhang; Andrew P. White; William A. Pastor; Maria Chondronikola; Labros Sidossis; Samuel Klein; Anastasia Kralli; Aaron M. Cypess; Steen B. Pedersen; Niels Jessen; Yu-Hua Tseng; Zachary Gerhart-H...; Patrick Seale; Davide Calebiro; Vincent Giguère; Lawrence Kazak
• Keywords: Thermogenin; Creatine; Creatine kinase

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 -adrenergic (AR) and β 3 -AR induces the expression genes futile creatine cycle 2,3 , early B cell factors, oestrogen-related receptors PGC1α are required for this response in vivo. triggers physical functional coupling between subtype (ADRA1A) Gα q to promote a manner dependent on effector proteins cycle, kinase tissue-non-specific alkaline phosphatase. Combined s selectively adipocytes continual rise whole-body energy expenditure, effect. Thus, ADRA1A–Gα –futile axis key regulator facultative adaptive thermogenesis.