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. 2023 Jun 28;46(11):2213–2236. doi: 10.1007/s40618-023-02125-0

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — Signalling pathways activated by drugs potentially affecting BAT activity and function: AMP-activated protein kinase (AMPK), adrenoceptor beta 3 (β3-AR), branched-chain amino acids (BCAA), branched-chain keto acids (BCKA), farnesoid X receptor (FXR), gastric inhibitory polypeptide receptor (GIPR), glucagon-like peptide 1 receptor (GLP-1R), Glucagon G-coupled receptor (GCGR), sirtuin-1 (SIRT1), peripheral nervous system (PNS), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α), phosphatidylinositol-3 kinase (PI3K), PR domain-containing protein 16 (PRDM16), protein kinase A (PKA), protein kinase B (AKT), p38α mitogen-activated protein kinase (p38 MAPK), ginsenoside Rb1 (Rb1), sympathetic nervous system (SNP), exchange protein directly activated by cAMP (EPAC), EPAC specific inhibitor (ESI-09), CCAAT enhancer-binding protein α (CEBPα), tricarboxylic acid (TCA) cycle, tumour necrosis factor receptor (TNFR), tumour necrosis factor α (TNF-α), thyroid receptor (TR)