| First Author | Park CH | Year | 2021 |
| Journal | Front Physiol | Volume | 12 |
| Pages | 780312 | PubMed ID | 34899399 |
| Mgi Jnum | J:320258 | Mgi Id | MGI:6836384 |
| Doi | 10.3389/fphys.2021.780312 | Citation | Park CH, et al. (2021) Protein Kinase SGK2 Is Induced by the beta3 Adrenergic Receptor-cAMP-PKA-PGC-1alpha/NT-PGC-1alpha Axis but Dispensable for Brown/Beige Adipose Tissue Thermogenesis. Front Physiol 12:780312 |
| abstractText | Brown and beige adipocytes are specialized to dissipate energy as heat. Sgk2, encoding a serine/threonine kinase, has been identified as a brown and beige adipocyte-specific gene in rodents and humans; however, its function in brown/beige adipocytes remains unraveled. Here, we examined the regulation and role of Sgk2 in brown/beige adipose tissue thermogenesis. We found that transcriptional coactivators PGC-1alpha and NT-PGC-1alpha activated by the beta3 adrenergic receptor-cAMP-PKA pathway are recruited to the Sgk2 promoter, triggering Sgk2 transcription in response to cold. SGK2 elevation was closely associated with increased serine/threonine phosphorylation of proteins carrying the consensus RxRxxS/T phosphorylation site. However, despite cold-dependent activation of SGK2, mice lacking Sgk2 exhibited normal cold tolerance at 4 degrees C. In addition, Sgk2(+/+) and Sgk2(-/-) mice induced comparable increases in energy expenditure during pharmacological activation of brown and beige adipose tissue with a beta3AR agonist. In vitro loss- and gain-of-function studies further demonstrated that Sgk2 ablation or activation does not alter thermogenic gene expression and mitochondrial respiration in brown adipocytes. Collectively, our results reveal a new signaling component SGK2, although dispensable for cold-induced thermogenesis that adds an additional layer of complexity to the beta3AR signaling network in brown/beige adipose tissue. |
