| First Author | Schmid S | Year | 2022 |
| Journal | Mol Metab | Volume | 66 |
| Pages | 101643 | PubMed ID | 36400401 |
| Mgi Jnum | J:351045 | Mgi Id | MGI:7410195 |
| Doi | 10.1016/j.molmet.2022.101643 | Citation | Schmid S, et al. (2022) PGC-1beta modulates catabolism and fiber atrophy in the fasting-response of specific skeletal muscle beds. Mol Metab 66:101643 |
| abstractText | OBJECTIVE: Skeletal muscle is a pivotal organ for the coordination of systemic metabolism, constituting one of the largest storage site for glucose, lipids and amino acids. Tight temporal orchestration of protein breakdown in times of fasting has to be balanced with preservation of muscle mass and function. However, the molecular mechanisms that control the fasting response in muscle are poorly understood. METHODS: We now have identified a role for the peroxisome proliferator-activated receptor gamma coactivator 1beta (PGC-1beta) in the regulation of catabolic pathways in this context in muscle-specific loss-of-function mouse models. RESULTS: Muscle-specific knockouts for PGC-1beta experience mitigated muscle atrophy in fasting, linked to reduced expression of myostatin, atrogenes, activation of AMP-dependent protein kinase (AMPK) and other energy deprivation signaling pathways. At least in part, the muscle fasting response is modulated by a negative effect of PGC-1beta on the nuclear factor of activated T-cells 1 (NFATC1). CONCLUSIONS: Collectively, these data highlight the complex regulation of muscle metabolism and reveal a new role for muscle PGC-1beta in the control of proteostasis in fasting. |
