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- Andrade 2021 Biochim Biophys Acta Mol Cell Biol Lipids + (The nutrient sensors peroxisome proliferat ā¦ The nutrient sensors peroxisome proliferator-activated receptor Ī³ (PPARĪ³) and mechanistic target of rapamycin complex 1 (mTORC1) closely interact in the regulation of adipocyte lipid storage. The precise mechanisms underlying this interaction and whether this extends to other metabolic processes and the endocrine function of adipocytes are still unknown. We investigated herein the involvement of mTORC1 as a mediator of the actions of the PPARĪ³ ligand rosiglitazone in subcutaneous inguinal white adipose tissue (iWAT) mass, endocrine function, lipidome, transcriptome and branched-chain amino acid (BCAA) metabolism. Mice bearing regulatory associated protein of mTOR (Raptor) deletion and therefore mTORC1 deficiency exclusively in adipocytes and littermate controls were fed a high-fat diet supplemented or not with the PPARĪ³ agonist rosiglitazone (30 mg/kg/day) for 8 weeks and evaluated for iWAT mass, lipidome, transcriptome (Rnaseq), respiration and BCAA metabolism. Adipocyte mTORC1 deficiency not only impaired iWAT adiponectin transcription, synthesis and secretion, PEPCK mRNA levels, triacylglycerol synthesis and BCAA oxidation and mRNA levels of related proteins but also completely blocked the upregulation in these processes induced by pharmacological PPARĪ³ activation with rosiglitazone. Mechanistically, adipocyte mTORC1 deficiency impairs PPARĪ³ transcriptional activity by reducing PPARĪ³ protein content, as well as by downregulating C/EBPĪ±, a co-partner and facilitator of PPARĪ³. In conclusion, mTORC1 and PPARĪ³ are essential partners involved in the regulation of subcutaneous adipose tissue adiponectin production and secretion and BCAA oxidative metabolism.d secretion and BCAA oxidative metabolism.)
