View source for Andrade 2021 Biochim Biophys Acta Mol Cell Biol Lipids

{{Publication
|title=Andrade ML, Gilio GR, Perandini LA, Peixoto AS, Moreno MF, Castro E, Oliveira TE, Vieira TS, Ortiz-Silva M, Thomazelli CA, Chaves-Filho AB, Belchior T, Chimin P, Magdalon J, Ivison R, Pant D, Tsai L, Yoshinaga MY, Miyamoto S, Festuccia WT (2021) PPARγ-induced upregulation of subcutaneous fat adiponectin secretion, glyceroneogenesis and BCAA oxidation requires mTORC1 activity. Biochim Biophys Acta Mol Cell Biol Lipids 1866:158967.
|info=[https://pubmed.ncbi.nlm.nih.gov/34004356/ PMID: 34004356 Open Access]
|authors=Andrade Maynara L, Gilio Gustavo R, Perandini Luiz A, Peixoto Albert S, Moreno Mayara F, Castro Erique, Oliveira Tiago E, Vieira Thayna S, Ortiz-Silva Milene, Thomazelli Caroline A, Chaves-Filho Adriano B, Belchior Thiago, Chimin Patricia, Magdalon Juliana, Ivison Rachael, Pant Deepti, Tsai Linus, Yoshinaga Marcos Y, Miyamoto Sayuri, Festuccia William T
|year=2021
|journal=Biochim Biophys Acta Mol Cell Biol Lipids
|abstract=The nutrient sensors peroxisome proliferator-activated receptor γ (PPARγ) 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 PPARγ 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 PPARγ 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 PPARγ activation with rosiglitazone. Mechanistically, adipocyte mTORC1 deficiency impairs PPARγ transcriptional activity by reducing PPARγ protein content, as well as by downregulating C/EBPα, a co-partner and facilitator of PPARγ. In conclusion, mTORC1 and PPARγ are essential partners involved in the regulation of subcutaneous adipose tissue adiponectin production and secretion and BCAA oxidative metabolism.
|keywords=Adiponectin secretion, BCAA oxidation, C/EBPα, Glyceroneogenesis, PPARγ, Subcutaneous adipose tissue, mTORC1
|editor=[[Reiswig R]]
|mipnetlab=BR Sao Paulo Festuccia W
}}
{{Labeling
|area=Respiration, Genetic knockout;overexpression, Pharmacology;toxicology
|organism=Mouse
|tissues=Fat
|instruments=Oxygraph-2k
|additional=2021-07
}}