Difference between revisions of "Porras 2017 Stem Cells"
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Latest revision as of 10:43, 24 June 2019
Porras DP, Abbaszadeh M, Bhattacharya D, D'Souza NC, Edjiu NR, Perry CG, Scimรจ A (2017) p107 determines a metabolic checkpoint required for adipocyte lineage fates. Stem Cells 35:1378-91. |
Porras DP, Abbaszadeh M, Bhattacharya D, D'Souza NC, Edjiu NR, Perry CG, Scime A (2017) Stem Cells
Abstract: We show that the transcriptional corepressor p107 orchestrates a metabolic checkpoint that determines adipocyte lineage fates for non-committed progenitors. p107 accomplishes this when stem cell commitment would normally occur in growth arrested cells. p107-deficient embryonic progenitors are characterized by a metabolic state resembling aerobic glycolysis that is necessary for their pro-thermogenic fate. Indeed, during growth arrest they have a reduced capacity for NADH partitioning between the cytoplasm and mitochondria. Intriguingly, this occurred despite an increase in the capacity for mitochondrial oxidation of non-glucose substrates. The significance of metabolic reprogramming is underscored by the disruption of glycolytic capacities in p107-depleted progenitors that reverted their fates from pro-thermogenic to white adipocytes. Moreover, the manipulation of glycolytic capacity on nonspecified embryonic and adult progenitors forced their beige fat commitment. These innovative findings introduce a new approach to increase pro-thermogenic adipocytes based on simply promoting aerobic glycolysis to manipulate nonspecified progenitor fate decisions. Stem Cells 2017.
ยฉ 2017 AlphaMed Press. โข Keywords: Aerobic glycolysis, Beige/brown adipocytes, Metabolism, Progenitor fate, p107 โข Bioblast editor: Kandolf G โข O2k-Network Lab: CA Toronto Perry CG
Labels: MiParea: Respiration, Genetic knockout;overexpression
Organism: Mouse
Tissue;cell: Fat, Fibroblast
Preparation: Intact cells
Coupling state: LEAK, OXPHOS
Pathway: F, N
HRR: Oxygraph-2k