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Poster Presentations
Day 1, June 22（Sun.）
Room P (Maesato East, Foyer, Ocean Wing)
- 1P-PM-38
Mitochondrial Acetyl-CoA Potentiates Beige Adipocyte Thermogenesis through BNIP3-mediated Mitophagy
(1CBDD,TMU, 2PhD Program for CBDD,TMU, 3Master Program in Clinical Genomics and Proteomics, TMU, 4Medical Sciences, NDMC, 5Department of Research and Development, NDMC)
oYii-Jwu Lo1,2, Tsui-Chin Huang1,2,3, Hsin-Yi Chang4,5
In previous studies, we noticed that the protein acetylation altered rapidly in response to forskolin treatment, a critical signal triggering lipolysis in adipocytes, which revealed a specific PTM crosstalk on acetyl-CoA (AcCoA) metabolism is involved in adipocyte thermogenesis. AcCoA a key substrate for lysine acetylation. We applied pharmacological inhibitors or metabolic stimulators to manipulate the subcellular level of AcCoA. Since AcCoA is membrane impermeable, it is of interest to elucidate the compartmentalized regulatory roles upon white adipocyte browning. We found that AcCoA replenishing agents decreased the lipid accumulation and lowered the pro-adipogenic marker expression. Elevation of mitochondrial AcCoA in mature beige adipocytes triggered the mRNA and protein expression in the UCP1 to determine thermogenesis upregulation. Next, we performed a mass spectrometry-based quantitative proteomics analysis and found that reduction of the protein level of Bnip3 appeared both while increasing mitochondrial AcCoA and β3-adrenergic agonist stimulation. We suggested that diminished Bnip3 attenuated mitophagy to prolong the half-life of mitochondria to support thermogenic needs. Elevation of mitochondrial AcCoA increased mitochondria biomass and reduced colocalization of LC3 and mitochondria. The mitochondrial AcCoA prevented mitophay was restored by Bnip3 overexpression, suggesting that the compartmentalization effect of AcCoA is pivotal in regulating functionality in beige adipocytes.