磷酸化
碎片(计算)
线粒体
化学
细胞生物学
感知
氧化磷酸化
生物
生物化学
神经科学
生态学
作者
Sinika Henschke,Hendrik Nolte,Judith Magoley,Tatjana Kleele,Claus Brandt,A. Christine Hausen,Claudia M. Wunderlich,Corinna A. Bauder,Philipp Aschauer,Suliana Manley,Thomas Langer,F. Thomas Wunderlich,Jens C. Brüning
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2024-04-26
卷期号:384 (6694): 438-446
被引量:3
标识
DOI:10.1126/science.adk1005
摘要
Liver mitochondria play a central role in metabolic adaptations to changing nutritional states, yet their dynamic regulation upon anticipated changes in nutrient availability has remained unaddressed. Here, we found that sensory food perception rapidly induced mitochondrial fragmentation in the liver through protein kinase B/AKT (AKT)–dependent phosphorylation of serine 131 of the mitochondrial fission factor (MFFS131). This response was mediated by activation of hypothalamic pro-opiomelanocortin (POMC)–expressing neurons. A nonphosphorylatable MFF S131G knock-in mutation abrogated AKT-induced mitochondrial fragmentation in vitro. In vivo, MFF S131G knock-in mice displayed altered liver mitochondrial dynamics and impaired insulin-stimulated suppression of hepatic glucose production. Thus, rapid activation of a hypothalamus–liver axis can adapt mitochondrial function to anticipated changes of nutritional state in control of hepatic glucose metabolism.
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