期刊
CELL REPORTS
卷 26, 期 8, 页码 2212-+出版社
CELL PRESS
DOI: 10.1016/j.celrep.2019.01.087
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资金
- DAE-TIFR (Government of India) [12P-0122]
- Department of Biotechnology (DBT, India) [BT/PR4972/AGR/36/714/2012]
Inability to mediate fed-fast transitions in the liver is known to cause metabolic dysfunctions and diseases. Intuitively, a failure to inhibit futile translation of state-specific transcripts during fed-fast cycles would abrogate dynamic physiological transitions. Here, we have discovered hepatic fed microRNAs that target fasting-induced genes and are essential for a refed transition. Our findings highlight the role of these fed microRNAs in orchestrating system-level control over liver physiology and whole-body energetics. By targeting SIRT1, PGC1 alpha, and their down-stream genes, fed microRNAs regulate metabolic and mitochondrial pathways. MicroRNA expression, processing, and RISC loading oscillate during these cycles and possibly constitute an anticipatory mechanism. Fed-microRNA oscillations are deregulated during aging. Scavenging of hepatic fed microRNAs causes uncontrolled gluconeogenesis and failure in the catabolic-to-anabolic switching upon feeding, which are hallmarks of metabolic diseases. Besides identifying mechanisms that enable efficient physio-logical toggling, our study highlights fed microRNAs as candidate therapeutic targets.
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