Abstract:
: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, PGC1α, and their downstream 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 physiological toggling, our study highlights fed microRNAs as candidate therapeutic targets.
journal_name
Cell Repjournal_title
Cell reportsauthors
Maniyadath B,Chattopadhyay T,Verma S,Kumari S,Kulkarni P,Banerjee K,Lazarus A,Kokane SS,Shetty T,Anamika K,Kolthur-Seetharam Udoi
10.1016/j.celrep.2019.01.087subject
Has Abstractpub_date
2019-02-19 00:00:00pages
2212-2226.e7issue
8issn
2211-1247pii
S2211-1247(19)30123-8journal_volume
26pub_type
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