Loss of Hepatic Oscillatory Fed microRNAs Abrogates Refed Transition and Causes Liver Dysfunctions.

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 Rep

journal_title

Cell reports

authors

Maniyadath B,Chattopadhyay T,Verma S,Kumari S,Kulkarni P,Banerjee K,Lazarus A,Kokane SS,Shetty T,Anamika K,Kolthur-Seetharam U

doi

10.1016/j.celrep.2019.01.087

subject

Has Abstract

pub_date

2019-02-19 00:00:00

pages

2212-2226.e7

issue

8

issn

2211-1247

pii

S2211-1247(19)30123-8

journal_volume

26

pub_type

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