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Hepatic Ago2-mediated RNA silencing controls energy metabolism linked to AMPK activation and obesity-associated pathophysiology.

Abstract：

:RNA silencing inhibits mRNA translation. While mRNA translation accounts for the majority of cellular energy expenditure, it is unclear if RNA silencing regulates energy homeostasis. Here, we report that hepatic Argonaute 2 (Ago2)-mediated RNA silencing regulates both intrinsic energy production and consumption and disturbs energy metabolism in the pathogenesis of obesity. Ago2 regulates expression of specific miRNAs including miR-802, miR-103/107, and miR-148a/152, causing metabolic disruption, while simultaneously suppressing the expression of genes regulating glucose and lipid metabolism, including Hnf1β, Cav1, and Ampka1. Liver-specific Ago2-deletion enhances mitochondrial oxidation and ATP consumption associated with mRNA translation, which results in AMPK activation, and improves obesity-associated pathophysiology. Notably, hepatic Ago2-deficiency improves glucose metabolism in conditions of insulin receptor antagonist treatment, high-fat diet challenge, and hepatic AMPKα1-deletion. The regulation of energy metabolism by Ago2 provides a novel paradigm in which RNA silencing plays an integral role in determining basal metabolic activity in obesity-associated sequelae.

journal_name

Nat Commun

journal_title

Nature communications

authors

Zhang C,Seo J,Murakami K,Salem ESB,Bernhard E,Borra VJ,Choi K,Yuan CL,Chan CC,Chen X,Huang T,Weirauch MT,Divanovic S,Qi NR,Thomas HE,Mercer CA,Siomi H,Nakamura T

doi

10.1038/s41467-018-05870-6

subject

Has Abstract

pub_date

2018-09-10 00:00:00

pages

3658

issue

1

issn

2041-1723

pii

10.1038/s41467-018-05870-6

journal_volume

9

pub_type

杂志文章

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