Hepatic arginase 2 (Arg2) is sufficient to convey the therapeutic metabolic effects of fasting. View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2019-12

AUTHORS

Yiming Zhang, Cassandra B Higgins, Hannah M Fortune, Phillip Chen, Alicyn I Stothard, Allyson L Mayer, Benjamin M Swarts, Brian J DeBosch

ABSTRACT

Caloric restriction and intermittent fasting are emerging therapeutic strategies against obesity, insulin resistance and their complications. However, the effectors that drive this response are not completely defined. Here we identify arginase 2 (Arg2) as a fasting-induced hepatocyte factor that protects against hepatic and peripheral fat accumulation, hepatic inflammatory responses, and insulin and glucose intolerance in obese murine models. Arg2 is upregulated in fasting conditions and upon treatment with the hepatocyte glucose transporter inhibitor trehalose. Hepatocyte-specific Arg2 overexpression enhances basal thermogenesis, and protects from weight gain, insulin resistance, glucose intolerance, hepatic steatosis and hepatic inflammation in diabetic mouse models. Arg2 suppresses expression of the regulator of G-protein signalling (RGS) 16, and genetic RGS16 reconstitution reverses the effects of Arg2 overexpression. We conclude that hepatocyte Arg2 is a critical effector of the hepatic glucose fasting response and define a therapeutic target to mitigate the complications of obesity and non-alcoholic fatty liver disease. More... »

PAGES

1587

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41467-019-09642-8

DOI

http://dx.doi.org/10.1038/s41467-019-09642-8

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1113300700

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30962478


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