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Biologically active, high levels of interleukin-22 inhibit hepatic gluconeogenesis but do not affect obesity and its metabolic consequences

Overview of attention for article published in Cell & Bioscience, May 2015
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Title
Biologically active, high levels of interleukin-22 inhibit hepatic gluconeogenesis but do not affect obesity and its metabolic consequences
Published in
Cell & Bioscience, May 2015
DOI 10.1186/s13578-015-0015-0
Pubmed ID
Authors

Ogyi Park, Sung Hwan Ki, Mingjiang Xu, Hua Wang, Dechun Feng, Joseph Tam, Douglas Osei-Hyiaman, George Kunos, Bin Gao

Abstract

Interleukin-22 (IL-22), a cytokine with important functions in anti-microbial defense and tissue repair, has been recently suggested to have beneficial effects in obesity and metabolic syndrome in some but not in other studies. Here, we re-examined the effects of IL-22 on obesity, insulin resistance, and hepatic glucose metabolism. Genetic deletion of IL-22 did not affect high-fat-diet (HFD)-induced obesity and insulin resistance. IL-22 transgenic mice with relatively high levels of circulating IL-22 (~600 pg/ml) were completely resistant to Concanavalin A-induced liver injury but developed the same degree of high fat diet (HFD)-induced obesity, insulin resistance, and fatty liver as the wild-type littermate controls. Similarly, chronic treatment with recombinant mouse IL-22 (rmIL-22) protein did not affect HFD-induced obesity and the associated metabolic syndrome. In vivo treatment with a single dose of rmIL-22 downregulated the hepatic expression of gluconeogenic genes and subsequently inhibited hepatic gluconeogenesis and reduced blood glucose levels both in HFD-fed and streptozotocin (STZ)-treated mice without affecting insulin production. In vitro exposure of mouse primary hepatocytes to IL-22 suppressed glucose production and the expression of gluconeogenic genes. These inhibitory effects were partially reversed by blocking STAT3 or the AMPK signaling pathway. Biologically active, high levels of IL-22 do not affect obesity and the associated metabolic syndrome. Acute treatment with IL-22 inhibits hepatic gluconeogenesis, which is mediated via the activation of STAT3 and AMPK in hepatocytes.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 258 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 258 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 8 3%
Researcher 8 3%
Student > Master 6 2%
Student > Postgraduate 2 <1%
Professor 2 <1%
Other 3 1%
Unknown 229 89%
Readers by discipline Count As %
Medicine and Dentistry 9 3%
Agricultural and Biological Sciences 7 3%
Immunology and Microbiology 6 2%
Biochemistry, Genetics and Molecular Biology 2 <1%
Pharmacology, Toxicology and Pharmaceutical Science 1 <1%
Other 2 <1%
Unknown 231 90%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 13 June 2015.
All research outputs
#4,348,280
of 5,223,626 outputs
Outputs from Cell & Bioscience
#127
of 149 outputs
Outputs of similar age
#145,039
of 178,145 outputs
Outputs of similar age from Cell & Bioscience
#8
of 8 outputs
Altmetric has tracked 5,223,626 research outputs across all sources so far. This one is in the 1st percentile – i.e., 1% of other outputs scored the same or lower than it.
So far Altmetric has tracked 149 research outputs from this source. They receive a mean Attention Score of 2.0. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
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