1
40
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Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1074/jbc.M116.737015" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/jbc.M116.737015</a>
Pages
22482–22495
Issue
43
Volume
291
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
MitoNEET Deficiency Alleviates Experimental Alcoholic Steatohepatitis in Mice by Stimulating Endocrine Adiponectin-Fgf15 Axis.
Publisher
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The Journal of biological chemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-10
Subject
The topic of the resource
*adiponectin; *alcohol; *intestine; *iron; *liver injury; *Signal Transduction; Adiponectin/genetics/*metabolism; Alcoholic/genetics/*metabolism/pathology; Animals; Fatty Liver; Fibroblast Growth Factors/genetics/*metabolism; Humans; Iron-Binding Proteins/metabolism; Knockout; Male; Membrane Proteins/*deficiency/metabolism; Mice; NF-kappa B/genetics/metabolism; Sirtuin 1/genetics/metabolism
Creator
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Hu Xudong; Jogasuria Alvin; Wang Jiayou; Kim Chunki; Han Yoonhee; Shen Hong; Wu Jiashin; You Min
Description
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MitoNEET (mNT) (CDGSH iron-sulfur domain-containing protein 1 or CISD1) is an outer mitochondrial membrane protein that donates 2Fe-2S clusters to apo-acceptor proteins. In the present study, using a global mNT knock-out (mNTKO) mouse model, we investigated the in vivo functional role of mNT in the development of alcoholic steatohepatitis. Experimental alcoholic steatohepatitis was achieved by pair feeding wild-type (WT) and mNTKO mice with Lieber-DeCarli ethanol-containing diets for 4 weeks. Strikingly, chronically ethanol-fed mNTKO mice were completely resistant to ethanol-induced steatohepatitis as revealed by dramatically reduced hepatic triglycerides, decreased hepatic cholesterol level, diminished liver inflammatory response, and normalized serum ALT levels. Mechanistic studies demonstrated that ethanol administration to mNTKO mice induced two pivotal endocrine hormones, namely, adipose-derived adiponectin and gut-derived fibroblast growth factor 15 (Fgf15). The elevation in circulating levels of adiponectin and Fgf15 led to normalized hepatic and serum levels of bile acids, limited hepatic accumulation of toxic bile, attenuated inflammation, and amelioration of liver injury in the ethanol-fed mNTKO mice. Other potential mechanisms such as reduced oxidative stress, activated Sirt1 signaling, and diminished NF-kappaB activity also contribute to hepatic improvement in the ethanol-fed mNTKO mice. In conclusion, the present study identified adiponectin and Fgf15 as pivotal adipose-gut-liver metabolic coordinators in mediating the protective action of mNT deficiency against development of alcoholic steatohepatitis in mice. Our findings may help to establish mNT as a novel therapeutic target and pharmacological inhibition of mNT may be beneficial for the prevention and treatment of human alcoholic steatohepatitis.
Identifier
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<a href="http://doi.org/10.1074/jbc.M116.737015" target="_blank" rel="noreferrer noopener">10.1074/jbc.M116.737015</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*adiponectin
*alcohol
*intestine
*iron
*liver injury
*Signal Transduction
2016
Adiponectin/genetics/*metabolism
Alcoholic/genetics/*metabolism/pathology
Animals
Department of Pharmaceutical Sciences
Fatty Liver
Fibroblast Growth Factors/genetics/*metabolism
Han Yoonhee
Hu Xudong
Humans
Iron-Binding Proteins/metabolism
Jogasuria Alvin
Kim Chunki
Knockout
Male
Membrane Proteins/*deficiency/metabolism
Mice
NEOMED College of Pharmacy
NF-kappa B/genetics/metabolism
Shen Hong
Sirtuin 1/genetics/metabolism
The Journal of biological chemistry
Wang Jiayou
Wu Jiashin
You Min
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1038/srep34117" target="_blank" rel="noreferrer noopener">http://doi.org/10.1038/srep34117</a>
Pages
34117–34117
Volume
6
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Myeloid Cell-Specific Lipin-1 Deficiency Stimulates Endocrine Adiponectin-FGF15 Axis and Ameliorates Ethanol-Induced Liver Injury in Mice.
Publisher
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Scientific reports
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-09
Subject
The topic of the resource
Adiponectin/*blood; Alcoholic/blood/*genetics/metabolism; Animal; Animals; Disease Models; Fatty Liver; Fibroblast Growth Factors/*blood; Gene Knockout Techniques; Lipid Metabolism; Male; Mice; Myeloid Cells/*metabolism; NF-kappa B/metabolism; Nuclear Proteins/*deficiency; Organ Specificity; Phosphatidate Phosphatase/*deficiency; Signal Transduction
Creator
An entity primarily responsible for making the resource
Wang Jiayou; Kim Chunki; Jogasuria Alvin; Han Yoonhee; Hu Xudong; Wu Jiashin; Shen Hong; Chrast Roman; Finck Brian N; You Min
Description
An account of the resource
Lipin-1 is a phosphatidate phosphohydrolase (PAP) required for the generation of diacylglycerol during glycerolipid synthesis, and exhibits dual functions in the regulation of lipid metabolism. Lipin-1 has been implicated in the pathogenesis of alcoholic liver disease (ALD). In the present study, we assessed lipin-1 function in myeloid cells in ALD using a myeloid cell-specific lipin-1 knockout (mLipin-1KO) mouse model. Utilizing the Gao-binge ethanol feeding protocol, matched mLipin-1KO mice and littermate loxP control (WT) mice were pair-fed with either an ethanol-containing diet or an ethanol-free diet (control). Surprisingly, deletion of lipin-1 in myeloid cells dramatically attenuated liver inflammatory responses and ameliorated liver injury that would normally occur following the ethanol feeding protocol, but slightly exacerbated the ethanol-induced steatosis in mice. Mechanistically, myeloid cell-specific lipin-1 deficiency concomitantly increased the fat-derived adiponectin and ileum-derived fibroblast growth factor (FGF) 15. In concordance with concerted elevation of circulating adiponectin and FGF15, myeloid cell-specific lipin-1 deficiency diminished hepatic nuclear factor kappa B (NF-kappaB) activity, limited liver inflammatory responses, normalized serum levels of bile acids, and protected mice from liver damage after ethanol challenge. Our novel data demonstrate that myeloid cell-specific deletion of lipin-1 ameliorated inflammation and alcoholic hepatitis in mice via activation of endocrine adiponectin-FGF15 signaling.
Identifier
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<a href="http://doi.org/10.1038/srep34117" target="_blank" rel="noreferrer noopener">10.1038/srep34117</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2016
Adiponectin/*blood
Alcoholic/blood/*genetics/metabolism
Animal
Animals
Chrast Roman
Department of Pharmaceutical Sciences
Disease Models
Fatty Liver
Fibroblast Growth Factors/*blood
Finck Brian N
Gene Knockout Techniques
Han Yoonhee
Hu Xudong
Jogasuria Alvin
Kim Chunki
Lipid Metabolism
Male
Mice
Myeloid Cells/*metabolism
NEOMED College of Pharmacy
NF-kappa B/metabolism
Nuclear Proteins/*deficiency
Organ Specificity
Phosphatidate Phosphatase/*deficiency
Scientific reports
Shen Hong
Signal Transduction
Wang Jiayou
Wu Jiashin
You Min