1
40
1
-
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/10.1002/hep.29305" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hep.29305</a>
Pages
1854–1865
Issue
6
Volume
66
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
Small heterodimer partner deletion prevents hepatic steatosis and when combined with farnesoid X receptor loss protects against type 2 diabetes in mice.
Publisher
An entity responsible for making the resource available
Hepatology (Baltimore, Md.)
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-12
Subject
The topic of the resource
Animals; Body Weight/genetics; Cytoplasmic and Nuclear/*physiology; Diabetes Mellitus; Fatty Liver/*genetics; Knockout; Lipid Metabolism/genetics; Mice; Receptors; Type 2/*genetics
Creator
An entity primarily responsible for making the resource
Akinrotimi Oludemilade; Riessen Ryan; VanDuyne Philip; Park Jung Eun; Lee Yoon-Kwang; Wong Lee-Jun; Zavacki Ann M; Schoonjans Kristina; Anakk Sayeepriyadarshini
Description
An account of the resource
Nuclear receptors farnesoid X receptor (FXR) and small heterodimer partner (SHP) are important regulators of bile acid, lipid, and glucose homeostasis. Here, we show that global Fxr (-/-) Shp(-/-) double knockout (DKO) mice are refractory to weight gain, glucose intolerance, and hepatic steatosis when challenged with high-fat diet. DKO mice display an inherently increased capacity to burn fat and suppress de novo hepatic lipid synthesis. Moreover, DKO mice were also very active and that correlated well with the observed increase in phosphoenolpyruvate carboxykinase expression, type IA fibers, and mitochondrial function in skeletal muscle. Mechanistically, we demonstrate that liver-specific Shp deletion protects against fatty liver development by suppressing expression of peroxisome proliferator-activated receptor gamma 2 and lipid-droplet protein fat-specific protein 27 beta. CONCLUSION: These data suggest that Fxr and Shp inactivation may be beneficial to combat diet-induced obesity and uncover that hepatic SHP is necessary to promote fatty liver disease. (Hepatology 2017;66:1854-1865).
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/hep.29305" target="_blank" rel="noreferrer noopener">10.1002/hep.29305</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).
2017
Akinrotimi Oludemilade
Anakk Sayeepriyadarshini
Animals
Body Weight/genetics
Cytoplasmic and Nuclear/*physiology
Department of Integrative Medical Sciences
Diabetes Mellitus
Fatty Liver/*genetics
Hepatology (Baltimore, Md.)
Knockout
Lee Yoon-Kwang
Lipid Metabolism/genetics
Mice
NEOMED College of Medicine
Park Jung Eun
Receptors
Riessen Ryan
Schoonjans Kristina
Type 2/*genetics
VanDuyne Philip
Wong Lee-Jun
Zavacki Ann M