1
40
7
-
Text
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<a href="http://doi.org/10.1002/hep4.1487" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hep4.1487</a>
Pages
527-539
Issue
4
Volume
4
ISSN
2471-254X 2471-254X
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<a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1002/hep4.1487" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1002/hep4.1487</a>
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Update Year & Number
June 2020 Update I
NEOMED College
NEOMED College of Medicine; NEOMED College of Graduate Studies
NEOMED Department
Department of Integrative Medical Sciences; NEOMED Postdoc Publications
Dublin Core
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Title
A name given to the resource
Hepatocyte-Specific Expression of Human Carboxylesterase 1 Attenuates Diet-Induced Steatohepatitis and Hyperlipidemia in Mice.
Publisher
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Hepatology communications
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-04
Subject
The topic of the resource
decreases blood-lipids; deficiency; dyslipidemia; hepatic steatosis; lipotoxicity; Liver; protects; receptor-alpha; reduces atherosclerosis; transgenic expression
Creator
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Xu Yanyong; Zhu Yingdong; Bawa Fathima Cassim; Hu Shuwei; Pan Xiaoli; Yin Liya; Zhang Yanqiao
Description
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Rodents have at least five carboxylesterase 1 (Ces1) genes, whereas there is only one CES1 gene in humans, raising the question as to whether human CES1 and mouse Ces1 genes share the same functions. In this study, we investigate the role of human CES1 in the development of steatohepatitis or dyslipidemia in C57BL/6 mice. Hepatocyte-specific expression of human CES1 prevented Western diet or alcohol-induced steatohepatitis and hyperlipidemia. Mechanistically, human CES1 induced lipolysis and fatty acid oxidation, leading to a reduction in hepatic triglyceride and free fatty acid levels. Human CES1 also reduced hepatic-free cholesterol levels and induced low-density lipoprotein receptor. In addition, human CES1 induced hepatic lipoprotein lipase and apolipoprotein C-II expression. Conclusion: Hepatocyte-specific overexpression of human CES1 attenuates diet-induced steatohepatitis and hyperlipidemia.
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<a href="http://doi.org/10.1002/hep4.1487" target="_blank" rel="noreferrer noopener">10.1002/hep4.1487</a>
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journalArticle
2020
Bawa Fathima Cassim
decreases blood-lipids
deficiency
Department of Integrative Medical Sciences
dyslipidemia
hepatic steatosis
Hepatology communications
Hu Shuwei
Journal Article
journalArticle
June 2020 Update I
lipotoxicity
Liver
NEOMED College of Graduate Studies
NEOMED College of Medicine
NEOMED College of Medicine Postdoc
NEOMED Postdoc Publications
Pan Xiaoli
protects
receptor-alpha
reduces atherosclerosis
transgenic expression
Xu Yanyong
Yin Liya
Zhang Yanqiao
Zhu Yingdong
-
Text
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URL Address
<a href="http://doi.org/10.1002/hep4.1341" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hep4.1341</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
763-775
Issue
6
Volume
3
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
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Title
A name given to the resource
Lipocalin‐2 Protects Against Diet‐Induced Nonalcoholic Fatty Liver Disease by Targeting Hepatocytes.
Publisher
An entity responsible for making the resource available
Hepatology Communications
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-06
Subject
The topic of the resource
FATTY liver; LIPOCALIN; LIVER disease treatment
Creator
An entity primarily responsible for making the resource
Xu Yanyong; Zhu Yingdong; Jadhav Kavita; Li Yuanyuan; Sun Huihui; Yin Liya; Kasumov Takhar; Chen Xiaoli; Zhang Yanqiao
Description
An account of the resource
Hepatocytes are the major source of hepatic lipocalin‐2 (LCN2), which is up‐regulated in response to inflammation, injury, or metabolic stress. So far, the role of hepatocyte‐derived LCN2 in the development of nonalcoholic fatty liver disease (NAFLD) remains unknown. Herein we show that overexpression of human LCN2 in hepatocytes protects against high fat/high cholesterol/high fructose (HFCF) diet–induced liver steatosis and nonalcoholic steatohepatitis by promoting lipolysis and fatty acid oxidation (FAO) and inhibiting de novo lipogenesis (DNL), lipid peroxidation, and apoptosis. LCN2 fails to reduce triglyceride accumulation in hepatocytes lacking sterol regulatory element‐binding protein 1. In contrast, Lcn2−/− mice have defective lipolysis, increased lipid peroxidation and apoptosis, and exacerbated NAFLD after being fed an HFCF diet. In primary hepatocytes, Lcn2 deficiency stimulates de novo lipogenesis but inhibits FAO. Conclusion: The current study indicates that hepatocyte LCN2 protects against diet‐induced NAFLD by regulating lipolysis, FAO, DNL, lipid peroxidation, and apoptosis. Targeting hepatocyte LCN2 may be useful for treatment of NAFLD. [ABSTRACT FROM AUTHOR]
Identifier
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<a href="http://doi.org/10.1002/hep4.1341" target="_blank" rel="noreferrer noopener">10.1002/hep4.1341</a>
2019
Chen Xiaoli
Department of Integrative Medical Sciences
Fatty Liver
Hepatology communications
Jadhav Kavita
Kasumov Takhar
Li Yuanyuan
LIPOCALIN
LIVER disease treatment
NEOMED College of Medicine
September 2019 Update
Sun Huihui
Xu Yanyong
Yin Liya
Zhang Yanqiao
Zhu Yingdong
-
Text
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URL Address
<a href="http://doi.org/10.1002/hep4.1333" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hep4.1333</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).
Pages
656-669
Issue
5
Volume
3
Dublin Core
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Title
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Adipose‐Specific Lipin‐1 Overexpression Renders Hepatic Ferroptosis and Exacerbates Alcoholic Steatohepatitis in Mice.
Publisher
An entity responsible for making the resource available
Hepatology Communications
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-05
Subject
The topic of the resource
APOPTOSIS; FATTY liver; PROTEIN expression
Creator
An entity primarily responsible for making the resource
Zhou Zhou; Ye Ting Jie; Bonavita Gregory; Daniels Michael; Kainrad Noah; Jogasuria Alvin; You Min
Description
An account of the resource
Lipin‐1 is a Mg2+‐dependent phosphatidic acid phosphohydrolase involved in the generation of diacylglycerol during synthesis of phospholipids and triglycerides. Ethanol‐mediated inhibitory effects on adipose‐specific lipin‐1 expression were associated with experimental steatohepatitis in rodents. In the present study, using an adipose‐specific lipin‐1 overexpression transgenic (Lpin1‐Tg) mouse model, we tested a hypothesis that adipose‐specific lipin‐1 overexpression in mice might dampen ethanol‐induced liver damage. Experimental alcoholic steatohepatitis was induced by pair‐feeding ethanol to Lpin1‐Tg and wild‐type (WT) mice using the chronic‐plus‐binge ethanol feeding protocol. Unexpectedly, following the chronic‐plus‐binge ethanol challenge, Lpin1‐Tg mice exhibited much more pronounced steatosis, exacerbated inflammation, augmented elevation of serum liver enzymes, hepatobiliary damage, and fibrogenic responses compared with the WT mice. Mechanistically, overexpression of adipose lipin‐1 in mice facilitated the onset of hepatic ferroptosis, which is an iron‐dependent form of cell death, and subsequently induced ferroptotic liver damage in mice under ethanol exposure. Concurrently, adipose lipin‐1 overexpression induced defective adiponectin signaling pathways in ethanol‐fed mice. Conclusion: We identified ferroptosis as a mechanism in mediating the detrimental effects of adipose‐specific lipin‐1 overexpression in mice under chronic‐plus‐binge ethanol exposure. Our present study sheds light on potential therapeutic approaches for the prevention and treatment of human alcoholic steatohepatitis. [ABSTRACT FROM AUTHOR]
Identifier
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<a href="http://doi.org/10.1002/hep4.1333" target="_blank" rel="noreferrer noopener">10.1002/hep4.1333</a>
2019
Apoptosis
Bonavita Gregory
Daniels Michael
Department of Pharmaceutical Sciences
Fatty Liver
Hepatology communications
Jogasuria Alvin
June 2019 Update
Kainrad Noah
NEOMED College of Pharmacy
PROTEIN expression
Ye Ting Jie
You Min
Zhou Zhou
-
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/hep4.1129" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hep4.1129</a>
Pages
99–112
Issue
1
Volume
2
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
Deficiency of cholesterol 7alpha-hydroxylase in bile acid synthesis exacerbates alcohol-induced liver injury in mice.
Publisher
An entity responsible for making the resource available
Hepatology communications
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-01
Creator
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Donepudi Ajay C; Ferrell Jessica M; Boehme Shannon; Choi Hueng-Sik; Chiang John Y L
Description
An account of the resource
Alcoholic fatty liver disease (AFLD) is a major risk factor for cirrhosis-associated liver diseases. Studies demonstrate that alcohol increases serum bile acids in humans and rodents. AFLD has been linked to cholestasis, although the physiologic relevance of increased bile acids in AFLD and the underlying mechanism of increasing the bile acid pool by alcohol feeding are still unclear. In this study, we used mouse models either deficient of or overexpressing cholesterol 7alpha-hydroxylase (Cyp7a1), the rate-limiting and key regulatory enzyme in bile acid synthesis, to study the effect of alcohol drinking in liver metabolism and inflammation. Mice were challenged with chronic ethanol feeding (10 days) plus a binge dose of alcohol by oral gavage (5 g/kg body weight). Alcohol feeding reduced bile acid synthesis gene expression but increased the bile acid pool size, hepatic triglycerides and cholesterol, and inflammation and injury in wild-type mice and aggravated liver inflammation and injury in Cyp7a1-deficient mice. Interestingly, alcohol-induced hepatic inflammation and injury were ameliorated in Cyp7a1 transgenic mice. Conclusion: Alcohol feeding alters hepatic bile acid and cholesterol metabolism to cause liver inflammation and injury, while maintenance of bile acid and cholesterol homeostasis protect against alcohol-induced hepatic inflammation and injury. Our findings indicate that CYP7A1 plays a key role in protection against alcohol-induced steatohepatitis. (Hepatology Communications 2018;2:99-112).
Identifier
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<a href="http://doi.org/10.1002/hep4.1129" target="_blank" rel="noreferrer noopener">10.1002/hep4.1129</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).
2018
Boehme Shannon
Chiang John Y L
Choi Hueng-Sik
Department of Integrative Medical Sciences
Donepudi Ajay C
Ferrell Jessica M
Hepatology communications
NEOMED College of Medicine
-
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/hep4.1127" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hep4.1127</a>
Pages
1002–1004
Issue
10
Volume
1
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
Targeting bile acids and lipotoxicity for NASH treatment.
Publisher
An entity responsible for making the resource available
Hepatology communications
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-12
Creator
An entity primarily responsible for making the resource
Chiang John Y L
Identifier
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<a href="http://doi.org/10.1002/hep4.1127" target="_blank" rel="noreferrer noopener">10.1002/hep4.1127</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
Chiang John Y L
Department of Integrative Medical Sciences
Hepatology communications
NEOMED College of Medicine
-
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/hep4.1120" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hep4.1120</a>
Pages
1085–1098
Issue
10
Volume
1
Dublin Core
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Title
A name given to the resource
Hairy and enhancer of split 6 prevents hepatic lipid accumulation through inhibition of Pparg2 expression.
Publisher
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Hepatology communications
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-12
Creator
An entity primarily responsible for making the resource
Park Jung Eun; Lee Mikang; Kim Seong-Chul; Zhang Yanqiao; Hardwick James P; Lee Yoon-Kwang
Description
An account of the resource
Peroxisome proliferator-activated receptor gamma (PPARgamma) is a master regulator for white adipocyte differentiation and lipid storage. The increased level of hepatic PPARgamma2 isoform reprograms liver for lipid storage and causes abnormal fat accumulation in certain pathophysiologic conditions. The current study aimed to investigate a role of transcriptional repressor hairy and enhancer of split 6 (HES6) in the regulation of Pparg2 expression and hepatic steatosis induced by diet. Liver-specific overexpression of Hes6 using adenovirus reduced Pparg2 messenger RNA levels by 90% and hepatic triglyceride accumulation by 22% compared to the levels in mice injected with an adenoviral empty vector with Western diet feeding. In sharp contrast, silencing Hes6 gene expression using short hairpin RNA increased hepatic lipid accumulation and Pparg2 messenger RNA levels by 70% and 4-fold, respectively. To locate hepatocyte nuclear factor 4 alpha (HNF4alpha) binding site(s), through which repressional activity of HES6 is mediated, a 2.5-kb Pparg2 promoter-driven luciferase reporter was constructed for transient transfection assays. Subsequently, chromatin immunoprecipitation and electrophoretic mobility shift assays were performed. An HNF4alpha binding consensus sequence was identified at 903 base pairs upstream from the transcription start site of Pparg2. Deletion or point mutation of the sequence in a luciferase reporter containing the Pparg2 promoter abolished HNF4alpha-mediated activation in HeLa cells. Chromatin immunoprecipitation and electrophoretic mobility shift assays further confirmed direct recruitment and binding of HNF4alpha to the site. Gene expression analysis with liver samples from subjects with nonalcoholic steatohepatitis suggested that the axis of the Hes6-Hnf4a-Pparg2 transcriptional cascade is also responsible for hepatic fat accumulation in humans. Conclusion: HES6 represses Pparg2 gene expression, thereby preventing hepatic lipid accumulation induced by chronic Western diet feeding or pathophysiologic conditions. (Hepatology Communications 2017;1:1085-1098).
Identifier
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<a href="http://doi.org/10.1002/hep4.1120" target="_blank" rel="noreferrer noopener">10.1002/hep4.1120</a>
Rights
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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).
2017
Department of Integrative Medical Sciences
Hardwick James P
Hepatology communications
Kim Seong-Chul
Lee Mikang
Lee Yoon-Kwang
NEOMED College of Medicine
Park Jung Eun
Zhang Yanqiao
-
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/hep4.1066" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hep4.1066</a>
Pages
675–690
Issue
7
Volume
1
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
Increased ethanol-inducible cytochrome P450-2E1 and cytochrome P450 isoforms in exosomes of alcohol-exposed rodents and patients with alcoholism through oxidative and endoplasmic reticulum stress.
Publisher
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Hepatology communications
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-09
Creator
An entity primarily responsible for making the resource
Cho Young-Eun; Mezey Esteban; Hardwick James P; Salem Norman Jr; Clemens Dahn L; Song Byoung-Joon
Description
An account of the resource
This study investigated the role of ethanol-inducible cytochrome P450-2E1 (CYP2E1) in enhancing CYP2E1 and other P450 proteins in extracellular vesicles (EVs) from alcohol-exposed rodents and human patients with alcoholism and their effects on oxidative hepatocyte injury. Female Fischer rats and wild-type or Cyp2e1-null mice were exposed to three oral doses of binge ethanol or dextrose control at 12-hour intervals. Plasma EV and hepatic proteins from alcohol-exposed rodents, patients with alcoholism, and their respective controls were isolated and characterized. The number of EVs and the amounts of EV CYP2E1, CYP2A, CYP1A1/2, and CYP4B proteins were markedly elevated in both patients with alcoholism and alcohol-exposed rats and mice. The number of EVs and EV P450 proteins were significantly reduced in ethanol-exposed rats fed a diet containing polyunsaturated fatty acids. The increased number of EVs and EV CYP2E1 and other P450 isoforms in alcohol-exposed wild types were significantly reduced in the corresponding Cyp2e1-null mice. EV CYP2E1 amounts depended on increased oxidative and endoplasmic reticulum (ER) stress because their levels were decreased by cotreatment with the antioxidant N-acetylcysteine or the CYP2E1 inhibitor chlormethiazole but increased by ER stress-inducer thapsigargin, which was blocked by 4-phenylbutyric acid. Furthermore, cell death rates were elevated when primary hepatocytes or human hepatoma cells were exposed to EVs from alcohol-exposed rodents and patients with alcoholism, demonstrating that EVs from alcohol-exposed rats and patients with alcoholism are functional and can promote cell death by activating the apoptosis signaling pathway, including phospho-c-Jun
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/hep4.1066" target="_blank" rel="noreferrer noopener">10.1002/hep4.1066</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
Cho Young-Eun
Clemens Dahn L
Department of Integrative Medical Sciences
Hardwick James P
Hepatology communications
Mezey Esteban
NEOMED College of Medicine
Salem Norman Jr
Song Byoung-Joon