1
40
4
-
Text
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URL Address
<a href="http://doi.org/10.1002/hep.26714" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hep.26714</a>
Pages
1761–1771
Issue
5
Volume
59
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
Hepatic carboxylesterase 1 is essential for both normal and farnesoid X receptor-controlled lipid homeostasis.
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
2014
2014-05
Subject
The topic of the resource
*Homeostasis; *Lipid Metabolism; Animals; Carboxylic Ester Hydrolases/*physiology; Cholesterol/blood; Cytoplasmic and Nuclear/*physiology; Fatty Acids/metabolism; Inbred C57BL; Lipogenesis; Liver/*enzymology; Mice; Receptors; Sterol Regulatory Element Binding Protein 1/physiology; Triglycerides/metabolism
Creator
An entity primarily responsible for making the resource
Xu Jiesi; Li Yuanyuan; Chen Wei-Dong; Xu Yang; Yin Liya; Ge Xuemei; Jadhav Kavita; Adorini Luciano; Zhang Yanqiao
Description
An account of the resource
UNLABELLED: Nonalcoholic fatty liver disease (NAFLD) is one of the major health concerns worldwide. Farnesoid X receptor (FXR) is considered a therapeutic target for treatment of NAFLD. However, the mechanism by which activation of FXR lowers hepatic triglyceride (TG) levels remains unknown. Here we investigated the role of hepatic carboxylesterase 1 (CES1) in regulating both normal and FXR-controlled lipid homeostasis. Overexpression of hepatic CES1 lowered hepatic TG and plasma glucose levels in both wild-type and diabetic mice. In contrast, knockdown of hepatic CES1 increased hepatic TG and plasma cholesterol levels. These effects likely resulted from the TG hydrolase activity of CES1, with subsequent changes in fatty acid oxidation and/or de novo lipogenesis. Activation of FXR induced hepatic CES1, and reduced the levels of hepatic and plasma TG as well as plasma cholesterol in a CES1-dependent manner. CONCLUSION: Hepatic CES1 plays a critical role in regulating both lipid and carbohydrate metabolism and FXR-controlled lipid homeostasis.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/hep.26714" target="_blank" rel="noreferrer noopener">10.1002/hep.26714</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).
*Homeostasis
*Lipid Metabolism
2014
Adorini Luciano
Animals
Carboxylic Ester Hydrolases/*physiology
Chen Wei-Dong
Cholesterol/blood
Cytoplasmic and Nuclear/*physiology
Department of Integrative Medical Sciences
Fatty Acids/metabolism
Ge Xuemei
Hepatology (Baltimore, Md.)
Inbred C57BL
Jadhav Kavita
Li Yuanyuan
Lipogenesis
Liver/*enzymology
Mice
NEOMED College of Medicine
Receptors
Sterol Regulatory Element Binding Protein 1/physiology
Triglycerides/metabolism
Xu Jiesi
Xu Yang
Yin Liya
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/10.1161/ATVBAHA.110.217828" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/ATVBAHA.110.217828</a>
Pages
328–336
Issue
2
Volume
31
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
Hepatic hepatocyte nuclear factor 4alpha is essential for maintaining triglyceride and cholesterol homeostasis.
Publisher
An entity responsible for making the resource available
Arteriosclerosis, thrombosis, and vascular biology
Date
A point or period of time associated with an event in the lifecycle of the resource
2011
2011-02
Subject
The topic of the resource
Adenoviridae/genetics; Animal; Animals; Cells; Cholesterol; Cholesterol/*metabolism; Cultured; Fatty Liver/metabolism/physiopathology; HDL/metabolism; Hepatocyte Nuclear Factor 4/drug effects/genetics/*physiology; Hepatocytes/cytology/*metabolism; Homeostasis/genetics/*physiology; Inbred C57BL; Lipid Metabolism/genetics/physiology; Mice; Models; RNA; Small Interfering/genetics/pharmacology; Triglycerides/*metabolism; VLDL/metabolism
Creator
An entity primarily responsible for making the resource
Yin Liya; Ma Huiyan; Ge Xuemei; Edwards Peter A; Zhang Yanqiao
Description
An account of the resource
OBJECTIVE: Loss-of-function mutations in human hepatocyte nuclear factor 4alpha (HNF4alpha) are associated with maturity-onset diabetes of the young and lipid disorders. However, the mechanisms underlying the lipid disorders are poorly understood. In this study, we determined the effect of acute loss or augmentation of hepatic HNF4alpha function on lipid homeostasis. METHODS AND RESULTS: We generated an adenovirus expressing LacZ (Ad-shLacZ) or short hairpin RNA of Hnf4alpha (Ad-shHnf4alpha). Tail vain injection of C57BL/6J mice with Ad-shHnf4alpha reduced hepatic Hnf4alpha expression and resulted in striking phenotypes, including the development of fatty liver and a \textgreater80% decrease in plasma levels of triglycerides, total cholesterol, and high-density lipoprotein cholesterol. These latter changes were associated with reduced hepatic lipogenesis and impaired very-low-density lipoprotein secretion. Deficiency in hepatic Hnf4alpha did not affect intestinal cholesterol absorption despite decreased expression of genes involved in bile acid synthesis. Consistent with the loss-of-function data, overexpression of Hnf4alpha induced numerous genes involved in lipid metabolism in isolated primary hepatocytes. Interestingly, many of these HNF4alpha-regulated genes were not induced in wild-type mice that overexpressed hepatic Hnf4alpha. Because of selective gene regulation, mice overexpressing hepatic Hnf4alpha had unchanged plasma triglyceride levels and decreased plasma cholesterol levels. CONCLUSIONS: Loss of hepatic HNF4alpha results in severe lipid disorder as a result of dysregulation of multiple genes involved in lipid metabolism. In contrast, augmentation of hepatic HNF4alpha activity lowers plasma cholesterol levels but has no effect on plasma triglyceride levels because of selective gene regulation. Our data indicate that hepatic HNF4alpha is essential for controlling the basal expression of numerous genes involved in lipid metabolism and is indispensable for maintaining normal lipid homeostasis.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/ATVBAHA.110.217828" target="_blank" rel="noreferrer noopener">10.1161/ATVBAHA.110.217828</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).
2011
Adenoviridae/genetics
Animal
Animals
Arteriosclerosis, thrombosis, and vascular biology
Cells
Cholesterol
Cholesterol/*metabolism
Cultured
Department of Integrative Medical Sciences
Edwards Peter A
Fatty Liver/metabolism/physiopathology
Ge Xuemei
HDL/metabolism
Hepatocyte Nuclear Factor 4/drug effects/genetics/*physiology
Hepatocytes/cytology/*metabolism
Homeostasis/genetics/*physiology
Inbred C57BL
Lipid Metabolism/genetics/physiology
Ma Huiyan
Mice
Models
NEOMED College of Medicine
RNA
Small Interfering/genetics/pharmacology
Triglycerides/*metabolism
VLDL/metabolism
Yin Liya
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/10.1194/jlr.M015859" target="_blank" rel="noreferrer noopener">http://doi.org/10.1194/jlr.M015859</a>
Pages
1561–1568
Issue
8
Volume
52
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
Aldo-keto reductase 1B7 is a target gene of FXR and regulates lipid and glucose homeostasis.
Publisher
An entity responsible for making the resource available
Journal of lipid research
Date
A point or period of time associated with an event in the lifecycle of the resource
2011
2011-08
Subject
The topic of the resource
*Aldehyde Reductase/genetics/metabolism; Adenoviridae; Animal; Animals; Blood Glucose/*metabolism; Cholesterol/analysis; Cytoplasmic and Nuclear/genetics/*metabolism; Diabetes Mellitus/genetics/*metabolism/physiopathology; Disease Models; Fatty Liver/genetics/*metabolism/physiopathology; Gene Expression; Genetic Vectors; Gluconeogenesis/genetics; Homeostasis; Humans; Liver/*metabolism/physiopathology; Malondialdehyde/blood; Mice; Polymerase Chain Reaction; Receptors; Transfection; Transgenic; Triglycerides/analysis
Creator
An entity primarily responsible for making the resource
Ge Xuemei; Yin Liya; Ma Huiyan; Li Tiangang; Chiang John Y L; Zhang Yanqiao
Description
An account of the resource
Aldo-keto reductase 1B7 (AKR1B7) is proposed to play a role in detoxification of by-products of lipid peroxidation. In this article, we show that activation of the nuclear receptor farnesoid X receptor (FXR) induces AKR1B7 expression in the liver and intestine, and reduces the levels of malondialdehyde (MDA), the end product of lipid peroxidation, in the intestine but not in the liver. To determine whether AKR1B7 regulates MDA levels in vivo, we overexpressed AKR1B7 in the liver. Overexpression of AKR1B7 in the liver had no effect on hepatic or plasma MDA levels. Interestingly, hepatic expression of AKR1B7 significantly lowered plasma glucose levels in both wild-type and diabetic db/db mice, which was associated with reduced hepatic gluconeogenesis. Hepatic expression of AKR1B7 also significantly lowered hepatic triglyceride and cholesterol levels in db/db mice. These data reveal a novel function for AKR1B7 in lipid and glucose metabolism and suggest that AKR1B7 may not play a role in detoxification of lipid peroxides in the liver. AKR1B7 may be a therapeutic target for treatment of fatty liver disease associated with diabetes mellitus.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1194/jlr.M015859" target="_blank" rel="noreferrer noopener">10.1194/jlr.M015859</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).
*Aldehyde Reductase/genetics/metabolism
2011
Adenoviridae
Animal
Animals
Blood Glucose/*metabolism
Chiang John Y L
Cholesterol/analysis
Cytoplasmic and Nuclear/genetics/*metabolism
Department of Integrative Medical Sciences
Diabetes Mellitus/genetics/*metabolism/physiopathology
Disease Models
Fatty Liver/genetics/*metabolism/physiopathology
Ge Xuemei
Gene Expression
Genetic Vectors
Gluconeogenesis/genetics
Homeostasis
Humans
Journal of lipid research
Li Tiangang
Liver/*metabolism/physiopathology
Ma Huiyan
Malondialdehyde/blood
Mice
NEOMED College of Medicine
Polymerase Chain Reaction
Receptors
Transfection
Transgenic
Triglycerides/analysis
Yin Liya
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/10.1210/me.2011-1157" target="_blank" rel="noreferrer noopener">http://doi.org/10.1210/me.2011-1157</a>
Pages
272–280
Issue
2
Volume
26
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
Loss of FXR protects against diet-induced obesity and accelerates liver carcinogenesis in ob/ob mice.
Publisher
An entity responsible for making the resource available
Molecular endocrinology (Baltimore, Md.)
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-02
Subject
The topic of the resource
Adipose Tissue; Adiposity/genetics; Animals; Brown/pathology; Carcinoma/etiology/*genetics; Cell Transformation; Cytoplasmic and Nuclear/*deficiency/genetics; Diet; Dietary Fats/metabolism; Energy Metabolism/genetics; Female; Gene Knockout Techniques; Glucose Intolerance/complications/genetics; High-Fat/*adverse effects; Intestinal Absorption; Knockout; Leptin/deficiency/genetics; Liver Neoplasms/etiology/*genetics; Liver/pathology; Male; Mice; Muscle; Neoplastic/genetics; Obese; Obesity/*etiology/genetics; Receptors; Sex Factors; Skeletal/metabolism; Weight Gain/genetics
Creator
An entity primarily responsible for making the resource
Zhang Yanqiao; Ge Xuemei; Heemstra Lydia A; Chen Wei-Dong; Xu Jiesi; Smith Joseph L; Ma Huiyan; Kasim Neda; Edwards Peter A; Novak Colleen M
Description
An account of the resource
Farnesoid X receptor (FXR) is known to play important regulatory roles in bile acid, lipid, and carbohydrate metabolism. Aged (\textgreater12 months old) Fxr(-/-) mice also develop spontaneous liver carcinomas. In this report, we used three mouse models to investigate the role of FXR deficiency in obesity. As compared with low-density lipoprotein receptor (Ldlr) knockout (Ldlr(-/-)) mice, the Ldlr(-/-)Fxr(-/-) double-knockout mice were highly resistant to diet-induced obesity, which was associated with increased expression of genes involved in energy metabolism in the skeletal muscle and brown adipose tissue. Such a striking effect of FXR deficiency on obesity on an Ldlr(-/-) background led us to investigate whether FXR deficiency alone is sufficient to affect obesity. As compared with wild-type mice, Fxr(-/-) mice showed resistance to diet-induced weight gain. Interestingly, only female Fxr(-/-) mice showed significant resistance to diet-induced obesity, which was accompanied by increased energy expenditure in these mice. Finally, we determined the effect of FXR deficiency on obesity in a genetically obese and diabetic mouse model. We generated ob(-/-)Fxr(-/-) mice that were deficient in both Leptin and Fxr. On a chow diet, ob(-/-)Fxr(-/-) mice gained less body weight and had reduced body fat mass as compared with ob/ob mice. In addition, we observed liver carcinomas in 43% of young (\textless11 months old) Ob(-/-)Fxr(-/-) mice. Together these data indicate that loss of FXR prevents diet-induced or genetic obesity and accelerates liver carcinogenesis under diabetic conditions.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1210/me.2011-1157" target="_blank" rel="noreferrer noopener">10.1210/me.2011-1157</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).
2012
Adipose Tissue
Adiposity/genetics
Animals
Brown/pathology
Carcinoma/etiology/*genetics
Cell Transformation
Chen Wei-Dong
Cytoplasmic and Nuclear/*deficiency/genetics
Diet
Dietary Fats/metabolism
Edwards Peter A
Energy Metabolism/genetics
Female
Ge Xuemei
Gene Knockout Techniques
Glucose Intolerance/complications/genetics
Heemstra Lydia A
High-Fat/*adverse effects
Intestinal Absorption
Kasim Neda
Knockout
Leptin/deficiency/genetics
Liver Neoplasms/etiology/*genetics
Liver/pathology
Ma Huiyan
Male
Mice
Molecular endocrinology (Baltimore, Md.)
Muscle
Neoplastic/genetics
Novak Colleen M
Obese
Obesity/*etiology/genetics
Receptors
Sex Factors
Skeletal/metabolism
Smith Joseph L
Weight Gain/genetics
Xu Jiesi
Zhang Yanqiao