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40
16
-
Text
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<a href="http://doi.org/10.1016/j.ebiom.2020.102754" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.ebiom.2020.102754</a>
Pages
102754
Volume
55
ISSN
2352-3964 2352-3964
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Update Year & Number
June 2020 Update II
NEOMED College
NEOMED College of Medicine
NEOMED Department
Department of Integrative Medical Sciences
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Targeting the gut microbiota for treating colitis: Is FGF19 a magic bullet?
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EBioMedicine
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2020
2020-05
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Chiang John Y L; Ferrell Jessica M
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<a href="http://doi.org/10.1016/j.ebiom.2020.102754" target="_blank" rel="noreferrer noopener">10.1016/j.ebiom.2020.102754</a>
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journalArticle
2020
Chiang John Y L
Department of Integrative Medical Sciences
EBioMedicine
Ferrell Jessica M
journalArticle
June 2020 Update II
NEOMED College of Medicine
-
Text
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<a href="http://doi.org/10.1002/cld.861" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/cld.861</a>
Pages
91-94
Issue
3
Volume
15
ISSN
2046-2484 2046-2484
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June 2020 Update I
NEOMED College
NEOMED College of Medicine
NEOMED Department
Department of Integrative Medical Sciences
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Title
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Bile Acid Biology, Pathophysiology, and Therapeutics.
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Clinical liver disease
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2020
2020-03
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Chiang John Y L; Ferrell Jessica M
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http://aasldpubs.onlinelibrary.wiley.com/hub/journal/10.1002/(ISSN)2046-2484/vide o/15-3-reading-chiang a video presentation of this article http://aasldpubs.onlinelibrary.wiley.com/hub/journal/10.1002/(ISSN)2046-2484/vide o/15-3-interview-chiang an interview with the author.
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<a href="http://doi.org/10.1002/cld.861" target="_blank" rel="noreferrer noopener">10.1002/cld.861</a>
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journalArticle
2020
Chiang John Y L
Clinical liver disease
Department of Integrative Medical Sciences
Ferrell Jessica M
Journal Article
journalArticle
June 2020 Update I
NEOMED College of Graduate Studies
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.
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<a href="http://doi.org/10.1152/ajpgi.00223.2019" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpgi.00223.2019</a>
Pages
G554-G573
Issue
3
Volume
318
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<a href="http://ezproxy.neomed.idm.oclc.org/login?url=http://doi.org/10.1152/ajpgi.00223.2019" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1152/ajpgi.00223.2019</a>
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Update Year & Number
March 2020 Update
NEOMED College
NEOMED College of Medicine; NEOMED College of Graduate Studies
NEOMED Department
Department of Integrative Medical Sciences
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Title
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Bile acid receptors FXR and TGR5 signaling in fatty liver diseases and therapy.
Publisher
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American journal of physiology. Gastrointestinal and liver physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-03
Subject
The topic of the resource
bile acid metabolism; liver diseases; farnesoid X receptor; alcoholic and nonalcoholic fatty; bile acid therapies; Takeda G protein-coupled receptor 5
Creator
An entity primarily responsible for making the resource
Chiang John Y L; Ferrell Jessica M
Description
An account of the resource
Bile acid synthesis is the most significant pathway for catabolism of cholesterol and for maintenance of whole body cholesterol homeostasis. Bile acids are physiological detergents that absorb, distribute, metabolize, and excrete nutrients, drugs, and xenobiotics. Bile acids also are signal molecules and metabolic integrators that activate nuclear farnesoid X receptor (FXR) and membrane Takeda G protein-coupled receptor 5 (TGR5; i.e., G protein-coupled bile acid receptor 1) to regulate glucose, lipid, and energy metabolism. The gut-to-liver axis plays a critical role in the transformation of primary bile acids to secondary bile acids, in the regulation of bile acid synthesis to maintain composition within the bile acid pool, and in the regulation of metabolic homeostasis to prevent hyperglycemia, dyslipidemia, obesity, and diabetes. High-fat and high-calorie diets, dysbiosis, alcohol, drugs, and disruption of sleep and circadian rhythms cause metabolic diseases, including alcoholic and nonalcoholic fatty liver diseases, obesity, diabetes, and cardiovascular disease. Bile acid-based drugs that target bile acid receptors are being developed for the treatment of metabolic diseases of the liver.
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<a href="http://doi.org/10.1152/ajpgi.00223.2019" target="_blank" rel="noreferrer noopener">10.1152/ajpgi.00223.2019</a>
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Journal Article
2020
alcoholic and nonalcoholic fatty
American journal of physiology. Gastrointestinal and liver physiology
Bile acid metabolism
bile acid therapies
Chiang John Y L
Department of Integrative Medical Sciences
Farnesoid X receptor
Ferrell Jessica M
Liver Diseases
NEOMED College of Graduate Studies
NEOMED College of Medicine
Takeda G protein-coupled receptor 5
-
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.
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n/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
1378A
Issue
1
Volume
70
ISSN
0270-9139
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Title
A name given to the resource
BILE ACID RECEPTORS FXR AND TGR IN LIVER FIBROSIS AND INFLAMMATION: STUDY OF FXR/TGR5 DOUBLE KNOCKOUT MICE
Publisher
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Hepatology
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-10
Creator
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Ferrell Jessica M; Boehme Shannon; Gilliland Tricia; Chiang John Y L
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n/a
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Journal Article
2019
Boehme Shannon
Chiang John Y L
Department of Integrative Medical Sciences
Ferrell Jessica M
Gilliland Tricia
Hepatology
Journal Article
NEOMED College of Medicine
November 2019 Update
-
Text
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<a href="https://e-dmj.org/Synapse/Data/PDFData/2004DMJ/dmj-43-257.pdf" target="_blank" rel="noreferrer noopener">http://doi.org/10.4093/dmj.2019.0043</a>
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Pages
257-272
Issue
3
Volume
43
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Title
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Understanding Bile Acid Signaling in Diabetes: From Pathophysiology to Therapeutic Targets.
Publisher
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Diabetes & Metabolism Journal
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
BILE acids; Bile acids and salts; cholesterol 7-alpha-hydroxylase; Cytoplasmic and Nuclear; Endocrinology & Metabolism; FARNESOID X receptor; farnesoid-x-receptor; FATTY liver; fatty liver-disease; G protein coupled receptors; G-protein-coupled; Gastrointestinal microbiome; growth-factor 19; gut microbiota; hepatic steatosis; improves insulin sensitivity; liver disease; metabolic; Non-alcoholic fatty; Non-alcoholic Fatty Liver Disease; nuclear; receptor; Receptors; serum fgf21 levels; syndrome
Creator
An entity primarily responsible for making the resource
Ferrell Jessica M; Chiang John Y L
Description
An account of the resource
Diabetes and obesity have reached an epidemic status worldwide. Diabetes increases the risk for cardiovascular disease and nonalcoholic fatty liver disease. Primary bile acids are synthesized in hepatocytes and are transformed to secondary bile acids in the intestine by gut bacteria. Bile acids are nutrient sensors and metabolic integrators that regulate lipid, glucose, and energy homeostasis by activating nuclear farnesoid X receptor and membrane Takeda G protein-coupled receptor 5. Bile acids control gut bacteria overgrowth, species population, and protect the integrity of the intestinal barrier. Gut bacteria, in turn, control circulating bile acid composition and pool size. Dysregulation of bile acid homeostasis and dysbiosis causes diabetes and obesity. Targeting bile acid signaling and the gut microbiome have therapeutic potential for treating diabetes, obesity, and non-alcoholic fatty liver disease. [ABSTRACT FROM AUTHOR]
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.4093/dmj.2019.0043" target="_blank" rel="noreferrer noopener">10.4093/dmj.2019.0043</a>
2019
BILE acids
Bile Acids and Salts
Chiang John Y L
cholesterol 7-alpha-hydroxylase
Cytoplasmic and Nuclear
Department of Integrative Medical Sciences
Diabetes & Metabolism Journal
Endocrinology & Metabolism
Farnesoid X receptor
farnesoid-x-receptor
Fatty Liver
fatty liver-disease
Ferrell Jessica M
G protein coupled receptors
G-protein-coupled
Gastrointestinal Microbiome
growth-factor 19
gut microbiota
hepatic steatosis
improves insulin sensitivity
Liver disease
Metabolic
NEOMED College of Medicine
Non-alcoholic fatty
Non-alcoholic Fatty Liver Disease
nuclear
Receptor
Receptors
September 2019 Update
serum fgf21 levels
Syndrome
-
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.
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<a href="http://doi.org/10.4093/dmj.2019.0043" target="_blank" rel="noreferrer noopener">http://doi.org/10.4093/dmj.2019.0043</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
257-272
Issue
3
Volume
43
Dublin Core
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Title
A name given to the resource
Understanding Bile Acid Signaling in Diabetes: From Pathophysiology to Therapeutic Targets
Publisher
An entity responsible for making the resource available
Diabetes & Metabolism Journal
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
Bile acids and salts; cytoplasmic and nuclear; G-protein-coupled; Gastrointestinal microbiome; Non-alcoholic fatty liver disease; Receptors
Creator
An entity primarily responsible for making the resource
Ferrell Jessica M; Chiang John Y L
Description
An account of the resource
Diabetes and obesity have reached an epidemic status worldwide. Diabetes increases the risk for cardiovascular disease and non-alcoholic fatty liver disease. Primary bile acids are synthesized in hepatocytes and are transformed to secondary bile acids in the intestine by gut bacteria. Bile acids are nutrient sensors and metabolic integrators that regulate lipid, glucose, and energy homeostasis by activating nuclear farnesoid X receptor and membrane Takeda G protein-coupled receptor 5. Bile acids control gut bacteria overgrowth, species population, and protect the integrity of the intestinal barrier. Gut bacteria, in turn, control circulating bile acid composition and pool size. Dysregulation of bile acid homeostasis and dysbiosis causes diabetes and obesity. Targeting bile acid signaling and the gut microbiome have therapeutic potential for treating diabetes, obesity, and non-alcoholic fatty liver disease.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.4093/dmj.2019.0043" target="_blank" rel="noreferrer noopener">10.4093/dmj.2019.0043</a>
2019
Bile Acids and Salts
Chiang John Y L
Cytoplasmic and Nuclear
Department of Integrative Medical Sciences
Diabetes & Metabolism Journal
Ferrell Jessica M
G-protein-coupled
Gastrointestinal Microbiome
June 2019 Update
NEOMED College of Medicine
Non-alcoholic Fatty Liver Disease
Receptors
-
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/10.1146/annurev-nutr-082018-124344" target="_blank" rel="noreferrer noopener">http://doi.org/10.1146/annurev-nutr-082018-124344</a>
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Title
A name given to the resource
Bile Acids as Metabolic Regulators and Nutrient Sensors
Publisher
An entity responsible for making the resource available
Annual Review of Nutrition
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-04
Creator
An entity primarily responsible for making the resource
Chiang John Y L; Ferrell Jessica M
Description
An account of the resource
Bile acids facilitate nutrient absorption and are endogenous ligands for nuclear receptors that regulate lipid and energy metabolism. The brain-gut-liver axis plays an essential role in maintaining overall glucose, bile, and immune homeostasis. Fasting and feeding transitions alter nutrient content in the gut, which influences bile acid composition and pool size. In turn, bile acid signaling mediates lipid and glucose use and protection against inflammation. Altered bile acid metabolism resulting from gene mutations, high-fat diets, alcohol, or circadian disruption can contribute to cholestatic and inflammatory diseases, diabetes, and obesity. Bile acids and their derivatives are valuable therapeutic agents for treating these inflammatory metabolic diseases. Expected final online publication date for the Annual Review of Nutrition Volume 39 is August 21, 2019. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.
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<a href="http://doi.org/10.1146/annurev-nutr-082018-124344" target="_blank" rel="noreferrer noopener">10.1146/annurev-nutr-082018-124344</a>
2019
Annual Review of Nutrition
Chiang John Y L
Department of Integrative Medical Sciences
Ferrell Jessica M
June 2019 Update
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/hep.29857" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hep.29857</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
1574-1588
Issue
4
Volume
68
Dublin Core
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Title
A name given to the resource
Intestine farnesoid X receptor agonist and the gut microbiota activate G-protein bile acid receptor-1 signaling to improve metabolism.
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
2018
2018-10
Subject
The topic of the resource
Male; Animals; Mice; Random Allocation; Sensitivity and Specificity; *Signal Transduction; Lipid Metabolism; Bile Acids and Salts/*metabolism; GTP-Binding Proteins/*metabolism; Receptors; Inbred C57BL; Animal; Disease Models; G-Protein-Coupled/*metabolism; Gastrointestinal Microbiome/*drug effects; Glucagon-Like Peptide 1/metabolism; Cytoplasmic and Nuclear/*antagonists & inhibitors/pharmacology
Creator
An entity primarily responsible for making the resource
Pathak Preeti; Xie Cen; Nichols Robert G; Ferrell Jessica M; Boehme Shannon; Krausz Kristopher W; Patterson Andrew D; Gonzalez Frank J; Chiang John Y L
Description
An account of the resource
Bile acids activate farnesoid X receptor (FXR) and G protein-coupled bile acid receptor-1 (aka Takeda G protein-coupled receptor-5 [TGR5]) to regulate bile acid metabolism and glucose and insulin sensitivity. FXR and TGR5 are coexpressed in the enteroendocrine L cells, but their roles in integrated regulation of metabolism are not completely understood. We reported recently that activation of FXR induces TGR5 to stimulate glucagon-like peptide-1 (GLP-1) secretion to improve insulin sensitivity and hepatic metabolism. In this study, we used the intestine-restricted FXR agonist fexaramine (FEX) to study the effect of activation of intestinal FXR on the gut microbiome, bile acid metabolism, and FXR and TGR5 signaling. The current study revealed that FEX markedly increased taurolithocholic acid, increased secretion of fibroblast growth factors 15 and 21 and GLP-1, improved insulin and glucose tolerance, and promoted white adipose tissue browning in mice. Analysis of 16S ribosomal RNA sequences of the gut microbiome identified the FEX-induced and lithocholic acid-producing bacteria Acetatifactor and Bacteroides. Antibiotic treatment completely reversed the
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/hep.29857" target="_blank" rel="noreferrer noopener">10.1002/hep.29857</a>
*Signal Transduction
2018
Animal
Animals
Bile Acids and Salts/*metabolism
Boehme Shannon
Chiang John Y L
Cytoplasmic and Nuclear/*antagonists & inhibitors/pharmacology
Department of Integrative Medical Sciences
Disease Models
Ferrell Jessica M
G-Protein-Coupled/*metabolism
Gastrointestinal Microbiome/*drug effects
Glucagon-Like Peptide 1/metabolism
Gonzalez Frank J
GTP-Binding Proteins/*metabolism
Hepatology (Baltimore, Md.)
Inbred C57BL
Krausz Kristopher W
Lipid Metabolism
Male
Mice
NEOMED College of Medicine
Nichols Robert G
Pathak Preeti
Patterson Andrew D
Random Allocation
Receptors
Sensitivity and Specificity
Xie Cen
-
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/10.3727/105221618X15156018385515" target="_blank" rel="noreferrer noopener">http://doi.org/10.3727/105221618X15156018385515</a>
Pages
71–87
Issue
2
Volume
18
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
Bile Acid Metabolism in Liver Pathobiology.
Publisher
An entity responsible for making the resource available
Gene expression
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-05
Creator
An entity primarily responsible for making the resource
Chiang John Y L; Ferrell Jessica M
Description
An account of the resource
Bile acids facilitate intestinal nutrient absorption and biliary cholesterol secretion to maintain bile acid homeostasis, which is essential for protecting liver and other tissues and cells from cholesterol and bile acid toxicity. Bile acid metabolism is tightly regulated by bile acid synthesis in the liver and bile acid biotransformation in the intestine. Bile acids are endogenous ligands that activate a complex network of nuclear receptor farnesoid X receptor and membrane G protein-coupled bile acid receptor-1 to regulate hepatic lipid and glucose metabolic homeostasis and energy metabolism. The gut-to-liver axis plays a critical role in the regulation of enterohepatic circulation of bile acids, bile acid pool size, and bile acid composition. Bile acids control gut bacteria overgrowth, and gut bacteria metabolize bile acids to regulate host metabolism. Alteration of bile acid metabolism by high-fat diets, sleep disruption, alcohol, and drugs reshapes gut microbiome and causes dysbiosis, obesity, and metabolic disorders. Gender differences in bile acid metabolism, FXR signaling, and gut microbiota have been linked to higher prevalence of fatty liver disease and hepatocellular carcinoma in males. Alteration of bile acid homeostasis contributes to cholestatic liver diseases, inflammatory diseases in the digestive system, obesity, and diabetes. Bile acid-activated receptors are potential therapeutic targets for developing drugs to treat metabolic disorders.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.3727/105221618X15156018385515" target="_blank" rel="noreferrer noopener">10.3727/105221618X15156018385515</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).
2018
Chiang John Y L
Department of Integrative Medical Sciences
Ferrell Jessica M
Gene Expression
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/10.1194/jlr.M064709" target="_blank" rel="noreferrer noopener">http://doi.org/10.1194/jlr.M064709</a>
Pages
1144–1154
Issue
7
Volume
57
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
Cholesterol 7alpha-hydroxylase-deficient mice are protected from high-fat/high-cholesterol diet-induced metabolic disorders.
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
2016
2016-07
Subject
The topic of the resource
*bile acids and salt/metabolism; *cholesterol/diet; *lipids; *liver; Animal; Animals; Bile Acids and Salts/genetics/metabolism; Cholesterol 7-alpha-Hydroxylase/*genetics/metabolism; Cholesterol/*metabolism; Diet; Disease Models; Exhalation/genetics; Glucose/metabolism; High-Fat; Homeostasis; Humans; Lipid Metabolism/genetics; Liver/enzymology/pathology; Metabolic Diseases/*genetics/metabolism; Mice
Creator
An entity primarily responsible for making the resource
Ferrell Jessica M; Boehme Shannon; Li Feng; Chiang John Y L
Description
An account of the resource
Cholesterol 7alpha-hydroxylase (CYP7A1) is the first and rate-limiting enzyme in the conversion of cholesterol to bile acids in the liver. In addition to absorption and digestion of nutrients, bile acids play a critical role in the regulation of lipid, glucose, and energy homeostasis. We have backcrossed Cyp7a1(-/-) mice in a mixed B6/129Sv genetic background to C57BL/6J mice to generate Cyp7a1(-/-) mice in a near-pure C57BL/6J background. These mice survive well and have normal growth and a bile acid pool size approximately 60% of WT mice. The expression of the genes in the alternative bile acid synthesis pathway are upregulated, resulting in a more hydrophilic bile acid composition with reduced cholic acid (CA). Surprisingly, Cyp7a1(-/-) mice have improved glucose sensitivity with reduced liver triglycerides and fecal bile acid excretion, but increased fecal fatty acid excretion and respiratory exchange ratio (RER) when fed a high-fat/high-cholesterol diet. Supplementing chow and Western diets with CA restored bile acid composition, reversed the glucose tolerant phenotype, and reduced the RER. Our current study points to a critical role of bile acid composition, rather than bile acid pool size, in regulation of glucose, lipid, and energy metabolism to improve glucose and insulin tolerance, maintain metabolic homeostasis, and prevent high-fat diet-induced metabolic disorders.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1194/jlr.M064709" target="_blank" rel="noreferrer noopener">10.1194/jlr.M064709</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).
*bile acids and salt/metabolism
*cholesterol/diet
*Lipids
*Liver
2016
Animal
Animals
Bile Acids and Salts/genetics/metabolism
Boehme Shannon
Chiang John Y L
Cholesterol 7-alpha-Hydroxylase/*genetics/metabolism
Cholesterol/*metabolism
Department of Integrative Medical Sciences
Diet
Disease Models
Exhalation/genetics
Ferrell Jessica M
Glucose/metabolism
High-Fat
Homeostasis
Humans
Journal of lipid research
Li Feng
Lipid Metabolism/genetics
Liver/enzymology/pathology
Metabolic Diseases/*genetics/metabolism
Mice
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/10.1016/j.jcmgh.2015.08.003" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.jcmgh.2015.08.003</a>
Pages
664–677
Issue
6
Volume
1
Dublin Core
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Title
A name given to the resource
Short-term circadian disruption impairs bile acid and lipid homeostasis in mice.
Publisher
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Cellular and molecular gastroenterology and hepatology
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-11
Subject
The topic of the resource
bile acid synthesis; Circadian rhythm; lipid metabolism
Creator
An entity primarily responsible for making the resource
Ferrell Jessica M; Chiang John Y L
Description
An account of the resource
BACKGROUND & AIMS: Bile acids are physiological detergents that also activate nuclear receptors to regulate glucose and lipid homeostasis. Cholesterol 7alpha-hydroxylase (Cyp7a1), the rate-limiting enzyme that converts cholesterol to bile acids, is transcriptionally regulated by bile acids and circadian rhythms. Fasting, nutrients and the circadian clock critically control hepatic bile acid and lipid homeostasis, while circadian misalignment is associated with metabolic syndrome in humans. To delineate these interactions, we employed a sleep disruption model to induce circadian disruption and examined hepatic metabolism with respect to bile acids, lipids and clock gene expression. METHODS: B6xC57 mice were maintained on chow or Western diet and were sleep disrupted for 6 hr/day for 5 days. Mice were sacrificed at 4 hr intervals over 24 hr. Hepatic metabolic genes were examined, and bile acid pool and lipid profiles were measured over 24 hr. RESULTS: Sleep disruption significantly suppressed circadian expression of core clock genes, genes involved in lipid metabolism, and key regulators of Cyp7a1 as well as Cyp7a1 expression itself. Sleep disruption abolished the peak in serum cholesterol and increased liver and serum free fatty acids. Bile acid pool size was increased while liver bile acids were decreased. ChIP assay revealed HNF4alpha and Dbp occupancies were suppressed at the Cyp7a1 promoter in sleep-disrupted mice. When coupled with Western diet, sleep disruption abolished liver clock rhythms and elevated free fatty acids. CONCLUSIONS: This study suggests that even short-term circadian disruption dramatically alters hepatic clock gene expression, bile acid metabolism and lipid homeostasis to contribute to dyslipidemia.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.jcmgh.2015.08.003" target="_blank" rel="noreferrer noopener">10.1016/j.jcmgh.2015.08.003</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).
2015
Bile acid synthesis
Cellular and molecular gastroenterology and hepatology
Chiang John Y L
Circadian Rhythm
Department of Integrative Medical Sciences
Ferrell Jessica M
Lipid Metabolism
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/10.1016/j.bbalip.2014.04.008" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.bbalip.2014.04.008</a>
Pages
19–29
Issue
1
Volume
1851
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
Bile acid signaling in lipid metabolism: metabolomic and lipidomic analysis of lipid and bile acid markers linked to anti-obesity and anti-diabetes in mice.
Publisher
An entity responsible for making the resource available
Biochimica et biophysica acta
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-01
Subject
The topic of the resource
Animals; bile acid metabolism; Bile Acids and Salts/genetics/*metabolism; Cholesterol 7-alpha-Hydroxylase/genetics/metabolism; CYP7A1; Diabetes Mellitus/genetics/*metabolism; Diet; farnesoid X receptor (FXR); Female; Glucose/genetics/metabolism; High-Fat/methods; Homeostasis; Inbred C57BL; Insulin Resistance; Intestinal Mucosa/metabolism; Lipid Metabolism/*physiology; lipidomics; Liver/metabolism; Male; Metabolome/*genetics; Metabolomics/methods; Mice; Obesity/genetics/*metabolism; Rats; Signal Transduction; tauro-beta-muricholic acid; Taurocholic Acid/analogs & derivatives/genetics/metabolism; Transgenic
Creator
An entity primarily responsible for making the resource
Qi Yunpeng; Jiang Changtao; Cheng Jie; Krausz Kristopher W; Li Tiangang; Ferrell Jessica M; Gonzalez Frank J; Chiang John Y L
Description
An account of the resource
Bile acid synthesis is the major pathway for catabolism of cholesterol. Cholesterol 7alpha-hydroxylase (CYP7A1) is the rate-limiting enzyme in the bile acid biosynthetic pathway in the liver and plays an important role in regulating lipid, glucose and energy metabolism. Transgenic mice overexpressing CYP7A1 (CYP7A1-tg mice) were resistant to high-fat diet (HFD)-induced obesity, fatty liver, and diabetes. However the mechanism of resistance to HFD-induced obesity of CYP7A1-tg mice has not been determined. In this study, metabolomic and lipidomic profiles of CYP7A1-tg mice were analyzed to explore the metabolic alterations in CYP7A1-tg mice that govern the protection against obesity and insulin resistance by using ultra-performance liquid chromatography-coupled with electrospray ionization quadrupole time-of-flight mass spectrometry combined with multivariate analyses. Lipidomics analysis identified seven lipid markers including lysophosphatidylcholines, phosphatidylcholines, sphingomyelins and ceramides that were significantly decreased in serum of HFD-fed CYP7A1-tg mice. Metabolomics analysis identified 13 metabolites in bile acid synthesis including taurochenodeoxycholic acid, taurodeoxycholic acid, tauroursodeoxycholic acid, taurocholic acid, and tauro-beta-muricholic acid (T-beta-MCA) that differed between CYP7A1-tg and wild-type mice. Notably, T-beta-MCA, an antagonist of the farnesoid X receptor (FXR) was significantly increased in intestine of CYP7A1-tg mice. This study suggests that reducing 12alpha-hydroxylated bile acids and increasing intestinal T-beta-MCA may reduce high fat diet-induced increase of phospholipids, sphingomyelins and ceramides, and ameliorate diabetes and obesity. This article is part of a Special Issue entitled Linking transcription to physiology in lipodomics.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.bbalip.2014.04.008" target="_blank" rel="noreferrer noopener">10.1016/j.bbalip.2014.04.008</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).
2015
Animals
Bile acid metabolism
Bile Acids and Salts/genetics/*metabolism
Biochimica et biophysica acta
Cheng Jie
Chiang John Y L
Cholesterol 7-alpha-Hydroxylase/genetics/metabolism
CYP7A1
Department of Integrative Medical Sciences
Diabetes Mellitus/genetics/*metabolism
Diet
farnesoid X receptor (FXR)
Female
Ferrell Jessica M
Glucose/genetics/metabolism
Gonzalez Frank J
High-Fat/methods
Homeostasis
Inbred C57BL
Insulin Resistance
Intestinal Mucosa/metabolism
Jiang Changtao
Krausz Kristopher W
Li Tiangang
Lipid Metabolism/*physiology
lipidomics
Liver/metabolism
Male
Metabolome/*genetics
Metabolomics/methods
Mice
NEOMED College of Medicine
Obesity/genetics/*metabolism
Qi Yunpeng
Rats
Signal Transduction
tauro-beta-muricholic acid
Taurocholic Acid/analogs & derivatives/genetics/metabolism
Transgenic
-
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/10.1016/j.apsb.2015.01.003" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.apsb.2015.01.003</a>
Pages
113–122
Issue
2
Volume
5
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
Circadian rhythms in liver metabolism and disease.
Publisher
An entity responsible for making the resource available
Acta pharmaceutica Sinica. B
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-03
Subject
The topic of the resource
ARC; arcuate nucleus; BMAL1; brain and muscle ARNT-like 1; CAR; cholesterol 7alpha-hydroxylase; circadian locomotor output cycles kaput; Circadian rhythm; CLOCK; constitutive androstane receptor; CRY; cryptochrome; CYP7A1; CYPs; cytochrome P450 enzymes; D-site binding protein; DBP; E-box; emergency medical technician; EMT; enhance box; FAA; familial advanced sleep-phase syndrome; farnesoid-X receptor; FASPS; FEO; food anticipatory activity; food entrainable oscillator; forkhead box O3; FOXO3; FXR; G protein-coupled bile acid receptor; glucose transporter 2; GLUT2; HDAC3; hepatic leukemia factor; HIP; histone deacetylase 3; HLF; hypoxia inducing protein; LDL; Liver; liver receptor homolog 1; low-density lipoprotein; LRH1; Metabolic syndrome; NAD+; nicotinamide adenine dinucleotide; PER; period; retinohypothalamic tract; retinoid-related orphan receptor alpha; RHT; ROR-response element; RORalpha; RORE; SCN; SHP; SIRT1; sirtuin 1; small heterodimer partner; suprachiasmatic nucleus; TEF; TGR5; thyrotroph embryonic factor; transcriptional translational feedback loop; TTFL; Type 2 diabetes
Creator
An entity primarily responsible for making the resource
Ferrell Jessica M; Chiang John Y L
Description
An account of the resource
Mounting research evidence demonstrates a significant negative impact of circadian disruption on human health. Shift work, chronic jet lag and sleep disturbances are associated with increased incidence of metabolic syndrome, and consequently result in obesity, type 2 diabetes and dyslipidemia. Here, these associations are reviewed with respect to liver metabolism and disease.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.apsb.2015.01.003" target="_blank" rel="noreferrer noopener">10.1016/j.apsb.2015.01.003</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).
2015
Acta pharmaceutica Sinica. B
ARC
arcuate nucleus
BMAL1
brain and muscle ARNT-like 1
CAR
Chiang John Y L
cholesterol 7alpha-hydroxylase
circadian locomotor output cycles kaput
Circadian Rhythm
CLOCK
constitutive androstane receptor
CRY
cryptochrome
CYP7A1
CYPs
cytochrome P450 enzymes
D-site binding protein
DBP
Department of Integrative Medical Sciences
E-box
emergency medical technician
EMT
enhance box
FAA
familial advanced sleep-phase syndrome
farnesoid-X receptor
FASPS
FEO
Ferrell Jessica M
food anticipatory activity
food entrainable oscillator
forkhead box O3
FOXO3
FXR
G protein-coupled bile acid receptor
glucose transporter 2
GLUT2
HDAC3
hepatic leukemia factor
Hip
histone deacetylase 3
HLF
hypoxia inducing protein
LDL
Liver
liver receptor homolog 1
Low-density lipoprotein
LRH1
Metabolic syndrome
NAD+
NEOMED College of Medicine
nicotinamide adenine dinucleotide
PER
period
retinohypothalamic tract
retinoid-related orphan receptor alpha
RHT
ROR-response element
RORalpha
RORE
SCN
SHP
SIRT1
sirtuin 1
small heterodimer partner
suprachiasmatic nucleus
TEF
TGR5
thyrotroph embryonic factor
transcriptional translational feedback loop
TTFL
Type 2 diabetes
-
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
An entity primarily responsible for making the resource
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
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/hep4.1129" target="_blank" rel="noreferrer noopener">10.1002/hep4.1129</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).
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/hep.30513" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hep.30513</a>
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 both farnesoid X receptor and Takeda G protein-coupled receptor 5 exacerbated liver fibrosis 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
2019
2019-01
Subject
The topic of the resource
Bile acid metabolism; FXR; gene expression; hepatic fibrosis; TGR5
Creator
An entity primarily responsible for making the resource
Ferrell Jessica M; Pathak Preeti; Boehme Shannon; Gilliland Tricia; Chiang John Y L
Description
An account of the resource
Activation of the nuclear bile acid receptor farnesoid X receptor (FXR) protects against hepatic inflammation and injury, while Takeda G protein-coupled receptor 5 (TGR5) promotes adipose tissue browning and energy metabolism. Here, we examined the physiological and metabolic effects of the deficiency of these two bile acid receptors on hepatic metabolism and injury in mice. Fxr/Tgr5 double knockout mice (DKO) were generated for metabolic phenotyping. Male DKO mice fed chow diet had reduced liver lipid levels but increased serum cholesterol levels. Liver Cyp7a1 activity and Cyp8b1 mRNA levels were induced, while ileum FXR target genes were suppressed in DKO mice compared to WT mice. Bile acid pool size was increased in DKO mice, with increased tauro-cholic acid and decreased tauro-muricholic acids. RNA sequencing analysis of the liver transcriptome revealed that bile acid synthesis and fibrosis gene expression levels are increased in chow-fed DKO mice compared to WT mice and the top regulated pathways are involved in steroid/cholesterol biosynthesis, liver cirrhosis and connective tissue disease. Cholestyramine treatment further induced Cyp7a1 mRNA and protein in DKO mice, and increased bile acid pool size, while cholic acid also induced Cyp7a1 in DKO mice, suggesting impaired bile acid feedback regulation. Western diet containing 0.2% cholesterol increased oxidative stress and markers of liver fibrosis, but not hepatic steatosis in DKO mice. In conclusion, FXR and TGR5 play critical roles in protecting the liver from inflammation and fibrosis. Deficiency of both of these bile acid receptors in mice increased cholic acid synthesis and bile acid pool, liver fibrosis and inflammation. FXR and TGR5 double knockout mice may be a novel mouse model for liver fibrosis. This article is protected by copyright. All rights reserved.
Identifier
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<a href="http://doi.org/10.1002/hep.30513" target="_blank" rel="noreferrer noopener">10.1002/hep.30513</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).
2019
Bile acid metabolism
Boehme Shannon
Chiang John Y L
Department of Integrative Medical Sciences
Ferrell Jessica M
FXR
Gene Expression
Gilliland Tricia
hepatic fibrosis
Hepatology (Baltimore, Md.)
NEOMED College of Medicine
Pathak Preeti
TGR5
-
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.29857" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hep.29857</a>
Pages
1574–1588
Issue
4
Volume
68
Dublin Core
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Title
A name given to the resource
Intestine farnesoid X receptor agonist and the gut microbiota activate G-protein bile acid receptor-1 signaling to improve metabolism.
Publisher
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Hepatology (Baltimore, Md.)
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-10
Creator
An entity primarily responsible for making the resource
Pathak Preeti; Xie Cen; Nichols Robert G; Ferrell Jessica M; Boehme Shannon; Krausz Kristopher W; Patterson Andrew D; Gonzalez Frank J; Chiang John Y L
Description
An account of the resource
Bile acids activate farnesoid X receptor (FXR) and G protein-coupled bile acid receptor-1 (aka Takeda G protein-coupled receptor-5 [TGR5]) to regulate bile acid metabolism and glucose and insulin sensitivity. FXR and TGR5 are coexpressed in the enteroendocrine L cells, but their roles in integrated regulation of metabolism are not completely understood. We reported recently that activation of FXR induces TGR5 to stimulate glucagon-like peptide-1 (GLP-1) secretion to improve insulin sensitivity and hepatic metabolism. In this study, we used the intestine-restricted FXR agonist fexaramine (FEX) to study the effect of activation of intestinal FXR on the gut microbiome, bile acid metabolism, and FXR and TGR5 signaling. The current study revealed that FEX markedly increased taurolithocholic acid, increased secretion of fibroblast growth factors 15 and 21 and GLP-1, improved insulin and glucose tolerance, and promoted white adipose tissue browning in mice. Analysis of 16S ribosomal RNA sequences of the gut microbiome identified the FEX-induced and lithocholic acid-producing bacteria Acetatifactor and Bacteroides. Antibiotic treatment completely reversed the
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/hep.29857" target="_blank" rel="noreferrer noopener">10.1002/hep.29857</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).
2018
Boehme Shannon
Chiang John Y L
Department of Integrative Medical Sciences
Ferrell Jessica M
Gonzalez Frank J
Hepatology (Baltimore, Md.)
Krausz Kristopher W
NEOMED College of Medicine
Nichols Robert G
Pathak Preeti
Patterson Andrew D
Xie Cen