1
40
6
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Hyperlink
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URL
https://doi.org/10.1016/j.jbc.2023.103070
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
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My lifelong dedication to bile acid research
Creator
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JohnY L Chiang
Date
A point or period of time associated with an event in the lifecycle of the resource
2023
Description
An account of the resource
It is a great honor to be invited to write a reflection of my lifelong bile acid research for the Journal of Biological Chemistry, the premier biochemistry journal in which I am proud to have published 24 manuscripts. I published 21 manuscripts in the Journal of Lipid Research, also a journal of American Society of Biochemistry and Molecular Biology. I started my reflection from my early education in Taiwan, my coming to America for graduate study, my postdoctoral training in cytochrome P450 research, and my lifelong bile acid research career at the not so "visible" Northeast Ohio Medical University. I have witnesses and help to transform this sleepy rural medical school to a well-funded powerhouse in liver research. Writing this reflection of my long, exciting, and rewarding journey in bile acid research brought back many good memories. I am proud of my scientific contribution. I attribute my lifelong academic success to working hard, perseverance, good mentoring, and networking. I hope that this reflection of my academic career may provide guidance to younger investigators who are pursuing academic teaching and research and might inspire the next generation of researchers in biochemistry and metabolic diseases.
Source
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J Biol Chem
. 2023 Feb 24;103070. doi: 10.1016/j.jbc.2023.103070. Online ahead of print.
Language
A language of the resource
English.
2023
Bile acid synthesis
cholesterol 7α-hydroxylase
CYP7A1
FXR
metabolism and regulation
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/10.1016/s1388-1981(02)00186-5" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/s1388-1981(02)00186-5</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
63-73
Issue
1
Volume
1583
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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
On the mechanism of bile acid inhibition of rat sterol 12 alpha-hydroxylase gene (CYP8B1) transcription: roles of alpha-fetoprotein transcription factor and hepatocyte nuclear factor 4 alpha
Publisher
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Biochimica Et Biophysica Acta-Molecular and Cell Biology of Lipids
Date
A point or period of time associated with an event in the lifecycle of the resource
2002
2002-06
Subject
The topic of the resource
activation; bile acid synthesise; Biochemistry & Molecular Biology; Biophysics; biosynthesis; Cell Biology; cholesterol 7-alpha-hydroxylase gene; Cyp7a1; cytochrome P450; expression; feedback-regulation; gene regulation; liver microsomal metabolism; nuclear receptor; promoter; receptor; repression
Creator
An entity primarily responsible for making the resource
Yang Y Z; Zhang M; Eggertsen G; Chiang J Y L
Description
An account of the resource
The sterol 12alpha-hydroxylase (CYP8B1) is a key enzyme of the bile acid biosynthetic pathway. It regulates the composition of bile acids in bile, i.e. ratio between cholic acid (CA) and chenodeoxycholic acid (CDCA). In similarity with cholesterol 7alpha-hydroxylase (CYP7A1), this enzyme is subjected to a negative feedback regulation by bile acids, It has been recently reported that bile acid-activated famesoid X receptor (FXR) induces the small heterodimer partner (SHP) that interacts with alpha-fetoprotein transcription factor (FTF) and down-regulates CYP7A1 transcription. We studied whether the same mechanism also regulated rat CYP8B1 gene transcription. Feeding rats with CDCA caused a 40-50% decrease of CYP8B1 and hepatocyte nuclear factor 4alpha (HNF4alpha) mRNA expression levels. This was associated with an increase in FTF mRNA expression, but SHP mRNA expression was not altered. Electrophoretic mobility shift assay (EMSA) and transient transfection assay of promoter/reporter genes coupled to mutagenesis analysis identified a putative bile acid response element (BARE) that has an HNF4alpha binding site embedded in two overlapping FTF binding sites. Mutation of the HNF4alpha binding site markedly reduced basal promoter activity and its repression by bile acids. Cotransfection with FTF strongly repressed CYP8B1 transcription. Interestingly, HNF4alpha could overcome the inhibitory effects of FTF and bile acids. We conclude that FTF and HNF4alpha not only play critical roles on CYP8B1 gene transcription, but also mediate bile acid feedback inhibition. This study reveals a novel mechanism by which bile acids inhibit rat CYP8B1 gene transcription by inducing FTF and inhibiting HNF4alpha expression. (C) 2002 Elsevier Science B.V. All rights reserved.
Identifier
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<a href="http://doi.org/10.1016/s1388-1981(02)00186-5" target="_blank" rel="noreferrer noopener">10.1016/s1388-1981(02)00186-5</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2002
activation
bile acid synthesise
Biochemistry & Molecular Biology
Biochimica Et Biophysica Acta-Molecular and Cell Biology of Lipids
Biophysics
biosynthesis
Cell Biology
Chiang J Y L
cholesterol 7-alpha-hydroxylase gene
CYP7A1
cytochrome P450
Eggertsen G
expression
feedback-regulation
Gene Regulation
Journal Article
liver microsomal metabolism
Nuclear Receptor
promoter
Receptor
repression
Yang Y Z
Zhang M
-
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/10.1093/toxsci/kfy031" target="_blank" rel="noreferrer noopener">http://doi.org/10.1093/toxsci/kfy031</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
265-278
Issue
1
Volume
163
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
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Dublin Core
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Title
A name given to the resource
Bile Acid Sequestration by Cholestyramine Mitigates FGFR4 Inhibition-Induced ALT Elevation
Publisher
An entity responsible for making the resource available
Toxicological Sciences
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-05
Subject
The topic of the resource
7alpha-hydroxy-4-cholesten-3-one; aminotransferase; aspartate-aminotransferase isozymes; bile acids; Cyp7a1; FGF19; fibroblast-growth-factor; fibroblast-growth-factor; hepatocellular carcinoma; identification; induced liver-injury; Klotho beta; lipophilicity; liver injury; mitigation; nuclear receptor; serum; sinusoidal endothelial-cells; suppression; tgr5; Toxicology
Creator
An entity primarily responsible for making the resource
Schadt H S; Wolf A; Mahl J A; Wuersch K; Couttet P; Schwald M; Fischer A; Lienard M; Emotte C; Teng C H; Skuba E; Richardson T A; Manenti L; Weiss A; Porta D G; Fairhurst R A; Kullak-Ublick G A; Chibout S D; Pognan F; Kluwe W; Kinyamu-Akunda J
Description
An account of the resource
The FGF19- fibroblast growth factor receptor (FGFR4)-beta Klotho (KLB) pathway plays an important role in the regulation of bile acid (BA) homeostasis. Aberrant activation of this pathway has been described in the development and progression of a subset of liver cancers including hepatocellular carcinoma, establishing FGFR4 as an attractive therapeutic target for such solid tumors. FGF401 is a highly selective FGFR4 kinase inhibitor being developed for hepatocellular carcinoma, currently in phase I/II clinical studies. In preclinical studies in mice and dogs, oral administration of FGF401 led to induction of Cyp7a1., elevation of its peripheral marker 7alpha-hydroxy-4-cholesten-3-one, increased BA pool size, decreased serum cholesterol and diarrhea in dogs. FGF401 was also associated with increases of serum aminotransferases, primarily alanine aminotransferase (ALT), in the absence of any observable adverse histopathological findings in the liver, or in any other organs. We hypothesized that the increase in ALT could be secondary to increased BAs and conducted an investigative study in dogs with FGF401 and coadministration of the BA sequestrant cholestyramine (CHO). CHO prevented and reversed FGF401-related increases in ALT in dogs in parallel to its ability to reduce BAs in the circulation. Correlation analysis showed that FGF401-mediated increases in ALT strongly correlated with increases in taurolithocholic acid and taurodeoxycholic acid, the major secondary BAs in dog plasma, indicating a mechanistic link between ALT elevation and changes in BA pool hydrophobicity. Thus, CHO may offer the potential to mitigate elevations in serum aminotransferases in human subjects that are caused by targeted FGFR4 inhibition and elevated intracellular BA levels.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1093/toxsci/kfy031" target="_blank" rel="noreferrer noopener">10.1093/toxsci/kfy031</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2018
7alpha-hydroxy-4-cholesten-3-one
aminotransferase
aspartate-aminotransferase isozymes
BILE acids
Chibout S D
Couttet P
CYP7A1
Emotte C
Fairhurst R A
FGF19
fibroblast-growth-factor
Fischer A
Hepatocellular carcinoma
identification
induced liver-injury
Journal Article
Kinyamu-Akunda J
Klotho beta
Kluwe W
Kullak-Ublick G A
Lienard M
lipophilicity
Liver injury
Mahl J A
Manenti L
mitigation
Nuclear Receptor
Pognan F
Porta D G
Richardson T A
Schadt H S
Schwald M
serum
sinusoidal endothelial-cells
Skuba E
suppression
Teng C H
TGR5
Toxicological Sciences
Toxicology
Weiss A
Wolf A
Wuersch K
-
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.2016.10.002" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.jcmgh.2016.10.002</a>
Pages
245–260
Issue
2
Volume
3
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 the Enterohepatic Bile Acid Signaling Induces Hepatic Autophagy via a
Publisher
An entity responsible for making the resource available
Cellular and molecular gastroenterology and hepatology
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-03
Subject
The topic of the resource
4EBP-1; ACAT; acyl-CoA:cholesterol acyltransferase; CE; chloroquine; Cholesterol; cholesterol 7alpha-hydroxylase; cholesterol ester; cholestyramine; Cholestyramine; ChTM; CQ; CYP7A1; diet-induced obesity; DIO; endoplasmic reticulum; ER; eukaryotic translation initiation factor 4E-binding protein 1; Fatty Liver; FC; free cholesterol; glycogen synthase kinase 3beta; GSK3beta; HMG-CoA reductase; HMGCR; LC3; LDLR; LMP; low-density lipoprotein receptor; lysosome membrane permeabilization; messenger RNA; microtubule-associated protein 1A/1B-light chain 3; mRNA; mTOR; Nuclear Receptor; phosphatidylinositol; PI; plasma membrane; PM; S6; SREBP; sterol response element binding protein; the nutrient sensing mechanistic target of rapamycin; tibosomal protein S6
Creator
An entity primarily responsible for making the resource
Wang Yifeng; Ding Yifeng; Li Jibiao; Chavan Hemantkumar; Matye David; Ni Hong-Min; Chiang John Y L; Krishnamurthy Partha; Ding Wen-Xing; Li Tiangang
Description
An account of the resource
BACKGROUND & AIMS: Hepatic cholesterol accumulation and autophagy defects contribute to hepatocyte injury in fatty liver disease. Bile acid synthesis is a major pathway for cholesterol catabolism in the liver. This study aims to understand the molecular link between cholesterol and bile acid metabolism and hepatic autophagy activity. METHODS: The effects of cholesterol and cholesterol 7alpha-hydroxylase (CYP7A1) expression on autophagy and lysosome function were studied in cell models. The effects and mechanism of disrupting enterohepatic bile acid circulation on hepatic autophagy were studied in mice. RESULTS: The results first showed differential regulation of hepatic autophagy by free cholesterol and cholesterol ester, whereby a modest increase of cellular free cholesterol, but not cholesterol ester, impaired lysosome function and caused marked autolysosome accumulation. We found that CYP7A1 induction, either by cholestyramine feeding in mice or adenovirus-mediated CYP7A1 expression in hepatocytes, caused strong autophagy induction. Mechanistically, we showed that CYP7A1 expression markedly attenuated growth factor/AKT signaling activation of mechanistic target of rapamycin (mTOR), but not amino acid signaling to mTOR in vitro and in vivo. Metabolomics analysis further found that CYP7A1 induction not only decreased hepatic cholesterol but also altered phospholipid and sphingolipid compositions. Collectively, these results suggest that CYP7A1 induction interferes with growth factor activation of AKT/mTOR signaling possibly by altering membrane lipid composition. Finally, we showed that cholestyramine feeding restored impaired hepatic autophagy and improved metabolic homeostasis in Western diet-fed mice. CONCLUSIONS: This study identified a novel CYP7A1-AKT-mTOR signaling axis that selectively induces hepatic autophagy, which helps improve hepatocellular integrity and metabolic homeostasis.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.jcmgh.2016.10.002" target="_blank" rel="noreferrer noopener">10.1016/j.jcmgh.2016.10.002</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).
2017
4EBP-1
ACAT
acyl-CoA:cholesterol acyltransferase
CE
Cellular and molecular gastroenterology and hepatology
Chavan Hemantkumar
Chiang John Y L
chloroquine
Cholesterol
cholesterol 7alpha-hydroxylase
cholesterol ester
Cholestyramine
ChTM
CQ
CYP7A1
Department of Integrative Medical Sciences
diet-induced obesity
Ding Wen-Xing
Ding Yifeng
DIO
endoplasmic reticulum
ER
eukaryotic translation initiation factor 4E-binding protein 1
Fatty Liver
FC
free cholesterol
glycogen synthase kinase 3beta
GSK3beta
HMG-CoA reductase
HMGCR
Krishnamurthy Partha
LC3
LDLR
Li Jibiao
Li Tiangang
LMP
low-density lipoprotein receptor
lysosome membrane permeabilization
Matye David
messenger RNA
microtubule-associated protein 1A/1B-light chain 3
mRNA
mTOR
NEOMED College of Medicine
Ni Hong-Min
Nuclear Receptor
phosphatidylinositol
PI
plasma membrane
PM
S6
SREBP
sterol response element binding protein
the nutrient sensing mechanistic target of rapamycin
tibosomal protein S6
Wang Yifeng
-
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>
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).
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>
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).
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