1
40
3
-
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/10.3390/ijms21207472" target="_blank" rel="noreferrer noopener">http://doi.org/10.3390/ijms21207472</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).
Issue
20
Volume
21
ISSN
1422-0067 1422-0067
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<a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.3390/ijms21207472" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.3390/ijms21207472</a>
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Update Year & Number
October 2020 List
NEOMED College
NEOMED College of Pharmacy
NEOMED College of Graduate Studies
NEOMED Department
Department of Pharmacy Practice
Department of Pharmaceutical Sciences
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
Early pro-inflammatory remodeling of HDL proteome in a model of diet-induced obesity: 2H2O-metabolic labeling-based kinetic approach.
Publisher
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International Journal of Molecular Sciences
Date
A point or period of time associated with an event in the lifecycle of the resource
2020
2020-10-10
Subject
The topic of the resource
inflammation; NAFLD; proteome dynamics; dyslipidemia; insulin resistance; diet-induced obesity; acute-phase proteins; high-density lipoprotein; high-fat diet
Creator
An entity primarily responsible for making the resource
Sadana P;Lin Li;Aghayev M;Ilchenko S;Kasumov T
Description
An account of the resource
Mice fed a high-fat diet for 12 weeks or longer develop hyperglycemia, insulin resistance, dyslipidemia, and fatty liver. Additionally, a high-fat diet induces inflammation that remodels and affects the anti-inflammatory and antiatherogenic property of the high-density lipoprotein (HDL). However, the precise time course of metabolic disease progression and HDL remodeling remains unclear. Short-term (four weeks) high-fat feeding (60% fat calories) was performed in wild-type male C57BL/6J mice to gain insights into the early metabolic disease processes in conjunction with a HDL proteome dynamics analysis using a heavy water metabolic labeling approach. The high-fat diet-fed mice developed hyperglycemia, impaired glucose tolerance, hypercholesterolemia without hypertriglyceridemia or hepatic steatosis. A plasma HDL proteome dynamics analysis revealed increased turnover rates (and reduced half-lives) of several acute-phase response proteins involved in innate immunity, including complement C3 (12.77 ± 0.81 vs. 9.98 ± 1.20 h, p < 0.005), complement factor B (12.71 ± 1.01 vs. 10.85 ± 1.04 h, p < 0.05), complement Factor H (19.60 ± 1.84 vs. 16.80 ± 1.58 h, p < 0.05), and complement factor I (25.25 ± 1.29 vs. 19.88 ± 1.50 h, p < 0.005). Our findings suggest that an early immune response-induced inflammatory remodeling of the plasma HDL proteome precedes the diet-induced steatosis and dyslipidemia.
Identifier
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<a href="http://doi.org/10.3390/ijms21207472" target="_blank" rel="noreferrer noopener">10.3390/ijms21207472</a>
Format
The file format, physical medium, or dimensions of the resource
journalArticle
2020
acute-phase proteins
Aghayev M
Department of Pharmaceutical Sciences
Department of Pharmacy Practice
diet-induced obesity
dyslipidemia
high-density lipoprotein
High-fat diet
Ilchenko S
Inflammation
Insulin Resistance
International journal of molecular sciences
journalArticle
Kasumov T
Lin Li
NAFLD
NEOMED College of Graduate Studies
NEOMED College of Pharmacy
October 2020 List
Proteome dynamics
Sadana P
-
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.M016048" target="_blank" rel="noreferrer noopener">http://doi.org/10.1194/jlr.M016048</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
2234-2244
Issue
12
Volume
52
Search for Full-text
Locate full-text within NEOMED Library's e-journal collections
<p>Users with a NEOMED Library login can search for full-text journal articles at the following url: <a href="https://libraryguides.neomed.edu/home">https://libraryguides.neomed.edu/home</a></p>
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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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Dissociation of diabetes and obesity in mice lacking orphan nuclear receptor small heterodimer partner
Publisher
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Journal of Lipid Research
Date
A point or period of time associated with an event in the lifecycle of the resource
2011
2011-12
Subject
The topic of the resource
beta-oxidation; Biochemistry & Molecular Biology; birth-weight; diet-induced obesity; fatty-acid oxidation; hepatic steatosis; induced; insulin sensitivity; insulin-resistance; lipid-metabolism; liver; negative feedback-regulation; oxygen consumption; quotient; respiratory; retinoic acid; signaling pathways; skeletal-muscle
Creator
An entity primarily responsible for making the resource
Park Y J; Kim S C; Kim J; Anakk S; Lee J M; Tseng H T; Yechoor V; Park J; Choi J S; Jang H C; Lee K U; Novak C M; Moore D D; Lee Y K
Description
An account of the resource
Mixed background SHP(-/-) mice are resistant to diet-induced obesity due to increased energy expenditure caused by enhanced PGC-1 alpha expression in brown adipocytes. However, congenic SHP(-/-) mice on the C57BL/6 background showed normal expression of PGC-1 alpha and other genes involved in brown adipose tissue thermogenesis. Thus, we reinvestigated the impact of small heterodimer partner (SHP) deletion on diet-induced obesity and insulin resistance using congenic SHP(-/-) mice. Compared with their C57BL/6 wild-type counterparts, SHP(-/-) mice subjected to a 6 month challenge with a Western diet (WestD) were leaner but more glucose intolerant, showed hepatic insulin resistance despite decreased triglyceride accumulation and increased beta-oxidation, exhibited alterations in peripheral tissue uptake of dietary lipids, maintained a higher respiratory quotient, which did not decrease even after WestD feeding, and displayed islet dysfunction. Hepatic mRNA expression analysis revealed that many genes expressed higher in SHP(-/-) mice fed WestD were direct peroxisome proliferator-activated receptor alpha (PPAR alpha) targets. Indeed, transient transfection and chromatin immunoprecipitation verified that SHP strongly repressed PPAR alpha-mediated transactivation. SHP is a pivotal metabolic sensor controlling lipid homeostasis in response to an energy-laden diet through regulating PPAR alpha-mediated transactivation. The resultant hepatic fatty acid oxidation enhancement and dietary fat redistribution protect the mice from diet-induced obesity and hepatic steatosis but accelerate development of type 2 diabetes.-Park, Y. J., S. C. Kim, J. Kim, S. Anakk, J. M. Lee, H-T. Tseng, V. Yechoor, J. Park, J-S. Choi, H. C. Jang, K-U. Lee, C. M. Novak, D. D. Moore, and Y. K. Lee. Dissociation of diabetes and obesity in mice lacking orphan nuclear receptor small heterodimer partner. J. Lipid Res. 2011. 52: 2234-2244.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1194/jlr.M016048" target="_blank" rel="noreferrer noopener">10.1194/jlr.M016048</a>
Format
The file format, physical medium, or dimensions of the resource
Journal Article
2011
Anakk S
beta-oxidation
Biochemistry & Molecular Biology
birth-weight
Choi J S
diet-induced obesity
fatty-acid oxidation
hepatic steatosis
Induced
insulin sensitivity
insulin-resistance
Jang H C
Journal Article
Journal of lipid research
Kim J
Kim S C
Lee J M
Lee K U
Lee Y K
lipid-metabolism
Liver
Moore D D
negative feedback-regulation
Novak C M
Oxygen Consumption
Park J
Park Y J
quotient
respiratory
retinoic acid
signaling pathways
skeletal-muscle
Tseng H T
Yechoor V
-
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
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<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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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
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