1
40
8
-
Text
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URL Address
<a href="http://doi.org/10.1152/ajpendo.00193.2019" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpendo.00193.2019</a>
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Title
A name given to the resource
HDL Flux is Higher in Patients with Nonalcoholic Fatty Liver Disease
Publisher
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American Journal of Physiology. Endocrinology and Metabolism
Date
A point or period of time associated with an event in the lifecycle of the resource
2019
2019-09
Subject
The topic of the resource
haevy water; HDL; NAFLD; NASH; proteomics
October 2019 Update
Creator
An entity primarily responsible for making the resource
McCullough Arthur; Previs Stephen F; Dasarathy Jaividhya; Lee Kwangwon; Osme Abdullah; Kim Chunki; Ilchenko Serguei; Lorkowski Shuhui W; Smith Jonathan D; Dasarathy Srinivasan; Kasumov Takhar
Description
An account of the resource
Altered lipid metabolism and inflammation are involved in the pathogenesis of both non-alcoholic fatty liver disease (NAFLD) and cardiovascular disease (CVD). Even though high-density lipoprotein (HDL), a CVD protective marker, is decreased, whether HDL metabolism and function are perturbed in NAFLD are currently unknown. We examined the effect of NAFLD and disease severity on HDL metabolism and function in patients with biopsy-proven simple steatosis (SS), nonalcoholic steatohepatitis (NASH), and healthy controls. HDL turnover and HDL proteins dynamics in SS (n=7), NASH patients (n=8), and healthy controls (n=9) were studied in vivo. HDL maturation and remodeling, anti-oxidant, cholesterol efflux properties, and activities of lecithin cholesterol ester acyl transferase (LCAT) and cholesterol ester transfer protein (CETP) were quantified using in vitro assays. All NAFLD patients had increased turnover of both HDL cholesterol (HDLc, 0.16±0.09 vs. 0.34±0.18 day-1, P<0.05) and ApoAI (0.26±0.04 vs. 0.34±0.06 day-1, P<0.005) compared to healthy controls. The fractional catabolic rates (FCR) of other HDL proteins, including ApoAII (and ApoAIV were higher (P<0.05) in NAFLD patients who also had higher CETP activity, ApoAI/HDLc ratio (P<0.05). NAFLD-induced alterations were associated with lower antioxidant (114.2±46.6 vs 220.5±48.2 nml/ml●min) but higher total efflux properties of HDL (23.4±1.3 vs. 25.5±2.3 %) (both P<0.05) which was more pronounced in individuals with NASH. However, no differences were observed in either HDL turnover, antioxidant and cholesterol efflux functions of HDL or HDL proteins' turnover between SS and NASH subjects. Thus, HDL metabolism and function are altered in NAFLD without any significant differences between SS and NASH.
Identifier
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<a href="http://doi.org/10.1152/ajpendo.00193.2019" target="_blank" rel="noreferrer noopener">10.1152/ajpendo.00193.2019</a>
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2019
American journal of physiology. Endocrinology and metabolism
Dasarathy Jaividhya
Dasarathy Srinivasan
Department of Pharmaceutical Sciences
haevy water
HDL
Ilchenko Serguei
Kasumov Takhar
Kim Chunki
Lee Kwangwon
Lorkowski Shuhui W
McCullough Arthur
NAFLD
NASH
NEOMED College of Pharmacy
October 2019 Update
Osme Abdullah
Previs Stephen F
proteomics
Smith Jonathan D
-
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/10.2174/1874467208666150817112109" target="_blank" rel="noreferrer noopener">http://doi.org/10.2174/1874467208666150817112109</a>
Pages
226–236
Issue
3
Volume
10
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
Signal Transduction Mechanisms of Alcoholic Fatty Liver Disease: Emer ging Role of Lipin-1.
Publisher
An entity responsible for making the resource available
Current molecular pharmacology
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
1905-7
Subject
The topic of the resource
Humans; Animals; AMP-Activated Protein Kinases/metabolism; Signal Transduction; Lipid Metabolism; Fatty Liver; Liver/metabolism; lipid metabolism; alcoholic fatty liver disease; inflammation; Lipin-1; signal transduction; transcriptional regulators; Phosphatidate Phosphatase/*metabolism; Inflammation/metabolism; Ethanol/chemistry/*metabolism; Sirtuin 1/metabolism; Alcoholic/*metabolism/pathology
Creator
An entity primarily responsible for making the resource
You Min; Jogasuria Alvin; Lee Kwangwon; Wu Jiashin; Zhang Yanqiao; Lee Yoon-Kwang; Sadana Prabodh
Description
An account of the resource
Lipin-1, a mammalian phosphatidic acid phosphatase (PAP), is a bi-functional molecule involved in various signaling pathways via its function as a PAP enzyme in the triglyceride synthesis pathway and in the nucleus as a transcriptional co-regulator. In the liver, lipin-1 is known to play a vital role in controlling the lipid metabolism and inflammation process at multiple regulatory levels. Alcoholic fatty liver disease (AFLD) is one of the earliest forms of liver injury and approximately 8-20% of patients with simple steatosis can develop into more severe forms of liver injury, including steatohepatitis, fibrosis/ cirrhosis, and eventually hepatocellular carcinoma (HCC). The signal transduction mechanisms for alcohol-induced detrimental effects in liver involves alteration of complex and multiple signaling pathways largely governed by a central and upstream signaling system, namely, sirtuin 1 (SIRT1)-AMP activated kinase (AMPK) axis. Emerging evidence suggests a pivotal role of lipin-1 as a crucial downstream regulator of
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.2174/1874467208666150817112109" target="_blank" rel="noreferrer noopener">10.2174/1874467208666150817112109</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
alcoholic fatty liver disease
Alcoholic/*metabolism/pathology
AMP-Activated Protein Kinases/metabolism
Animals
Current molecular pharmacology
Department of Integrative Medical Sciences
Department of Pharmaceutical Sciences
Department of Pharmacy Practice
Ethanol/chemistry/*metabolism
Fatty Liver
Humans
Inflammation
Inflammation/metabolism
Jogasuria Alvin
Lee Kwangwon
Lee Yoon-Kwang
Lipid Metabolism
Lipin-1
Liver/metabolism
NEOMED College of Graduate Studies
NEOMED College of Medicine
NEOMED College of Pharmacy
Phosphatidate Phosphatase/*metabolism
Sadana Prabodh
Signal Transduction
Sirtuin 1/metabolism
transcriptional regulators
Wu Jiashin
You Min
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/jc.2017-01551" target="_blank" rel="noreferrer noopener">http://doi.org/10.1210/jc.2017-01551</a>
Pages
388–396
Issue
2
Volume
103
Dublin Core
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Title
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Glycation Reduces the Stability of ApoAI and Increases HDL Dysfunction in Diet-Controlled Type 2 Diabetes.
Publisher
An entity responsible for making the resource available
The Journal of clinical endocrinology and metabolism
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-02
Subject
The topic of the resource
Adult; Aged; Animal Studies; Animals; Apolipoprotein A-I/blood/*metabolism; Apolipoproteins – Blood; Apolipoproteins – Metabolism; Biochemical Phenomena; Case Control Studies; Case-Control Studies; Cells; Comparative Studies; Cultured; Diabetes Mellitus; Diet; Dyslipidemias/complications/diet therapy/*metabolism; Evaluation Research; Female; Funding Source; Glycosylation; HDL – Metabolism; HDL/*metabolism; Human; Humans; Hyperglycemia – Complications; Hyperglycemia – Diet Therapy; Hyperglycemia – Metabolism; Hyperglycemia/complications/diet therapy/*metabolism; Hyperlipidemia – Complications; Hyperlipidemia – Diet Therapy; Hyperlipidemia – Metabolism; Lipoproteins; Male; Mice; Middle Age; Middle Aged; Multicenter Studies; Protein Stability; Type 2 – Complications; Type 2 – Diet Therapy; Type 2 – Metabolism; Type 2/complications/*diet therapy/metabolism; Validation Studies
Creator
An entity primarily responsible for making the resource
Kashyap Sangeeta R; Osme Abdullah; Ilchenko Serguei; Golizeh Makan; Lee Kwangwon; Wang Shuhui; Bena James; Previs Stephen F; Smith Jonathan D; Kasumov Takhar
Description
An account of the resource
Context: Hyperglycemia plays a key role in the pathogenesis of cardiovascular complications of diabetes. Type 2 diabetes mellitus (T2DM) is associated with high-density lipoprotein (HDL) dysfunction and increased degradation of apolipoprotein I (ApoAI). The mechanism(s) of these changes is largely unknown. Objective: To study the role of hyperglycemia-induced glycation on ApoAI kinetics and stability in patients with diet-controlled T2DM. Design: 2H2O-metabolic labeling approach was used to study ApoAI turnover in patients with diet-controlled T2DM [n = 9 (5 F); 59.3 +/- 8.5 years] and matched healthy controls [n = 8 (4 F); 50.7 +/- 11.6 years]. The effect of Amadori glycation on in vivo ApoAI stability and the antioxidant and cholesterol efflux properties of HDL were assessed using a proteomics approach and in vitro assays. Results: Patients with T2DM had increased turnover of ApoAI and impaired cholesterol efflux and antioxidant properties of HDL. Glycated hemoglobin was negatively correlated with the half-life of ApoAI and cholesterol efflux function of HDL. Proteomics analysis identified several nonenzymatic early (Amadori) glycations of ApoAI at lysine sites. The kinetics analysis of glycated and native ApoAI peptides in patients with T2DM revealed that glycation resulted in a threefold shorter ApoAI half-life. Conclusions: The 2H2O method allowed the detection of early in vivo impairments in HDL metabolism and function that were related to hyperglycemia-induced glycation of ApoAI in T2DM.
Identifier
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<a href="http://doi.org/10.1210/jc.2017-01551" target="_blank" rel="noreferrer noopener">10.1210/jc.2017-01551</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2018
Adult
Aged
Animal Studies
Animals
Apolipoprotein A-I/blood/*metabolism
Apolipoproteins – Blood
Apolipoproteins – Metabolism
Bena James
Biochemical Phenomena
Case Control Studies
Case-Control Studies
Cells
Comparative Studies
Cultured
Department of Pharmaceutical Sciences
Diabetes Mellitus
Diet
Dyslipidemias/complications/diet therapy/*metabolism
Evaluation Research
Female
Funding Source
Glycosylation
Golizeh Makan
HDL – Metabolism
HDL/*metabolism
Human
Humans
Hyperglycemia – Complications
Hyperglycemia – Diet Therapy
Hyperglycemia – Metabolism
Hyperglycemia/complications/diet therapy/*metabolism
Hyperlipidemia – Complications
Hyperlipidemia – Diet Therapy
Hyperlipidemia – Metabolism
Ilchenko Serguei
Kashyap Sangeeta R
Kasumov Takhar
Lee Kwangwon
Lipoproteins
Male
Mice
Middle Age
Middle Aged
Multicenter Studies
NEOMED College of Pharmacy
Osme Abdullah
Previs Stephen F
Protein Stability
Smith Jonathan D
The Journal of clinical endocrinology and metabolism
Type 2 – Complications
Type 2 – Diet Therapy
Type 2 – Metabolism
Type 2/complications/*diet therapy/metabolism
Validation Studies
Wang Shuhui
-
Text
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URL Address
<a href="http://doi.org/10.1074/mcp.RA118.000961" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/mcp.RA118.000961</a>
Pages
2371–2386
Issue
12
Volume
17
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 Mitochondrial Defects in a Nonalcoholic Fatty Liver Disease Mouse Model Are Associated with Increased Degradation of Oxidative Phosphorylation Subunits.
Publisher
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Molecular & cellular proteomics : MCP
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-12
Subject
The topic of the resource
Energy metabolism; heavy water; Mass Spectrometry; metabolic labeling; Mitochondria function or biology; oxidative phosphorylation; Oxidative stress; Protein Degradation; Protein Turnover
Creator
An entity primarily responsible for making the resource
Lee Kwangwon; Haddad Andrew; Osme Abdullah; Kim Chunki; Borzou Ahmad; Ilchenko Sergei; Allende Daniela; Dasarathy Srinivasan; McCullough Arthur; Sadygov Rovshan G; Kasumov Takhar
Description
An account of the resource
Nonalcoholic fatty liver disease (NAFLD) is associated with hepatic mitochondrial dysfunction characterized by reduced ATP synthesis. We applied the (2)H2O-metabolic labeling approach to test the hypothesis that the reduced stability of oxidative phosphorylation proteins contributes to mitochondrial dysfunction in a diet-induced mouse model of NAFLD. A high fat diet containing cholesterol (a so-called Western diet (WD)) led to hepatic oxidative stress, steatosis, inflammation and mild fibrosis, all markers of NAFLD, in low density cholesterol (LDL) receptor deficient (LDLR(-/-)) mice. In addition, compared with controls (LDLR(-/-) mice on normal diet), livers from NAFLD mice had reduced citrate synthase activity and ATP content, suggesting mitochondrial impairment. Proteome dynamics study revealed that mitochondrial defects are associated with reduced average half-lives of mitochondrial proteins in NAFLD mice (5.41 +/- 0.46 versus 5.15 +/- 0.49 day, p \textless 0.05). In particular, the WD reduced stability of oxidative phosphorylation subunits, including cytochrome b-c1 complex subunit 1 (5.9 +/- 0.1 versus 3.4 +/- 0.8 day), ATP synthase subunit alpha (6.3 +/- 0.4 versus 5.5 +/- 0.4 day) and ATP synthase F(0) complex subunit B1 of complex V (8.5 +/- 0.6 versus 6.5 +/- 0.2 day) (p \textless 0.05). These changes were associated with impaired complex III and F0F1-ATP synthase activities. Markers of mitophagy were increased, but proteasomal degradation activity were reduced in NAFLD mice liver, suggesting that ATP deficiency because of reduced stability of oxidative phosphorylation complex subunits contributed to inhibition of ubiquitin-proteasome and activation of mitophagy. In conclusion, the (2)H2O-metabolic labeling approach shows that increased degradation of hepatic oxidative phosphorylation subunits contributed to mitochondrial impairment in NAFLD mice.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1074/mcp.RA118.000961" target="_blank" rel="noreferrer noopener">10.1074/mcp.RA118.000961</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2018
Allende Daniela
Borzou Ahmad
Dasarathy Srinivasan
Department of Pharmaceutical Sciences
Energy Metabolism
Haddad Andrew
Heavy water
Ilchenko Sergei
Kasumov Takhar
Kim Chunki
Lee Kwangwon
Mass spectrometry
McCullough Arthur
metabolic labeling
Mitochondria function or biology
Molecular & cellular proteomics : MCP
NEOMED College of Pharmacy
Osme Abdullah
oxidative phosphorylation
Oxidative Stress
Protein Degradation
Protein Turnover
Sadygov Rovshan G
-
Text
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URL Address
<a href="http://doi.org/10.1021/acs.jproteome.8b00417" target="_blank" rel="noreferrer noopener">http://doi.org/10.1021/acs.jproteome.8b00417</a>
Pages
3740–3748
Issue
11
Volume
17
Dublin Core
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Title
A name given to the resource
d2ome, Software for in Vivo Protein Turnover Analysis Using Heavy Water Labeling and LC-MS, Reveals Alterations of Hepatic Proteome Dynamics in a Mouse Model of NAFLD.
Publisher
An entity responsible for making the resource available
Journal of proteome research
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-11
Subject
The topic of the resource
40S ribosomal proteins; in vivo protein turnover; isotopomer quantification; metabolic labeling; NAFLD; nonlinear least-squares modeling; peak detection and integration; protein half-life; proteome dynamics; UPR
Creator
An entity primarily responsible for making the resource
Sadygov Rovshan G; Avva Jayant; Rahman Mahbubur; Lee Kwangwon; Ilchenko Sergei; Kasumov Takhar; Borzou Ahmad
Description
An account of the resource
Metabolic labeling with heavy water followed by LC-MS is a high throughput approach to study proteostasis in vivo. Advances in mass spectrometry and sample processing have allowed consistent detection of thousands of proteins at multiple time points. However, freely available automated bioinformatics tools to analyze and extract protein decay rate constants are lacking. Here, we describe d2ome-a robust, automated software solution for in vivo protein turnover analysis. d2ome is highly scalable, uses innovative approaches to nonlinear fitting, implements Grubbs' outlier detection and removal, uses weighted-averaging of replicates, applies a data dependent elution time windowing, and uses mass accuracy in peak detection. Here, we discuss the application of d2ome in a comparative study of protein turnover in the livers of normal vs Western diet-fed LDLR(-/-) mice (mouse model of nonalcoholic fatty liver disease), which contained 256 LC-MS experiments. The study revealed reduced stability of 40S ribosomal protein subunits in the Western diet-fed mice.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1021/acs.jproteome.8b00417" target="_blank" rel="noreferrer noopener">10.1021/acs.jproteome.8b00417</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2018
40S ribosomal proteins
Avva Jayant
Borzou Ahmad
Department of Pharmaceutical Sciences
Ilchenko Sergei
in vivo protein turnover
isotopomer quantification
Journal of proteome research
Kasumov Takhar
Lee Kwangwon
metabolic labeling
NAFLD
NEOMED College of Pharmacy
nonlinear least-squares modeling
peak detection and integration
protein half-life
Proteome dynamics
Rahman Mahbubur
Sadygov Rovshan G
UPR
-
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.freeradbiomed.2017.10.373" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.freeradbiomed.2017.10.373</a>
Pages
461–469
Volume
113
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Increased serotransferrin and ceruloplasmin turnover in diet-controlled patients with type 2 diabetes.
Publisher
An entity responsible for making the resource available
Free radical biology & medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-12
Subject
The topic of the resource
*Ceruloplasmin; *Deamidation; *Heavy water metabolic labeling; *High resolution mass spectrometry; *Iron metabolism; *LC-MS/MS; *Non-enzymatic glycation; *Oxidative stress; *Protein Processing; *Proteome dynamics; *Serotransferrin; *Type 2 diabetes mellitus; Adult; Amino Acid Sequence; Case-Control Studies; Ceruloplasmin/genetics/*metabolism; Deuterium/metabolism; Diabetes Mellitus; Diabetic; Diet; Female; Gene Expression Regulation; Glycated Hemoglobin A/genetics/metabolism; Glycosylation; Humans; Iron/*metabolism; Isotope Labeling; Male; Middle Aged; Oxidation-Reduction; Oxidative Stress; Post-Translational; Proteolysis; Transferrin/genetics/*metabolism; Type 2/diet therapy/genetics/*metabolism/pathology
Creator
An entity primarily responsible for making the resource
Golizeh Makan; Lee Kwangwon; Ilchenko Serguei; Osme Abdullah; Bena James; Sadygov Rovshan G; Kashyap Sangeeta R; Kasumov Takhar
Description
An account of the resource
Type 2 diabetes mellitus (T2DM) is associated with oxidative stress and perturbed iron metabolism. Serotransferrin (Trf) and ceruloplasmin (Cp) are two key proteins involved in iron metabolism and anti-oxidant defense. Non-enzymatic glycation and oxidative modification of plasma proteins are known to occur under hyperglycemia and oxidative stress. In this study, shotgun proteomics and (2)H2O-based metabolic labeling were used to characterize post-translational modifications and assess the kinetics of Trf and Cp in T2DM patients and matched controls in vivo. Six early lysine (Amadori) and one advanced arginine glycation were detected in Trf. No glycation, but five asparagine deamidations, were found in Cp. T2DM patients had increased fractional catabolic rates of both Trf and Cp that correlated with HbA1c (p \textless 0.05). The glycated Trf population was subject to an even faster degradation compared to the total Trf pool, suggesting that hyperglycemia contributed to an increased Trf degradation in T2DM patients. Enhanced production of Trf and Cp kept their levels stable. The changes in Trf and Cp turnover were associated with increased systemic oxidative stress without any alteration in iron status in T2DM. These findings can help better understand the potential role of altered Trf and Cp metabolism in the pathogenesis of T2DM and other diseases.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.freeradbiomed.2017.10.373" target="_blank" rel="noreferrer noopener">10.1016/j.freeradbiomed.2017.10.373</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).
*Ceruloplasmin
*Deamidation
*Heavy water metabolic labeling
*High resolution mass spectrometry
*Iron metabolism
*LC-MS/MS
*Non-enzymatic glycation
*Oxidative Stress
*Protein Processing
*Proteome dynamics
*Serotransferrin
*Type 2 diabetes mellitus
2017
Adult
Amino Acid Sequence
Bena James
Case-Control Studies
Ceruloplasmin/genetics/*metabolism
Department of Pharmaceutical Sciences
Deuterium/metabolism
Diabetes Mellitus
Diabetic
Diet
Female
Free radical biology & medicine
Gene Expression Regulation
Glycated Hemoglobin A/genetics/metabolism
Glycosylation
Golizeh Makan
Humans
Ilchenko Serguei
Iron/*metabolism
Isotope Labeling
Kashyap Sangeeta R
Kasumov Takhar
Lee Kwangwon
Male
Middle Aged
NEOMED College of Pharmacy
Osme Abdullah
Oxidation-Reduction
Oxidative Stress
Post-Translational
Proteolysis
Sadygov Rovshan G
Transferrin/genetics/*metabolism
Type 2/diet therapy/genetics/*metabolism/pathology
-
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.freeradbiomed.2016.03.032" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.freeradbiomed.2016.03.032</a>
Pages
13–21
Volume
96
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
A Western diet induced NAFLD in LDLR(-/)(-) mice is associated with reduced hepatic glutathione synthesis.
Publisher
An entity responsible for making the resource available
Free radical biology & medicine
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
*Flux; *Glutathione; *Heavy water; *Mass spectrometer; *NAFLD; *NASH; *Oxidative stress; *Western Diet; Animal; Animals; Antioxidants/metabolism; Diet; Disease Models; Glutathione/blood/*metabolism; Humans; LDL/blood/*genetics/metabolism; Liver/*metabolism/pathology; Mice; Non-alcoholic Fatty Liver Disease/blood/*genetics/pathology; Oxidative Stress/genetics; Receptors; Western/adverse effects
Creator
An entity primarily responsible for making the resource
Li Ling; Zhang Guo-Fang; Lee Kwangwon; Lopez Rocio; Previs Stephen F; Willard Belinda; McCullough Arthur; Kasumov Takhar
Description
An account of the resource
Oxidative stress plays a key role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). Glutathione is the major anti-oxidant involved in cellular oxidative defense, however there are currently no simple non-invasive methods for assessing hepatic glutathione metabolism in patients with NAFLD. As a primary source of plasma glutathione, liver plays an important role in interorgan glutathione homeostasis. In this study, we have tested the hypothesis that measurements of plasma glutathione turnover could be used to assess the hepatic glutathione metabolism in LDLR(-/)(-) mice, a mouse model of diet-induced NAFLD. Mice were fed a standard low fat diet (LFD) or a high fat diet containing cholesterol (a Western type diet (WD)). The kinetics of hepatic and plasma glutathione were quantified using the (2)H2O metabolic labeling approach. Our results show that a WD leads to reduced fractional synthesis rates (FSR) of hepatic (25%/h in LFD vs. 18%/h in WD, P\textless0.05) and plasma glutathione (43%/h in LFD vs. 21%/h in WD, P\textless0.05), without any significant effect on their absolute production rates (PRs). WD-induced concordant changes in both hepatic and plasma glutathione turnover suggest that the plasma glutathione turnover measurements could be used to assess hepatic glutathione metabolism. The safety, simplicity, and low cost of the (2)H2O-based glutathione turnover approach suggest that this method has the potential for non-invasive probing of hepatic glutathione metabolism in patients with NAFLD and other diseases.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.freeradbiomed.2016.03.032" target="_blank" rel="noreferrer noopener">10.1016/j.freeradbiomed.2016.03.032</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).
*Flux
*Glutathione
*Heavy water
*Mass spectrometer
*NAFLD
*NASH
*Oxidative Stress
*Western Diet
2016
Animal
Animals
Antioxidants/metabolism
Department of Pharmaceutical Sciences
Diet
Disease Models
Free radical biology & medicine
Glutathione/blood/*metabolism
Humans
Kasumov Takhar
LDL/blood/*genetics/metabolism
Lee Kwangwon
Li Ling
Liver/*metabolism/pathology
Lopez Rocio
McCullough Arthur
Mice
NEOMED College of Pharmacy
Non-alcoholic Fatty Liver Disease/blood/*genetics/pathology
Oxidative Stress/genetics
Previs Stephen F
Receptors
Western/adverse effects
Willard Belinda
Zhang Guo-Fang
-
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.ajpath.2016.05.006" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.ajpath.2016.05.006</a>
Pages
2417–2428
Issue
9
Volume
186
Dublin Core
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Title
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The Detrimental Role Played by Lipocalin-2 in Alcoholic Fatty Liver in Mice.
Publisher
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The American journal of pathology
Date
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2016
2016-09
Subject
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Alcoholic/*metabolism; Animal; Animals; Blotting; Disease Models; Fatty Liver; Humans; Inbred C57BL; Knockout; Lipocalin-2/*metabolism; Mice; Polymerase Chain Reaction; Western
Creator
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Cai Yan; Jogasuria Alvin; Yin Huquan; Xu Ming-Jiang; Hu Xudong; Wang Jiayou; Kim Chunki; Wu Jiashin; Lee Kwangwon; Gao Bin; You Min
Description
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We have previously shown that the ethanol-mediated elevation of lipocaline-2 (LCN2) is closely associated with the development of alcoholic fatty liver disease (AFLD) in mice. Herein, we aimed to understand the functional significance of LCN2 induction by ethanol and to explore its underlying mechanisms. We evaluated the effects of LCN2 in an in vitro cellular alcoholic steatosis model and in an animal study using wild-type and LCN2 knockout mice fed for 4 weeks with an ethanol-supplemented Lieber-DeCarli diet. In the cellular model of alcoholic steatosis, recombinant LCN2 or overexpression of LCN2 exacerbated ethanol-induced fat accumulation, whereas knocking down LCN2 prevented steatosis in hepatocytes exposed to ethanol. Consistently, removal of LCN2 partially but significantly alleviated alcoholic fatty liver injury in mice. Mechanistically, LCN2 mediates detrimental effects of ethanol in the liver via disrupted multiple signaling pathways, including aberrant nicotinamide phosphoribosyltransferase-sirtuin 1 axis, perturbed endocrine metabolic regulatory fibroblast growth factor 15/19 signaling, and impaired chaperone-mediated autophagy. Finally, compared with healthy human livers, liver samples from patients with AFLD had lower gene expression of several
Identifier
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<a href="http://doi.org/10.1016/j.ajpath.2016.05.006" target="_blank" rel="noreferrer noopener">10.1016/j.ajpath.2016.05.006</a>
Rights
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2016
Alcoholic/*metabolism
Animal
Animals
Blotting
Cai Yan
Department of Pharmaceutical Sciences
Disease Models
Fatty Liver
Gao Bin
Hu Xudong
Humans
Inbred C57BL
Jogasuria Alvin
Kim Chunki
Knockout
Lee Kwangwon
Lipocalin-2/*metabolism
Mice
NEOMED College of Pharmacy
Polymerase Chain Reaction
The American journal of pathology
Wang Jiayou
Western
Wu Jiashin
Xu Ming-Jiang
Yin Huquan
You Min