1
40
3
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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/B978-0-12-404717-4.00005-6" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/B978-0-12-404717-4.00005-6</a>
Pages
157–266
Volume
66
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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Eicosanoids in metabolic syndrome.
Publisher
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Advances in pharmacology (San Diego, Calif.)
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
1905-7
Subject
The topic of the resource
Adipose Tissue; Animals; Eicosanoids/*metabolism; Fatty Liver/etiology/immunology/metabolism; Humans; Immune System/immunology/metabolism; Lipid Metabolism; Metabolic Syndrome/complications/immunology/*metabolism/physiopathology; Non-alcoholic Fatty Liver Disease; Obesity/complications/immunology/metabolism; Sepsis/complications/immunology/metabolism; White/immunology/metabolism
Creator
An entity primarily responsible for making the resource
Hardwick James P; Eckman Katie; Lee Yoon-Kwang; Abdelmegeed Mohamed A; Esterle Andrew; Chilian William M; Chiang John Y; Song Byoung-Joon
Description
An account of the resource
Chronic persistent inflammation plays a significant role in disease pathology of cancer, cardiovascular disease, and metabolic syndrome (MetS). MetS is a constellation of diseases that include obesity, diabetes, hypertension, dyslipidemia, hypertriglyceridemia, and hypercholesterolemia. Nonalcoholic fatty liver disease (NAFLD) is associated with many of the MetS diseases. These metabolic derangements trigger a persistent inflammatory cascade, which includes production of lipid autacoids (eicosanoids) that recruit immune cells to the site of injury and subsequent expression of cytokines and chemokines that amplify the inflammatory response. In acute inflammation, the transcellular synthesis of antiinflammatory eicosanoids resolve inflammation, while persistent activation of the autacoid-cytokine-chemokine cascade in metabolic disease leads to chronic inflammation and accompanying tissue pathology. Many drugs targeting the eicosanoid pathways have been shown to be effective in the treatment of MetS, suggesting a common linkage between inflammation, MetS and drug metabolism. The cross-talk between inflammation and MetS seems apparent because of the growing evidence linking immune cell activation and metabolic disorders such as insulin resistance, dyslipidemia, and hypertriglyceridemia. Thus modulation of lipid metabolism through either dietary adjustment or selective drugs may become a new paradigm in the treatment of metabolic disorders. This review focuses on the mechanisms linking eicosanoid metabolism to persistent inflammation and altered lipid and carbohydrate metabolism in MetS.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/B978-0-12-404717-4.00005-6" target="_blank" rel="noreferrer noopener">10.1016/B978-0-12-404717-4.00005-6</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).
2013
Abdelmegeed Mohamed A
Adipose Tissue
Advances in pharmacology (San Diego, Calif.)
Animals
Chiang John Y
Chilian William M
Department of Integrative Medical Sciences
Eckman Katie
Eicosanoids/*metabolism
Esterle Andrew
Fatty Liver/etiology/immunology/metabolism
Hardwick James P
Humans
Immune System/immunology/metabolism
Lee Yoon-Kwang
Lipid Metabolism
Metabolic Syndrome/complications/immunology/*metabolism/physiopathology
NEOMED College of Medicine
Non-alcoholic Fatty Liver Disease
Obesity/complications/immunology/metabolism
Sepsis/complications/immunology/metabolism
Song Byoung-Joon
White/immunology/metabolism
-
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/bs.apha.2015.04.002" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/bs.apha.2015.04.002</a>
Pages
303–372
Volume
74
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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Translational Implications of the Alcohol-Metabolizing Enzymes, Including Cytochrome P450-2E1, in Alcoholic and Nonalcoholic Liver Disease.
Publisher
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Advances in pharmacology (San Diego, Calif.)
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015
Subject
The topic of the resource
Alcohol-metabolizing enzymes; Alcoholic/*enzymology/*metabolism; ALDH2; Animals; CYP2E1; Cytochrome P-450 CYP2E1/*metabolism; Ethanol/*metabolism; Humans; Liver disease; Liver Diseases; Mitochondrial dysfunction; Nitroxidative stress; Non-alcoholic Fatty Liver Disease/*enzymology/*metabolism; Posttranslational modifications
Creator
An entity primarily responsible for making the resource
Song Byoung-Joon; Akbar Mohammed; Jo Inho; Hardwick James P; Abdelmegeed Mohamed A
Description
An account of the resource
Fat accumulation (hepatic steatosis) in alcoholic and nonalcoholic fatty liver disease is a potentially pathologic condition which can progress to steatohepatitis (inflammation), fibrosis, cirrhosis, and carcinogenesis. Many clinically used drugs or some alternative medicine compounds are also known to cause drug-induced liver injury, which can further lead to fulminant liver failure and acute deaths in extreme cases. During liver disease process, certain cytochromes P450 such as the ethanol-inducible cytochrome P450-2E1 (CYP2E1) and CYP4A isozymes can be induced and/or activated by alcohol and/or high-fat diets and pathophysiological conditions such as fasting, obesity, and diabetes. Activation of these P450 isozymes, involved in the metabolism of ethanol, fatty acids, and various drugs, can produce reactive oxygen/nitrogen species directly and/or indirectly, contributing to oxidative modifications of DNA/RNA, proteins and lipids. In addition, aldehyde dehydrogenases including the mitochondrial low Km aldehyde dehydrogenase-2 (ALDH2), responsible for the metabolism of acetaldehyde and lipid aldehydes, can be inactivated by various hepatotoxic agents. These highly reactive acetaldehyde and lipid peroxides, accumulated due to ALDH2 suppression, can interact with cellular macromolecules DNA/RNA, lipids, and proteins, leading to suppression of their normal function, contributing to DNA mutations, endoplasmic reticulum stress, mitochondrial dysfunction, steatosis, and cell death. In this chapter, we specifically review the roles of the alcohol-metabolizing enzymes including the alcohol dehydrogenase, ALDH2, CYP2E1, and other enzymes in promoting liver disease. We also discuss translational research opportunities with natural and/or synthetic antioxidants, which can prevent or delay the onset of inflammation and liver disease.
Identifier
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<a href="http://doi.org/10.1016/bs.apha.2015.04.002" target="_blank" rel="noreferrer noopener">10.1016/bs.apha.2015.04.002</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
Abdelmegeed Mohamed A
Advances in pharmacology (San Diego, Calif.)
Akbar Mohammed
Alcohol-metabolizing enzymes
Alcoholic/*enzymology/*metabolism
ALDH2
Animals
CYP2E1
Cytochrome P-450 CYP2E1/*metabolism
Department of Integrative Medical Sciences
Ethanol/*metabolism
Hardwick James P
Humans
Jo Inho
Liver disease
Liver Diseases
Mitochondrial dysfunction
NEOMED College of Medicine
Nitroxidative stress
Non-alcoholic Fatty Liver Disease/*enzymology/*metabolism
Posttranslational modifications
Song Byoung-Joon
-
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/10.1155/2009/952734" target="_blank" rel="noreferrer noopener">http://doi.org/10.1155/2009/952734</a>
Pages
952734–952734
Volume
2009
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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PPAR/RXR Regulation of Fatty Acid Metabolism and Fatty Acid omega-Hydroxylase (CYP4) Isozymes: Implications for Prevention of Lipotoxicity in Fatty Liver Disease.
Publisher
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PPAR research
Date
A point or period of time associated with an event in the lifecycle of the resource
2009
1905-07
Creator
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Hardwick James P; Osei-Hyiaman Douglas; Wiland Homer; Abdelmegeed Mohamed A; Song Byoung-Joon
Description
An account of the resource
Fatty liver disease is a common lipid metabolism disorder influenced by the combination of individual genetic makeup, drug exposure, and life-style choices that are frequently associated with metabolic syndrome, which encompasses obesity, dyslipidemia, hypertension, hypertriglyceridemia, and insulin resistant diabetes. Common to obesity related dyslipidemia is the excessive storage of hepatic fatty acids (steatosis), due to a decrease in mitochondria beta-oxidation with an increase in both peroxisomal beta-oxidation, and microsomal omega-oxidation of fatty acids through peroxisome proliferator activated receptors (PPARs). How steatosis increases PPARalpha activated gene expression of fatty acid transport proteins, peroxisomal and mitochondrial fatty acid beta-oxidation and omega-oxidation of fatty acids genes regardless of whether dietary fatty acids are polyunsaturated (PUFA), monounsaturated (MUFA), or saturated (SFA) may be determined by the interplay of PPARs and HNF4alpha with the fatty acid transport proteins L-FABP and ACBP. In hepatic steatosis and steatohepatitis, the omega-oxidation cytochrome P450 CYP4A gene expression is increased even with reduced hepatic levels of PPARalpha. Although numerous studies have suggested the role ethanol-inducible CYP2E1 in contributing to increased oxidative stress, Cyp2e1-null mice still develop steatohepatitis with a dramatic increase in CYP4A gene expression. This strongly implies that CYP4A fatty acid omega-hydroxylase P450s may play an important role in the development of steatohepatitis. In this review and tutorial, we briefly describe how fatty acids are partitioned by fatty acid transport proteins to either anabolic or catabolic pathways regulated by PPARs, and we explore how medium-chain fatty acid (MCFA) CYP4A and long-chain fatty acid (LCFA) CYP4Fomega-hydroxylase genes are regulated in fatty liver. We finally propose a hypothesis that increased CYP4A expression with a decrease in CYP4F genes may promote the progression of steatosis to steatohepatitis.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1155/2009/952734" target="_blank" rel="noreferrer noopener">10.1155/2009/952734</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).
2009
Abdelmegeed Mohamed A
Department of Integrative Medical Sciences
Hardwick James P
NEOMED College of Medicine
Osei-Hyiaman Douglas
PPAR research
Song Byoung-Joon
Wiland Homer