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<a href="http://doi.org/10.1152/ajpgi.00343.2015" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpgi.00343.2015</a>
Pages
G799–807
Issue
10
Volume
310
Dublin Core
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Title
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Enhanced ethanol catabolism in orphan nuclear receptor SHP-null mice.
Publisher
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American journal of physiology. Gastrointestinal and liver physiology
Date
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2016
2016-05
Subject
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*acetaldehyde dehydrogenase; *alcoholic fatty liver disease; *inflammation; *small heterodimer partner; Acetates/blood; Alcoholic/genetics/*metabolism; Aldehyde Dehydrogenase; Animals; Cytoplasmic and Nuclear/deficiency/*genetics/metabolism; Ethanol/blood/*metabolism/toxicity; Inbred C57BL; Lipid Peroxidation; Liver Diseases; Liver/drug effects/metabolism; Male; Mice; Mitochondrial/genetics/metabolism; PPAR gamma/genetics/metabolism; Receptors
Creator
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Park Jung Eun; Lee Mikang; Mifflin Ryan; Lee Yoon-Kwang
Description
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Deficiency of the orphan nuclear hormone receptor small heterodimer partner (SHP, NR0B2) protects mice from diet-induced hepatic steatosis, in part, via repression of peroxisome proliferator-activated receptor (PPAR)-gamma2 (Pparg2) gene expression. Alcoholic fatty liver diseases (AFLD) share many common pathophysiological features with non-AFLD. To study the role of SHP and PPARgamma2 in AFLD, we used a strategy of chronic ethanol feeding plus a single binge ethanol feeding to challenge wild-type (WT) and SHP-null (SHP(-/-)) mice with ethanol. The ethanol feeding induced liver fat accumulation and mRNA expression of hepatic Pparg2 in WT mice, which suggests that a high level of PPARgamma2 is a common driving force for fat accumulation induced by ethanol or a high-fat diet. Interestingly, ethanol-fed SHP(-/-) mice displayed hepatic fat accumulation similar to that of ethanol-fed WT mice, even though their Pparg2 expression level remained lower. Mortality of SHP(-/-) mice after ethanol binge feeding was significantly reduced and their acetaldehyde dehydrogenase (Aldh2) mRNA level was higher than that of their WT counterparts. After an intoxicating dose of ethanol, SHP(-/-) mice exhibited faster blood ethanol clearance and earlier wake-up time than WT mice. Higher blood acetate, the end product of ethanol metabolism, and lower acetaldehyde levels were evident in the ethanol-challenged SHP(-/-) than WT mice. Ethanol-induced inflammatory responses and lipid peroxidation were also lower in SHP(-/-) mice. The current data show faster ethanol catabolism and extra fat storage through conversion of acetate to acetyl-CoA before its release into the circulation in this ethanol-feeding model in SHP(-/-) mice.
Identifier
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<a href="http://doi.org/10.1152/ajpgi.00343.2015" target="_blank" rel="noreferrer noopener">10.1152/ajpgi.00343.2015</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).
*acetaldehyde dehydrogenase
*alcoholic fatty liver disease
*Inflammation
*small heterodimer partner
2016
Acetates/blood
Alcoholic/genetics/*metabolism
Aldehyde Dehydrogenase
American journal of physiology. Gastrointestinal and liver physiology
Animals
Cytoplasmic and Nuclear/deficiency/*genetics/metabolism
Department of Integrative Medical Sciences
Ethanol/blood/*metabolism/toxicity
Inbred C57BL
Lee Mikang
Lee Yoon-Kwang
Lipid Peroxidation
Liver Diseases
Liver/drug effects/metabolism
Male
Mice
Mifflin Ryan
Mitochondrial/genetics/metabolism
NEOMED College of Medicine
Park Jung Eun
PPAR gamma/genetics/metabolism
Receptors