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An analysis of the effects of various compounds on alcohol and high-fat-diet-induced steatosis in rats and mice
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Text
TitleInfo
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Title
An analysis of the effects of various compounds on alcohol and high-fat-diet-induced steatosis in rats and mice
SubTitle
PartName
PartNumber
NonSort
Identifier
ETD_1494
Identifier
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http://hdl.rutgers.edu/1782.2/rucore10001600001.ETD.000051061
Language
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eng
Genre
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theses
Subject
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(authority = RUETD)
Topic
Neuroscience
Subject
(ID = SBJ-2);
(authority = ETD-LCSH)
Topic
Alcohol--Physiological effect
Subject
(ID = SBJ-3);
(authority = ETD-LCSH)
Topic
Liver--Diseases
Abstract
Excessive alcohol consumption is known to result in fatty liver, or steatosis. A high-fat, low-carbohydrate diet also results in fatty liver. Furthermore, fatty liver is known to precede cirrhosis in both animals and humans, and cirrhosis precedes primary hepatocellular carcinoma in humans. A series of studies was first undertaken to determine whether exercise and/or certain dietary manipulations could affect fatty liver. Long-Evans rats were given either a high-fat, low-carbohydrate or a high-carbohydrate, low-fat version of liquid diet with or without alcohol. Livers were analyzed for fat and measures of carbohydrate metabolism in liver and plasma were taken, as well as blood glucose alcohol concentrations. Next, added exercise (run wheel), caffeine, antioxidants such as Vitamin E, diphenyl-para-phenylene diamine (DPPD), and selenium were examined as were the dietary additives cranberry powder and soy protein. Finally, based on ambiguous results involving each agent separately, caffeine and DPPD were combined. Following the conclusion of rat studies, C57BL6 mice were given a modified version of the Leiber-deCarli liquid diet with alcohol. The calorie manipulation described above was repeated in mice to determine whether alcohol-induced fatty liver would be exacerbated in the presence of a high-fat diet. Subsequently, the dietary additives Vitamin E, DPPD and Trolox were added. Striatum was taken for HPLC, and livers were taken for liver fat analysis and malondialdehyde (MDA) assay (as a measure of oxidative stress) respectively. Finally, an experiment was undertaken to determine a time course for withdrawal seizures in mice.
In rats, differences in liver glycogen did not account for differences in liver fat. Exercise and caffeine both resulted in significant changes in weight gain, and while combined they appeared to reduce alcohol-induced fatty liver, the effect was not significant. Separately, no protective properties of either exercise or caffeine were observed. Vitamin E and selenium were found to exacerbate alcohol-induced fatty liver, while DPPD did not. Neither cranberry powder nor soy protein affected alcohol-induced fatty liver. DPPD combined with caffeine reduced alcohol-induced fatty liver significantly (p<0.05).
Adult mice were able to tolerate 4.5% ethanol in a high-fat liquid diet. The high-fat diet resulted in liver fat values significantly higher than high-carbohydrate when combined with alcohol. Vitamin E appeared to exacerbate fatty liver in mice, but differences were not significant. There were significant differences in oxidative stress; Vitamin E and Trolox reduced MDA significantly over diet plus alcohol alone. All animals experienced withdrawal seizures between 3 and 5 hours after removal of alcohol. There were significant differences in serotonin turnover (5HIAA/5HT) in animals fed a high-fat diet without alcohol vs. chow controls.
In rats, differences in liver glycogen did not account for differences in liver fat. Exercise and caffeine both resulted in significant changes in weight gain, and while combined they appeared to reduce alcohol-induced fatty liver, the effect was not significant. Separately, no protective properties of either exercise or caffeine were observed. Vitamin E and selenium were found to exacerbate alcohol-induced fatty liver, while DPPD did not. Neither cranberry powder nor soy protein affected alcohol-induced fatty liver. DPPD combined with caffeine reduced alcohol-induced fatty liver significantly (p<0.05).
Adult mice were able to tolerate 4.5% ethanol in a high-fat liquid diet. The high-fat diet resulted in liver fat values significantly higher than high-carbohydrate when combined with alcohol. Vitamin E appeared to exacerbate fatty liver in mice, but differences were not significant. There were significant differences in oxidative stress; Vitamin E and Trolox reduced MDA significantly over diet plus alcohol alone. All animals experienced withdrawal seizures between 3 and 5 hours after removal of alcohol. There were significant differences in serotonin turnover (5HIAA/5HT) in animals fed a high-fat diet without alcohol vs. chow controls.
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electronic resource
Extent
vii, 71 p. : ill.
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Note
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Ph.D.
Note
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Includes bibliographical references (p. 52-60)
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by Bonnie Nolan
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Nolan
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Bonnie
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Bonnie Nolan
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Wagner
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George
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chair
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Advisory Committee
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George C Wagner
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Kusnecov
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Alexander
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internal member
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Advisory Committee
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Alexander Kusnecov
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Martin
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Joseph
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internal member
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Advisory Committee
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Joseph V Martin
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Fisher
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Hans
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outside member
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Advisory Committee
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Hans Fisher
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Rutgers University
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degree grantor
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Graduate School - New Brunswick
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school
OriginInfo
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2009
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2009-01
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NjNbRU
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Title
Rutgers University Electronic Theses and Dissertations
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ETD
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TitleInfo
Title
Graduate School - New Brunswick Electronic Theses and Dissertations
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rucore19991600001
Identifier
(type = doi)
doi:10.7282/T3KS6RS0
Genre
(authority = ExL-Esploro)
ETD doctoral
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The author owns the copyright to this work.
Copyright
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Copyright protected
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Open
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Non-exclusive ETD license
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Author Agreement License
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I hereby grant to the Rutgers University Libraries and to my school the non-exclusive right to archive, reproduce and distribute my thesis or dissertation, in whole or in part, and/or my abstract, in whole or in part, in and from an electronic format, subject to the release date subsequently stipulated in this submittal form and approved by my school. I represent and stipulate that the thesis or dissertation and its abstract are my original work, that they do not infringe or violate any rights of others, and that I make these grants as the sole owner of the rights to my thesis or dissertation and its abstract. I represent that I have obtained written permissions, when necessary, from the owner(s) of each third party copyrighted matter to be included in my thesis or dissertation and will supply copies of such upon request by my school. I acknowledge that RU ETD and my school will not distribute my thesis or dissertation or its abstract if, in their reasonable judgment, they believe all such rights have not been secured. I acknowledge that I retain ownership rights to the copyright of my work. I also retain the right to use all or part of this thesis or dissertation in future works, such as articles or books.
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