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The effect of tea polyphenols on chronic disease: obesity, the metabolic syndrome, and colon cancer

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Title
The effect of tea polyphenols on chronic disease: obesity, the metabolic syndrome, and colon cancer
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Title
Obesity, the metabolic syndrome, and colon cancer
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Bose
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Mousumi
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Mousumi Bose
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yang
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chung
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chung s yang
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Reddy
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Bandaru S Reddy
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Storch
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Judith
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Judith Storch
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Suh
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Nanjoo
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Advisory Committee
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Nanjoo Suh
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Rutgers University
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degree grantor
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Graduate School - New Brunswick
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theses
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2007
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2007
Language
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English
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electronic
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xvi, 129 pages
Abstract
The prevalence of obesity and the metabolic syndrome has more than doubled in the last 30 years. Colon cancer is the second leading cause of cancer-related death in the United States. Many studies show beneficial effects of certain dietary constituents, including green tea, in the prevention of these diseases. In the first set of experiments, I determined the effect of (-)-epigallocatechin-3-gallate (EGCG) on weight gain and related factors in a high-fat diet-induced mouse model for obesity and the metabolic syndrome. I found that l6-week treatment of 0.32% EGCG in the diet (w/w) significantly reduced body weight gain ([greater than sign]50%) and body fat percentage (by 10%) in comparison to control mice. Visceral fat weight was significantly decreased by EGCG treatment. Biochemical measurements revealed that EGCG treatment significantly attenuated insulin resistance and plasma cholesterol. Liver pathologies were significantly lessened by EGCG, as indicated by decreased liver weight, triglyceride content, and transaminase release into plasma. Plasma monocyte chemoattractant protein (MCP-1) levels were also decreased by EGCG, suggesting reduction of inflammation by EGCG.
In the next set of experiments, I determined the effect of a combination of EGCG (0.16% in the drinking fluid) and fish oil in the diet (12% w/w), on intestinal tumorigenesis in ApcMin/+ mice. Combination treatment reduced tumor number by 53% compared to controls; at the doses used, neither agent alone had a significant effect. β-catenin nuclear positivity in intestinal adenomas from the combination group was lower than control mice, indicating modulation of Wnt signaling. Fish oil and the combination significantly reduced prostaglandin E2 levels in adenomas compared to controls, suggesting modulation of aberrant arachidonic acid metabolism. Akt phosphorylation in adenomas was significantly reduced in all treatment groups, which may have contributed to the observed increase in apoptosis. The results from these two studies indicate that long-term treatment with EGCG decreases risk for obesity and conditions associated with the metabolic syndrome, and that a combination of EGCG and fish oil can inhibit intestinal tumorigenesis in ApcMin/+ mice. These effects may be mediated through multiple mechanisms and should be addressed in future studies in the prevention of chronic disease.
Note (type = degree)
Ph.D.
Note (type = bibliography)
Includes bibliographical references (p. 104-127).
Subject (ID = SUBJ1); (authority = RUETD)
Topic
Nutritional Sciences
Subject (ID = SUBJ2); (authority = ETD-LCSH)
Topic
Plant polyphenols
Subject (ID = SUBJ3); (authority = ETD-LCSH)
Topic
Tea
Subject (ID = SUBJ4); (authority = ETD-LCSH)
Topic
Cancer
Subject (ID = SUBJ5); (authority = ETD-LCSH)
Topic
Obesity
Subject (ID = SUBJ6); (authority = ETD-LCSH)
Topic
Metabolic syndrome
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Graduate School - New Brunswick Electronic Theses and Dissertations
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rucore19991600001
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http://hdl.rutgers.edu/1782.2/rucore10001600001.ETD.15786
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ETD_343
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Identifier (type = doi)
doi:10.7282/T3T72HWK
Genre (authority = ExL-Esploro)
ETD doctoral
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Mousumi Bose
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Rutgers University. Graduate School - New Brunswick
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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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