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dc.creatorStine, Christina Nicole
dc.date.accessioned2012-06-07T23:09:20Z
dc.date.available2012-06-07T23:09:20Z
dc.date.created2001
dc.date.issued2001
dc.identifier.urihttps://hdl.handle.net/1969.1/ETD-TAMU-2001-THESIS-S7453
dc.descriptionDue to the character of the original source materials and the nature of batch digitization, quality control issues may be present in this document. Please report any quality issues you encounter to digital@library.tamu.edu, referencing the URI of the item.en
dc.descriptionIncludes bibliographical references (leaves 41-53).en
dc.descriptionIssued also on microfiche from Lange Micrographics.en
dc.description.abstractAlcohol consumption is occurring in the younger generation. It has been found that the sooner people started drinking the shorter they are. Alcohol has also been shown to reduce peak bone mass. Alcohol inhibits osteoblastic proliferation which is known to be regulated by insulin-like growth factor-I (IGF-I). This study was designed to determine if systemic and local IGF-I production is affected by alcohol consumption in a rat animal model. Experimental treatments included three groups; an alcohol-fed group, a pair-fed group that was matched in energy intake to the alcohol-fed group, and a pellet-fed group that was maintained on standard rat pellets for two weeks. Food was administered according to the Lieber-Decarli technique of ethanol administration, with alcohol-fed rats receiving 35% ethanol-derived calories and the pair-fed group receiving maltose-dextrin in substitute for ethanol. Both tibias and part of the liver were removed for analysis after 2-weeks on the diets. IGF-I mRNA in the liver and bone and IGF-I protein in plasma and bone were analyzed. There was a significant difference among all groups in their weight at sacrifice and percent weight change with the alcohol-fed group having the lowest weight. There was a significant reduction in plasma IGF-I in the alcohol-fed group with respect to the other two groups. No significant differences were found in bone IGF-I mRNA, liver mRNA, and bone IGF-I. The energy requirement for alcohol oxidation by the microsomal oxidase system may explain the alcohol-fed rats inability to gain weight. While IGF-I mRNA in the liver did not decrease significantly in response to ethanol, had this study been carried out longer a decrease might have been observed. Insulin-like growth factor binding protein (IGFBP)-1 has been shown to be increased in plasma in rats fed alcohol. This would increase IGF-I clearance to the tissues, lowering plasma IGF-I. This may explain why plasma IGF-I decreased while liver mRNA (main source of circulating IGF-I) did not. Many other factors also contribute to IGF-I production by bone. IGF-I is a complex system with many factors involved.en
dc.format.mediumelectronicen
dc.format.mimetypeapplication/pdf
dc.language.isoen_US
dc.publisherTexas A&M University
dc.rightsThis thesis was part of a retrospective digitization project authorized by the Texas A&M University Libraries in 2008. Copyright remains vested with the author(s). It is the user's responsibility to secure permission from the copyright holder(s) for re-use of the work beyond the provision of Fair Use.en
dc.subjectnutrition.en
dc.subjectMajor nutrition.en
dc.titleAnalyzing the effects of alcohol on IGF-I in bone and plasma and on IGF-I mRNA in the liver and boneen
dc.typeThesisen
thesis.degree.disciplinenutritionen
thesis.degree.nameM.S.en
thesis.degree.levelMastersen
dc.type.genrethesisen
dc.type.materialtexten
dc.format.digitalOriginreformatted digitalen


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