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dc.contributor.advisorvom Saal, Frederick S.en
dc.contributor.authorCoe, Benjamin Lloyd, 1981-en_US
dc.date.issued2006eng
dc.date.submitted2006 Springen
dc.descriptionThe entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file.en_US
dc.descriptionTitle from title screen of research.pdf file viewed on (February 6, 2007)en_US
dc.descriptionVita.en_US
dc.descriptionIncludes bibliographical references.en_US
dc.descriptionThesis (M.A.) University of Missouri-Columbia 2006.en_US
dc.descriptionDissertations, Academic -- University of Missouri--Columbia -- Biological sciences.en_US
dc.description.abstractObesity is a growing epidemic and a major health concern in the United States and elsewhere. The Fetal Basis of Adult Disease (FBAD) theory holds that events that occur during development can permanently alter gene expression throughout the lifetime of the individual. A link has emerged between fetal nutrition, birth weight, and metabolic profile in adulthood. Metabolic diseases represent a host of conditions relating to abnormal "programming" of nutrient management. We have developed a CD-1 mouse model which shows that fetuses within two body weight ranges at birth are at increased risk for developing metabolic diseases such as obesity, hypertension, cardiovascular disease, and Type II diabetes. It is not just individuals that are born with abnormally high birth weights (macrosomia) that are at risk for becoming overweight later in life. Paradoxically, this risk also applies for individuals who are born with extremely low birth weights, which are termed intrauterine growth restricted (IUGR). Mice identified with IUGR at birth show a dramatic increase in body weight during the first week post-weaning, which results in adult obesity and an altered metabolic profile for the remainder of their adult life. Preliminary studies indicate that when examined in adulthood, adipocytes in males identified with IUGR or macrosomia at birth showed evidence of differences in "programming" of expression of genes involved in fat cell differentiation and function. Certain xenoestrogens in the environment are known to interrupt the process of cell differentiation. Utilizing this model, we will be able to test the effects of these chemicals on individuals that already have a metabolic deficit. By examining the relationship of fetal nutrition and growth with endocrine disruption, greater evidence may emerge for the need of regulation of endocrine disrupting chemicals.en_US
dc.identifier.merlin.b57710417en_US
dc.identifier.otherCoeB-050506-T5202en_US
dc.identifier.urihttp://hdl.handle.net/10355/4636
dc.publisherUniversity of Missouri--Columbiaen_US
dc.relation.ispartof2006 Freely available theses (MU)en_US
dc.relation.ispartofcommunityUniversity of Missouri-Columbia. Graduate School. Theses and Dissertations. Theses. 2006 Theses
dc.subjectendocrine disrupting chemicals.en_US
dc.subjectendocrine disrupting chemicalsen_US
dc.subject.lcshObesityen_US
dc.subject.lcshMetabolism -- Disordersen_US
dc.subject.lcshFetus -- Developmenten_US
dc.subject.lcshFetus -- Growthen_US
dc.titleObesity: a growing concern about fetal nutritionen_US
dc.typeThesisen_US
thesis.degree.disciplineBiological scienceseng
thesis.degree.grantorUniversity of Missouri--Columbiaeng
thesis.degree.levelMastersen_US
thesis.degree.nameM.A.en_US


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