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dc.contributor.advisorvom Saal, Frederick S.eng
dc.contributor.authorCoe, Benjamin Lloyd, 1981-eng
dc.date.issued2006eng
dc.date.submitted2006 Springeng
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.eng
dc.descriptionTitle from title screen of research.pdf file viewed on (February 6, 2007)eng
dc.descriptionVita.eng
dc.descriptionIncludes bibliographical references.eng
dc.descriptionThesis (M.A.) University of Missouri-Columbia 2006.eng
dc.descriptionDissertations, Academic -- University of Missouri--Columbia -- Biological sciences.eng
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.eng
dc.identifier.merlin.b57710417eng
dc.identifier.otherCoeB-050506-T5202eng
dc.identifier.urihttp://hdl.handle.net/10355/4636eng
dc.languageEnglisheng
dc.publisherUniversity of Missouri--Columbiaeng
dc.relation.ispartofcollectionUniversity of Missouri--Columbia. Graduate School. Theses and Dissertationseng
dc.source.originalSubmitted by University of Missouri--Columbia Graduate School.eng
dc.subjectendocrine disrupting chemicals.eng
dc.subjectendocrine disrupting chemicalseng
dc.subject.lcshObesityeng
dc.subject.lcshMetabolism -- Disorderseng
dc.subject.lcshFetus -- Developmenteng
dc.subject.lcshFetus -- Growtheng
dc.titleObesity: a growing concern about fetal nutritioneng
dc.typeThesiseng
thesis.degree.disciplineBiological sciences (MU)eng
thesis.degree.grantorUniversity of Missouri--Columbiaeng
thesis.degree.levelMasterseng
thesis.degree.nameM.A.eng


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