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dc.contributor.author Meyers, Adrienne F. A. en_US
dc.date.accessioned 2007-05-17T12:39:21Z
dc.date.available 2007-05-17T12:39:21Z
dc.date.issued 1998-08-01T00:00:00Z en_US
dc.identifier.uri http://hdl.handle.net/1993/1524
dc.description.abstract Previous studies have documented that liver/body weight ratios and rates of hepatic DNA synthesis are decreased in a rat model of fetal alcohol syndrome (FAS). In an attempt to determine the mechanism(s) responsible for these findings, rates of liver maturation, liver histology, and the status of the growth hormone (GH)/insulin-like growth factor (IGF)/insulin-like growth factor binding protein (IGFBP) axis were documented in FAS pups during gestation and the post-partum period and compared with control animals. Pregnant Sprague-Dawley rats were fed a liquid diet containing ethanol as 36% of the total calories, an isocaloric control liquid diet, or had ad lib access to the control liquid diet throughout pregnancy. Dams were continued on their respective diets until weaning. Upon weaning, pups were fed control liquid diet until the time of sacrifice. Sacrifices were performed at gestational days 16 and 20 and post-partum days 1, 7, and 40. Albumin, alpha fetoprotein, growth hormone receptor, IGF-1, IGF-II, and IGFBP-1, -2, -3, -4 mRNA were documented at each time point by Northern Blot Analyses. In 40 day old pups, serum glucose, insulin, glucagon and insulin sensitivity were also determined by commercial assays and a rapid insulin sensitivity test (RIST) respectively. (Abstract shortened by UMI.) en_US
dc.format.extent 3706633 bytes
dc.format.extent 184 bytes
dc.format.mimetype application/pdf
dc.format.mimetype text/plain
dc.language en en_US
dc.language.iso en_US
dc.rights info:eu-repo/semantics/openAccess
dc.title Liver maldevelopment in the fetal alcohol syndrome en_US
dc.type info:eu-repo/semantics/masterThesis
dc.degree.discipline Pharmacology & Therapeutics en_US
dc.degree.level Master of Science (M.Sc.) en_US


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