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- W419785099 abstract "Several lines of evidence suggest that CFTR (the gene defective in cystic fibrosis) plays a role in proper development of the intestine. To analyze temporal aspects of CFTR requirement for post-natal phenotype, we transiently suppressed CFTR expression in the intestine of rat fetuses using antisense in utero gene therapy. Depending on the gestational age of the fetus, transient reduction of CFTR function resulted in phenotypes ranging from meconium ileus and subsequent death to obesity. Of particular interest are animals treated during day 17 (E17) of embryonic development. After birth, these animals display dysregulated production of hormones and neuropeptides responsible for promoting satiety, leading to increased food intake and excess body fat. We also observed significant peripheral tissue resistance to insulin, as indicated by clamp studies. Microarray analysis showed changes in gene expression in the intestine both before and after birth, and the results were confirmed by immunofluorescent staining. These data demonstrate that weight gain and insulin resistance in adults can result solely from subtle changes in gene expression during gestation expression during intestinal development results in a metabolic syndrome in the adult animal." @default.
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- W419785099 date "2009-04-01" @default.
- W419785099 modified "2023-09-23" @default.
- W419785099 title "Disruption of Development in the Intestinal Epithelium Leads to a Metabolic Syndrome in Adult Rats" @default.
- W419785099 doi "https://doi.org/10.1096/fasebj.23.1_supplement.473.2" @default.
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