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- W65716239 abstract "AbstractCitrin deficiency is a newly established disease entity involving adult-onset type II citrullinemia (CTLN2), neonatal intrahepatic cholestasis (NICCD), and failure to thrive with dyslipidemia (FTTDCD), all of which are caused by mutations in the SLC25A13 gene. To establish animal model of citrin deficiency, we had to introduce a mouse of a second gene knockout (KO), that of mitochondrial glycerol 3-phosphate dehydrogenase (mGPD) in addition to the Slc25a13 KO, or citrin (Ctrn)-KO. The resultant Ctrn/mGPD double-KO mice presented symptoms such as citrullinemia, hypoglycemia, growth retardation, and hyperammonemia that were enhanced by an enteral administration of sugars, indicative of an animal model of human citrin deficiency. This chapter describes the pathophysiology induced by the administration of sucrose, effects of diet and dietary supplements on the body weight and food intake of the double-KO mice, and possible therapeutic procedures suggested by the results.KeywordsIncrease Food IntakeUrea Cycle DisorderActive Electron Transport SystemCitrin DeficiencySucrose LoadThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves." @default.
- W65716239 created "2016-06-24" @default.
- W65716239 creator A5025837026 @default.
- W65716239 date "2014-01-01" @default.
- W65716239 modified "2023-09-25" @default.
- W65716239 title "An Animal Model of Citrin Deficiency, the Citrin/Mitochondrial Glycerol 3-Phosphate Dehydrogenase Double-Knockout Mouse" @default.
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- W65716239 doi "https://doi.org/10.1007/978-1-4939-0679-6_10" @default.
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