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• W3107375003 abstract "Mutations in any of the genes encoding the four subunits of succinate dehydrogenase (SDH), a mitochondrial membrane-bound enzyme complex that is involved in both the tricarboxylic acid cycle and the electron transport chain, can lead to a variety of disorders. Recognized conditions with such mutations include Leigh syndrome and hereditary tumors such as pheochromocytoma and paraganglioma (PPGL), renal cell carcinoma, and gastrointestinal stromal tumor. Tumors appear in SDH mutation carriers with dominant inheritance due to loss of heterozygosity in susceptible cells. Here, we describe a mouse model intended to reproduce hereditary PPGL through Cre-mediated loss of SDHC in cells that express tyrosine hydroxylase (TH), a compartment where PPGL is known to originate. We report that while there is modest expansion of TH+ glomus cells in the carotid body upon SDHC loss, PPGL is not observed in such mice, even in the presence of a conditional dominant negative p53 protein and chronic hypoxia. Instead, we report an unexpected phenotype of nondiabetic obesity beginning at about 20 weeks of age. We hypothesize that this obesity is caused by TH+ cell loss or altered phenotype in key compartments of the central nervous system responsible for regulating feeding behavior, coupled with metabolic changes due to loss of peripheral catecholamine production." @default.
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• W3107375003 date "2020-11-27" @default.
• W3107375003 modified "2023-10-18" @default.
• W3107375003 title "Unexpected obesity, rather than tumorigenesis, in a conditional mouse model of mitochondrial complex II deficiency" @default.
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• W3107375003 doi "https://doi.org/10.1096/fj.202002100r" @default.
• W3107375003 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7861419" @default.
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• W3107375003 hasPublicationYear "2020" @default.
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