Defects in mitophagy promote redox-driven metabolic syndrome in the absence of TP53INP1

@inproceedings{Seillier2015DefectsIM,
  title={Defects in mitophagy promote redox-driven metabolic syndrome in the absence of TP53INP1},
  author={Marion Seillier and Laurent Pouyet and Prudence N'guessan and Marie Nollet and Florence Capo and Fabienne Guillaumond and Laure Peyta and Jean-François Dumas and Annie Varrault and Gyslaine Bertrand and St{\'e}phanie Bonnafous and Albert Tran and Gargi Meur and Piero Marchetti and Magalie A. Ravier and St{\'e}phane Dalle and Philippe Gual and Dany Muller and Guy A Rutter and St{\'e}phane Servais and Juan L Iovanna and Alice Carrier},
  booktitle={EMBO molecular medicine},
  year={2015}
}
The metabolic syndrome covers metabolic abnormalities including obesity and type 2 diabetes (T2D). T2D is characterized by insulin resistance resulting from both environmental and genetic factors. A genome-wide association study (GWAS) published in 2010 identified TP53INP1 as a new T2D susceptibility locus, but a pathological mechanism was not identified. In this work, we show that mice lacking TP53INP1 are prone to redox-driven obesity and insulin resistance. Furthermore, we demonstrate that… CONTINUE READING
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