Communications Biology (Jul 2021)

Deletion of the diabetes candidate gene Slc16a13 in mice attenuates diet-induced ectopic lipid accumulation and insulin resistance

  • Tina Schumann,
  • Jörg König,
  • Christian von Loeffelholz,
  • Daniel F. Vatner,
  • Dongyan Zhang,
  • Rachel J. Perry,
  • Michel Bernier,
  • Jason Chami,
  • Christine Henke,
  • Anica Kurzbach,
  • Nermeen N. El-Agroudy,
  • Diana M. Willmes,
  • Dominik Pesta,
  • Rafael de Cabo,
  • John F. O´Sullivan,
  • Eric Simon,
  • Gerald I. Shulman,
  • Bradford S. Hamilton,
  • Andreas L. Birkenfeld

DOI
https://doi.org/10.1038/s42003-021-02279-8
Journal volume & issue
Vol. 4, no. 1
pp. 1 – 17

Abstract

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Schumann et al. demonstrate that the loss of a lactate transporter Slc16a13 increases mitochondrial respiration in the liver, which reduces hepatic lipid accumulation while increasing hepatic insulin sensitivity in mice fed a high-fat diet. This study suggests SLC16A13 as a potential target for the treatment of type 2 diabetes and non-alcoholic fatty liver disease.