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

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

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...

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Main Authors: 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
Format: article
Language:EN
Published: Nature Portfolio 2021
Subjects:
Biology (General)
QH301-705.5
Online Access:https://doaj.org/article/7ba53b89a38d4e43a575de6ad202ef08
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Summary: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.

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