Schumann 2021 Commun Biol

From Bioblast
Publications in the MiPMap
Schumann T, Koenig J, von Loeffelholz C, Vatner DF, Zhang D, Perry RJ, Bernier M, Chami J, Henke C, Kurzbach A, El-Agroudy NN, Willmes DM, Pesta D, de Cabo R, O Sullivan JF, Simon E, Shulman GI, Hamilton BS, Birkenfeld AL (2021) Deletion of the diabetes candidate gene Slc16a13 in mice attenuates diet-induced ectopic lipid accumulation and insulin resistance. Commun Biol 4:826.

Β» PMID: 34211098 Open Access

Schumann Tina, Koenig Joerg, von Loeffelholz Christian, Vatner Daniel F, Zhang Dongyan, Perry Rachel J, Bernier Michel, Chami Jason, Henke Christine, Kurzbach Anica, El-Agroudy Nermeen N, Willmes Diana M, Pesta Dominik, de Cabo Rafael, Sullivan John F O, Simon Eric, Shulman Gerald I, Hamilton Bradford S, Birkenfeld Andreas L (2021) Commun Biol

Abstract: Genome-wide association studies have identified SLC16A13 as a novel susceptibility gene for type 2 diabetes. The SLC16A13 gene encodes SLC16A13/MCT13, a member of the solute carrier 16 family of monocarboxylate transporters. Despite its potential importance to diabetes development, the physiological function of SLC16A13 is unknown. Here, we validate Slc16a13 as a lactate transporter expressed at the plasma membrane and report on the effect of Slc16a13 deletion in a mouse model. We show that Slc16a13 increases mitochondrial respiration in the liver, leading to reduced hepatic lipid accumulation and increased hepatic insulin sensitivity in high-fat diet fed Slc16a13 knockout mice. We propose a mechanism for improved hepatic insulin sensitivity in the context of Slc16a13 deficiency in which reduced intrahepatocellular lactate availability drives increased AMPK activation and increased mitochondrial respiration, while reducing hepatic lipid content. Slc16a13 deficiency thereby attenuates hepatic diacylglycerol-PKCΞ΅ mediated insulin resistance in obese mice. Together, these data suggest that SLC16A13 is a potential target for the treatment of type 2 diabetes and non-alcoholic fatty liver disease.

β€’ Bioblast editor: Plangger M β€’ O2k-Network Lab: DE Duesseldorf Roden M

Labels: MiParea: Respiration, Genetic knockout;overexpression  Pathology: Diabetes 

Organism: Mouse  Tissue;cell: Liver  Preparation: Intact cells 

Coupling state: LEAK, ROUTINE, OXPHOS, ET  Pathway: F, N, NS, ROX  HRR: Oxygraph-2k 


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