The pore-forming subunit MCU of the mitochondrial Ca²⁺ uniporter is required for normal glucose-stimulated insulin secretion in vitro and in vivo in mice.

ABSTRACT:

Aims/hypothesis

Mitochondrial oxidative metabolism is central to glucose-stimulated insulin secretion (GSIS). Whether Ca²⁺ uptake into pancreatic beta cell mitochondria potentiates or antagonises this process is still a matter of debate. Although the mitochondrial Ca²⁺ importer (MCU) complex is thought to represent the main route for Ca²⁺ transport across the inner mitochondrial membrane, its role in beta cells has not previously been examined in vivo.

Methods

Here, we inactivated the pore-forming subunit of the MCU, encoded by Mcu, selectively in mouse beta cells using Ins1^Cre-mediated recombination. Whole or dissociated pancreatic islets were isolated and used for live beta cell fluorescence imaging of cytosolic or mitochondrial

SUBMITTER: Georgiadou E 

PROVIDER: S-EPMC7286857 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature