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Vigueira 2014 Cell Rep

From Bioblast
Publications in the MiPMap
Vigueira PA, McCommis KS, Schweitzer GG, Remedi MS, Chambers KT, Fu X, McDonald WG, Cole SL, Colca JR, Kletzien RF, Burgess SC, Finck BN (2014) Mitochondrial pyruvate carrier 2 hypomorphism in mice leads to defects in glucose-stimulated insulin secretion. Cell Rep 7:2042-53.

Β» PMID: 24910426

Vigueira PA, McCommis KS, Schweitzer GG, Remedi MS, Chambers KT, Fu X, McDonald WG, Cole SL, Colca JR, Kletzien RF, Burgess SC, Finck BN (2014) Cell Rep

Abstract: Carrier-facilitated pyruvate transport across the inner mitochondrial membrane plays an essential role in anabolic and catabolic intermediary metabolism. Mitochondrial pyruvate carrier 2 (Mpc2) is believed to be a component of the complex that facilitates mitochondrial pyruvate import. Complete MPC2 deficiency resulted in embryonic lethality in mice. However, a second mouse line expressing an N-terminal truncated MPC2 protein (Mpc2Ξ”16) was viable but exhibited a reduced capacity for mitochondrial pyruvate oxidation. Metabolic studies demonstrated exaggerated blood lactate concentrations after pyruvate, glucose, or insulin challenge in Mpc2Ξ”16 mice. Additionally, compared with wild-type controls, Mpc2Ξ”16 mice exhibited normal insulin sensitivity but elevated blood glucose after bolus pyruvate or glucose injection. This was attributable to reduced glucose-stimulated insulin secretion and was corrected by sulfonylurea KATP channel inhibitor administration. Collectively, these data are consistent with a role for MPC2 in mitochondrial pyruvate import and suggest that Mpc2 deficiency results in defective pancreatic Ξ² cell glucose sensing.


β€’ O2k-Network Lab: US MO St Louis Finck B


Labels: MiParea: Respiration 

Stress:Mitochondrial disease  Organism: Mouse  Tissue;cell: Heart, Kidney  Preparation: Isolated mitochondria 


Coupling state: ET  Pathway: N, S  HRR: Oxygraph-2k