Eimre 2018 Oxid Med Cell Longev

From Bioblast
Jump to: navigation, search
Publications in the MiPMap
Eimre M, Paju K, Peet N, Kadaja L, Tarrend M, Kasvandik S, Seppet J, Ivask M, Orlova E, Kõks S (2018) Increased mitochondrial protein levels and bioenergetics in the musculus rectus femoris of Wfs1-deficient mice. Oxid Med Cell Longev 2018:3175313.

» PMID: 30584460 Open Access

Eimre M, Paju K, Peet N, Kadaja L, Tarrend M, Kasvandik S, Seppet J, Ivask M, Orlova E, Koks S (2018) Oxid Med Cell Longev

Abstract: Wfs1 deficiency leads to a progressive loss of plasma insulin concentration, which should reduce the consumption of glucose in insulin-dependent tissues, causing a variety of changes in intracellular energy metabolism. Our objective here was to assess the changes in the amount and function of mitochondrial proteins in different muscles of Wfs1-deficient mice. Mitochondrial functions were assayed by high-resolution oxygraphy of permeabilized muscle fibers; the protein amount was evaluated by liquid chromatography tandem mass spectrometry (LC/MS/MS) analysis and mRNA levels of the uncoupler proteins UCP2 and UCP3 by real-time PCR; and citrate synthase (CS) activity was determined spectrophotometrically in muscle homogenates. Compared to controls, there were no changes in proton leak and citrate synthase activity in the heart and m. soleus tissues of Wfs1-deficient mice, but significantly higher levels of both of these factors were observed in the m. rectus femoris; mitochondrial proteins and mRNA of UCP2 were also higher in the m. rectus femoris. ADP-stimulated state 3 respiration was lower in the m. soleus, remained unchanged in the heart, and was higher in the m. rectus femoris. The mitochondrial protein amount and activity are higher in Wfs1-deficient mice, as are mitochondrial proton leak and oxygen consumption in m. rectus femoris. These changes in muscle metabolism may be important for identifying the mechanisms responsible for Wolfram syndrome and diabetes.

Bioblast editor: Plangger M O2k-Network Lab: EE Tartu Paju K

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

Organism: Mouse  Tissue;cell: Skeletal muscle  Preparation: Permeabilized tissue  Enzyme: Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Complex V;ATP synthase 

Coupling state: LEAK, OXPHOS  Pathway: N, S, CIV, ROX  HRR: Oxygraph-2k