Naimi 2011 Clin Physiol Funct Imaging: Difference between revisions

From Bioblast
No edit summary
No edit summary
Β 
(16 intermediate revisions by 8 users not shown)
Line 1: Line 1:
{{Publication
{{Publication
|title=Naimi AI, Bourbeau J, Perrault H, Baril J, Wright-Paradis C, Rossi A, Taivassalo T, Sheel AW, RabΓΈl R, Dela F, Boushel R (2011) Altered mitochondrial regulation in quadriceps muscles of patients with COPD. Clin. Physiol. Funct. Imaging 31: 124-131.
|title=Naimi AI, Bourbeau J, Perrault H, Baril J, Wright-Paradis C, Rossi A, Taivassalo T, Sheel AW, RabΓΈl R, Dela F, Boushel RC (2011) Altered mitochondrial regulation in quadriceps muscles of patients with COPD. Clin Physiol Funct Imaging 31:124-31.
|info=[http://www.ncbi.nlm.nih.gov/pubmed/21091605 PMID:21091605]
|info=[http://www.ncbi.nlm.nih.gov/pubmed/21091605 PMID:21091605]
|authors=Naimi AI, Bourbeau J, Perrault H, Baril J, Wright-Paradis C, Rossi A, Taivassalo T, Sheel AW, Rabol R, Dela F, Boushel R
|authors=Naimi AI, Bourbeau J, Perrault H, Baril J, Wright-Paradis C, Rossi A, Taivassalo T, Sheel AW, Raboel R, Dela F, Boushel RC
|year=2011
|year=2011
|journal=Clin. Physiol. Funct. Imaging
|journal=Clin Physiol Funct Imaging
|abstract=Evidence exists for locomotor muscle impairment in patients with chronic obstructive pulmonary disease (COPD), including fiber type alterations and reduced mitochondrial oxidative capacity. In this study high-resolution respirometry was used to quantify oxygen flux in permeabilized fibres from biopsies of the vastus lateralis muscle in patients with COPD and compared to healthy control subjects. The main findings of this study were that (i) routine [[State 2]] respiration was higher in COPD; (ii) [[State 3]] respiration in the presence of ADP was similar in both groups with substrate supply of electrons to [[Complex I]] (COPD 38Β·28 Β± 3Β·58 versus control 42Β·85 Β± 3Β·10 pmol s(-1) mg tissue(-1) ), but O(2) flux with addition of succinate was lower in COPD patients (COPD 63Β·72 Β± 6Β·33 versus control 95Β·73 Β± 6Β·53 pmol s(-1) mg tissue(-1) ); (iii) excess capacity of [[cytochrome c oxidase]] in COPD patients was only ~50% that of control subjects. These results indicate that quadriceps muscle mitochondrial function is altered in patients with COPD. The regulatory mechanisms underlying these functional abnormalities remain to be uncovered.
|abstract=Evidence exists for locomotor muscle impairment in patients with chronic obstructive pulmonary disease (COPD), including fiber type alterations and reduced mitochondrial oxidative capacity. In this study high-resolution respirometry was used to quantify oxygen flux in permeabilized fibres from biopsies of the vastus lateralis muscle in patients with COPD and compared to healthy control subjects. The main findings of this study were that (i) routine [[State 2]] respiration was higher in COPD; (ii) [[State 3]] respiration in the presence of ADP was similar in both groups with substrate supply of electrons to [[Complex I]] (COPD 38Β·28 Β± 3Β·58 versus control 42Β·85 Β± 3Β·10 pmol s(-1) mg tissue(-1) ), but O(2) flux with addition of succinate was lower in COPD patients (COPD 63Β·72 Β± 6Β·33 versus control 95Β·73 Β± 6Β·53 pmol s(-1) mg tissue(-1) ); (iii) excess capacity of [[Complex_IV|cytochrome c oxidase]] in COPD patients was only ~50% that of control subjects. These results indicate that quadriceps muscle mitochondrial function is altered in patients with COPD. The regulatory mechanisms underlying these functional abnormalities remain to be uncovered.
|keywords=chronic obstructive pulmonary disease, mitochondrial respiration, skeletal muscle
|keywords=chronic obstructive pulmonary disease, mitochondrial respiration, skeletal muscle
|mipnetlab=DK_Copenhagen_Boushel R, DK_Copenhagen_Dela F
|mipnetlab=SE Stockholm Boushel RC, DK_Copenhagen_Dela F, CA_Montreal_Hepple RT, CA Vancouver Boushel RC, DK Copenhagen Larsen S
}}
}}
{{Labeling
{{Labeling
|organism=Human
|tissues=Skeletal muscle
|preparations=Permeabilized tissue
|enzymes=Complex I, Complex IV;cytochrome c oxidase
|injuries=Mitochondrial disease
|diseases=COPD
|couplingstates=OXPHOS
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
|injuries=Mitochondrial Disease; Degenerative Disease and Defect
|organism=Human
|tissues=Skeletal Muscle
|preparations=Permeabilized Cell or Tissue; Homogenate
|enzymes=Complex I, Complex IV; Cytochrome c Oxidase
|topics=Respiration; OXPHOS; ETS Capacity
}}
}}

Latest revision as of 05:23, 8 February 2020

Publications in the MiPMap
Naimi AI, Bourbeau J, Perrault H, Baril J, Wright-Paradis C, Rossi A, Taivassalo T, Sheel AW, RabΓΈl R, Dela F, Boushel RC (2011) Altered mitochondrial regulation in quadriceps muscles of patients with COPD. Clin Physiol Funct Imaging 31:124-31.

Β» PMID:21091605

Naimi AI, Bourbeau J, Perrault H, Baril J, Wright-Paradis C, Rossi A, Taivassalo T, Sheel AW, Raboel R, Dela F, Boushel RC (2011) Clin Physiol Funct Imaging

Abstract: Evidence exists for locomotor muscle impairment in patients with chronic obstructive pulmonary disease (COPD), including fiber type alterations and reduced mitochondrial oxidative capacity. In this study high-resolution respirometry was used to quantify oxygen flux in permeabilized fibres from biopsies of the vastus lateralis muscle in patients with COPD and compared to healthy control subjects. The main findings of this study were that (i) routine State 2 respiration was higher in COPD; (ii) State 3 respiration in the presence of ADP was similar in both groups with substrate supply of electrons to Complex I (COPD 38Β·28 Β± 3Β·58 versus control 42Β·85 Β± 3Β·10 pmol s(-1) mg tissue(-1) ), but O(2) flux with addition of succinate was lower in COPD patients (COPD 63Β·72 Β± 6Β·33 versus control 95Β·73 Β± 6Β·53 pmol s(-1) mg tissue(-1) ); (iii) excess capacity of cytochrome c oxidase in COPD patients was only ~50% that of control subjects. These results indicate that quadriceps muscle mitochondrial function is altered in patients with COPD. The regulatory mechanisms underlying these functional abnormalities remain to be uncovered. β€’ Keywords: chronic obstructive pulmonary disease, mitochondrial respiration, skeletal muscle

β€’ O2k-Network Lab: SE Stockholm Boushel RC, DK_Copenhagen_Dela F, CA_Montreal_Hepple RT, CA Vancouver Boushel RC, DK Copenhagen Larsen S


Labels: Pathology: COPD  Stress:Mitochondrial disease  Organism: Human  Tissue;cell: Skeletal muscle  Preparation: Permeabilized tissue  Enzyme: Complex I, Complex IV;cytochrome c oxidase 

Coupling state: OXPHOS 

HRR: Oxygraph-2k 


Cookies help us deliver our services. By using our services, you agree to our use of cookies.