Difference between revisions of "Karlsson 2016 Mitochondrion"
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{{Publication | {{Publication | ||
|title=Karlsson M, Ehinger JK, Piel S, Sjövall F, Henriksnäs J, Höglund U, Hansson MJ, Elmér E ( | |title=Karlsson M, Ehinger JK, Piel S, Sjövall F, Henriksnäs J, Höglund U, Hansson MJ, Elmér E (2016) Changes in energy metabolism due to acute rotenone-induced mitochondrial complex I dysfunction – an in vivo large animal model. Mitochondrion 31:56-62. | ||
|info=[https://www.ncbi.nlm.nih.gov/pubmed/27769952 PMID: 27769952] | |info=[https://www.ncbi.nlm.nih.gov/pubmed/27769952 PMID: 27769952] | ||
|authors=Karlsson M, Ehinger JK, Piel S, Sjoevall F, Henriksnaes J, Hoeglund U, Hansson MJ, Elmer E | |authors=Karlsson M, Ehinger JK, Piel S, Sjoevall F, Henriksnaes J, Hoeglund U, Hansson MJ, Elmer E | ||
|year= | |year=2016 | ||
|journal=Mitochondrion | |journal=Mitochondrion | ||
|abstract=Metabolic crisis is a clinical condition primarily affecting patients with inherent mitochondrial dysfunction in situations of augmented energy demand. To model this, ten pigs received an infusion of rotenone, a mitochondrial complex I inhibitor, or vehicle. Clinical parameters, blood gases, continuous indirect calorimetry, ''in vivo'' muscle oxygen tension, ''ex vivo'' mitochondrial respiration and metabolomics were assessed. Rotenone induced a progressive increase in blood lactate which was paralleled by an increase in oxygen tension in venous blood and skeletal muscle. There was an initial decrease in whole body oxygen utilization, and there was a trend towards inhibited mitochondrial respiration in platelets. While levels of succinate were decreased, other intermediates of glycolysis and the TCA cycle were increased. This model may be suited for evaluating pharmaceutical interventions aimed at counteracting metabolic changes due to complex I dysfunction. | |abstract=Metabolic crisis is a clinical condition primarily affecting patients with inherent mitochondrial dysfunction in situations of augmented energy demand. To model this, ten pigs received an infusion of rotenone, a mitochondrial complex I inhibitor, or vehicle. Clinical parameters, blood gases, continuous indirect calorimetry, ''in vivo'' muscle oxygen tension, ''ex vivo'' mitochondrial respiration and metabolomics were assessed. Rotenone induced a progressive increase in blood lactate which was paralleled by an increase in oxygen tension in venous blood and skeletal muscle. There was an initial decrease in whole body oxygen utilization, and there was a trend towards inhibited mitochondrial respiration in platelets. While levels of succinate were decreased, other intermediates of glycolysis and the TCA cycle were increased. This model may be suited for evaluating pharmaceutical interventions aimed at counteracting metabolic changes due to complex I dysfunction. | ||
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|tissues=Skeletal muscle, Platelet | |tissues=Skeletal muscle, Platelet | ||
|preparations=Intact cells | |preparations=Intact cells | ||
|couplingstates= | |couplingstates=ET | ||
|pathways=N, ROX | |pathways=N, ROX | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|additional=Labels, 2018-09, | |additional=Labels, 2018-09, | ||
}} | }} | ||
Latest revision as of 14:52, 18 October 2018
| Karlsson M, Ehinger JK, Piel S, Sjövall F, Henriksnäs J, Höglund U, Hansson MJ, Elmér E (2016) Changes in energy metabolism due to acute rotenone-induced mitochondrial complex I dysfunction – an in vivo large animal model. Mitochondrion 31:56-62. |
Karlsson M, Ehinger JK, Piel S, Sjoevall F, Henriksnaes J, Hoeglund U, Hansson MJ, Elmer E (2016) Mitochondrion
Abstract: Metabolic crisis is a clinical condition primarily affecting patients with inherent mitochondrial dysfunction in situations of augmented energy demand. To model this, ten pigs received an infusion of rotenone, a mitochondrial complex I inhibitor, or vehicle. Clinical parameters, blood gases, continuous indirect calorimetry, in vivo muscle oxygen tension, ex vivo mitochondrial respiration and metabolomics were assessed. Rotenone induced a progressive increase in blood lactate which was paralleled by an increase in oxygen tension in venous blood and skeletal muscle. There was an initial decrease in whole body oxygen utilization, and there was a trend towards inhibited mitochondrial respiration in platelets. While levels of succinate were decreased, other intermediates of glycolysis and the TCA cycle were increased. This model may be suited for evaluating pharmaceutical interventions aimed at counteracting metabolic changes due to complex I dysfunction. • Keywords: Animal model, Complex I, Energy metabolism, Metabolic crisis, Mitochondria • Bioblast editor: Plangger M • O2k-Network Lab: SE Lund Elmer E, US PA Philadelphia Kilbaugh T
Labels: MiParea: Respiration
Organism: Pig
Tissue;cell: Skeletal muscle, Platelet
Preparation: Intact cells
Coupling state: ET
Pathway: N, ROX
HRR: Oxygraph-2k
Labels, 2018-09
