Difference between revisions of "Serteyn 2014 Bioenergetics"
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the mitochondrial function before reaching the « mitochondrial dysfunction threshold » that may lead to the failure of | the mitochondrial function before reaching the « mitochondrial dysfunction threshold » that may lead to the failure of | ||
the dermal-epidermal interface. | the dermal-epidermal interface. | ||
|keywords=Horse, Laminitis, Mitochondria, | |keywords=Horse, Laminitis, Mitochondria, electron transfer-pathway, Energy metabolism dysfunction, Oxidative phosphorylation, Inflammation, Reactive oxygen species | ||
|mipnetlab=BE Liege Votion DM | |mipnetlab=BE Liege Votion DM | ||
}} | }} | ||
Revision as of 15:25, 20 October 2017
| Serteyn D, de la Rebière de Pouyade G, Sandersen C, Salciccia A, Grulke S, Mouithys-Mickalad A, Franck T, Lejeune JP, Ceusters Justine D (2014) Muscle mitochondrial dysfunction in horses affected by acute laminitis. Bioenergetics 3:1-7. |
Serteyn D, de la Rebiere de Pouyade G, Sandersen C, Salciccia A, Grulke S, Mouithys-Mickalad A, Franck T, Lejeune JP, Ceusters Justine D (2014) Bioenergetics
Abstract: Laminitis is a common and debilitating disease affecting horses and ponies. It often leads to the demise of the animal. Energy deficiency is suspected to entrain the disruption of the hemidesmosomes leading to the failure of the dermal-epidermal interface. The aim of this study was to measure the muscle mitochondrial function by high resolution respirometry. Muscle micro-biopsies were obtained from 11 horses affected by acute metabolic laminitis, 6 horses affected by acute laminitis resulting from a systemic inflammation response syndrome and 28 healthy horses distributed in 2 control groups: 17 horses with a body condition score [BSC, ranging from 0 (emaciated) to 5 (obese)] of 2 to 3 and 11 horses with a BSC of 4 to 5. During the acute phase of laminitis, a significant reduction of the muscle mitochondrial respiration was observed. The muscle mitochondrial dysfunction occurred independently of the etiology (metabolic disorder or systemic inflammation) leading to laminitis. The reduction of the oxidative phosphorylation and of the maximal respiratory capacity (after uncoupling) may induce depletion of the cell’s ATP content. If the same mitochondrial alteration occurs in the foot lamina, mitochondria targeting should be considered for the future, not only to better understand the physiopathology of the disease but also to maintain and to support the mitochondrial function before reaching the « mitochondrial dysfunction threshold » that may lead to the failure of the dermal-epidermal interface. • Keywords: Horse, Laminitis, Mitochondria, electron transfer-pathway, Energy metabolism dysfunction, Oxidative phosphorylation, Inflammation, Reactive oxygen species
• O2k-Network Lab: BE Liege Votion DM
Labels: MiParea: Respiration
Pathology: Obesity, Other
Organism: Horse Tissue;cell: Skeletal muscle Preparation: Permeabilized tissue
Coupling state: LEAK, OXPHOS, ETS"ETS" is not in the list (LEAK, ROUTINE, OXPHOS, ET) of allowed values for the "Coupling states" property.
Pathway: N, S, NS, ROX
HRR: Oxygraph-2k
