Difference between revisions of "Gnaiger 2013 Abstract ASMRM"
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Controversies persist currently if mitochondrial (mt) dysfunction plays a causative role during the onset and progression of type 2 diabetes [1,2], metabolic syndrome [3] and a wide range of degenerative diseases. BMI is an integrator of energy balance in active versus sedentary lifestyles, and the progression to obesity correlates with a loss of mt-density and the decline of OXPHOS capacity per muscle mass. Under sedentary conditions of diminished energy utilization and ‘diabesity’, reduction of mt-density may be adaptive, keeping hyperpolarization and ROS production in check. Below a threshold of low mt-density the adaptive range for downregulation of mt-biogenesis is exceeded. This marks the transition to a proinflammatory state (‘mitochondrial fever’), putting the cell at risk of further degeneration and cell death, with all sequelae of age-related diseases [4]. | |||
From a static point of view, deterioration of mt-structure (mt-DNA, proteins, membranes) causes dysfunction. From a dynamic perspective, the action of flows over time induces regeneration, explaining the preventive potential of physical exercise. Cause and effect are embedded in a network of feedback control and circular loops in degenerative diseases. | |||
|keywords=Preventive mitochondrial medicine, BMI, mt-density, OXPHOS capacity, diabesity | |keywords=Preventive mitochondrial medicine, BMI, mt-density, OXPHOS capacity, diabesity | ||
|mipnetlab=AT Innsbruck Gnaiger E | |mipnetlab=AT Innsbruck Gnaiger E | ||
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|journal=Abstract | |journal=Abstract | ||
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== References == | |||
#Goodpaster BH (2013) Mitochondrial deficiency is associated with insulin resistance. Diabetes 62: 1032-1035. | |||
#Holloszy JO (2013) "Deficiency" of mitochondria in muscle does not cause insulin resistance. Diabetes 62: 1036-1040. | |||
#Lee HK, Shim EB (2013) Extension of the mitochondria dysfunction hypothesis of metabolic syndrome to atherosclerosis with emphasis on the endocrine-disrupting chemicals and biophysical laws. J Diabetes Investig 4 : 19-33. | |||
#Burtscher M, Gnaiger E (2013) Physical activity and cardiovascular diseases: epidemiology and primary preventive and therapeutic targets. In: Wakabayashi I, Groschner K, ed, Interdisciplinary concepts in cardiovascular health. Springer: 127-144. | |||
== Afilliation == | |||
1- D. Swarovski Research Laboratory, Medical University of Innsbruck, 6020, 2OROBOROS INSTRUMENTS, Innsbruck, 6020, Austria. www.bioblast.at/index.php/MitoCom | |||
Email: [email protected] | |||
Revision as of 16:33, 21 October 2013
| Gnaiger E(2013) Loss of mitochondrial competence and degenerative disease: cause and effect. Abstract ASMRM-Seoul. |
Link: http://www.asmrm2013.com
Gnaiger E (2013)
Event: ASMRM
Controversies persist currently if mitochondrial (mt) dysfunction plays a causative role during the onset and progression of type 2 diabetes [1,2], metabolic syndrome [3] and a wide range of degenerative diseases. BMI is an integrator of energy balance in active versus sedentary lifestyles, and the progression to obesity correlates with a loss of mt-density and the decline of OXPHOS capacity per muscle mass. Under sedentary conditions of diminished energy utilization and ‘diabesity’, reduction of mt-density may be adaptive, keeping hyperpolarization and ROS production in check. Below a threshold of low mt-density the adaptive range for downregulation of mt-biogenesis is exceeded. This marks the transition to a proinflammatory state (‘mitochondrial fever’), putting the cell at risk of further degeneration and cell death, with all sequelae of age-related diseases [4]. From a static point of view, deterioration of mt-structure (mt-DNA, proteins, membranes) causes dysfunction. From a dynamic perspective, the action of flows over time induces regeneration, explaining the preventive potential of physical exercise. Cause and effect are embedded in a network of feedback control and circular loops in degenerative diseases.
• Keywords: Preventive mitochondrial medicine, BMI, mt-density, OXPHOS capacity, diabesity
• O2k-Network Lab: AT Innsbruck Gnaiger E
Labels: MiParea: Respiration, mt-Biogenesis;mt-density, Exercise physiology;nutrition;life style Pathology: Diabetes Stress:Mitochondrial Disease; Degenerative Disease and Defect"Mitochondrial Disease; Degenerative Disease and Defect" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property. Organism: Human
Regulation: Coupling efficiency;uncoupling, Substrate, Fatty Acid"Fatty Acid" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property. Coupling state: LEAK, OXPHOS
HRR: Oxygraph-2k
References
- Goodpaster BH (2013) Mitochondrial deficiency is associated with insulin resistance. Diabetes 62: 1032-1035.
- Holloszy JO (2013) "Deficiency" of mitochondria in muscle does not cause insulin resistance. Diabetes 62: 1036-1040.
- Lee HK, Shim EB (2013) Extension of the mitochondria dysfunction hypothesis of metabolic syndrome to atherosclerosis with emphasis on the endocrine-disrupting chemicals and biophysical laws. J Diabetes Investig 4 : 19-33.
- Burtscher M, Gnaiger E (2013) Physical activity and cardiovascular diseases: epidemiology and primary preventive and therapeutic targets. In: Wakabayashi I, Groschner K, ed, Interdisciplinary concepts in cardiovascular health. Springer: 127-144.
Afilliation
1- D. Swarovski Research Laboratory, Medical University of Innsbruck, 6020, 2OROBOROS INSTRUMENTS, Innsbruck, 6020, Austria. www.bioblast.at/index.php/MitoCom
Email: [email protected]
