Difference between revisions of "Gnaiger 2013 Abstract Neurocon Kolkata"

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{{Abstract
{{Abstract
|title=Gnaiger E (2013) Body mass index and the risk of neurodegeneration: from mitochondrial fitness to brain function. Abstract Neurocon 2013, Santiago Kolkata, India. Symposium: Neurocon 2013. January 17-20.  
|title=Gnaiger E (2013) Body mass index and the risk of neurodegeneration: from mitochondrial fitness to brain function. Abstract Neurocon 2013, Kolkata, India. Symposium: Neurocon 2013. January 17-20.
|info=[https://sites.google.com/site/neuroconkolkata/ Neurocon]
|info=[https://sites.google.com/site/neuroconkolkata/ Neurocon]
|authors=Gnaiger E
|authors=Gnaiger E
|year=2013
|year=2013
|event=Neurocon 2013
|event=Neurocon 2013
|abstract=Persistence of being overweight decreases the quality of life and increases the risk of developing early signs of neurodegeneration. Obesity and overweight are an emerging epidemic indicated by high body mass indexes, BMI>30 and >25 kg∙m­2. BMI is a lifestyle accumulator integrating the imbalance between daily deficits of physical exercise and unmatched caloric intake. In addition, regional distributions of BMI correlate with chronic exposure to persistent organic pollutants in the environment and food chains, and pharmacological accumulation in post-industrial societies. Whereas correlations between high BMI and reduced cognitive function are well established, the underlying mechanisms remain elusive. The present analysis provides a turning point for finding the mechanistic basis to explain how BMI is related to neurological and brain function. Three previously disparate lines of study substantiate the hypothesis that preservation of mental health with age is related to maintenance of mitochondrial competence expressed as the capacity of oxidative phosphorylation (OXPHOS). (i) OXPHOS capacity in vastus lateralis declines significantly with BMI increasing from normal to overweight in healthy young and middle-aged men and women. Diminished mitochondrial density in muscle fibres is the main cause for low OXPHOS capacity. (ii) OXPHOS capacity in skeletal muscle is a potential marker for mitochondrial function in other highly aerobic tissues such as heart and brain. (iii) Low OXPHOS capacity in all or specific areas of the brain is causally related to impaired cognitive function and neurodegenerative diseases. Taken together, declining OXPHOS capacity in skeletal muscle with increasing BMI is suggested to indicate systemic ‘mitochondrial fever’ in a pro-inflammatory state of oxidative stress and reduced mitochondrial biogenesis. This translates high BMI to the risk of neurodegenerative disease. The health benefits are emphasized of maintaining mitochondrial competence high particularly with progressive age, as achieved by a physically active and nutritionally balanced life style.  
|abstract=Persistence of being overweight decreases the quality of life and increases the risk of developing early signs of neurodegeneration. Obesity and overweight are an emerging epidemic indicated by high body mass indexes, BMI>30 and >25 kg/m­<sup>2</sup>. BMI is a lifestyle accumulator integrating the imbalance between daily deficits of physical exercise and unmatched caloric intake. In addition, regional distributions of BMI correlate with chronic exposure to persistent organic pollutants in the environment and food chains, and pharmacological accumulation in post-industrial societies. Whereas correlations between high BMI and reduced cognitive function are well established, the underlying mechanisms remain elusive. The present analysis provides a turning point for finding the mechanistic basis to explain how BMI is related to neurological and brain function. Three previously disparate lines of study substantiate the hypothesis that preservation of mental health with age is related to maintenance of mitochondrial competence expressed as the capacity of oxidative phosphorylation (OXPHOS). (i) OXPHOS capacity in vastus lateralis declines significantly with BMI increasing from normal to overweight in healthy young and middle-aged men and women. Diminished mitochondrial density in muscle fibres is the main cause for low OXPHOS capacity. (ii) OXPHOS capacity in skeletal muscle is a potential marker for mitochondrial function in other highly aerobic tissues such as heart and brain. (iii) Low OXPHOS capacity in all or specific areas of the brain is causally related to impaired cognitive function and neurodegenerative diseases. Taken together, declining OXPHOS capacity in skeletal muscle with increasing BMI is suggested to indicate systemic ‘mitochondrial fever’ in a pro-inflammatory state of oxidative stress and reduced mitochondrial biogenesis. This translates high BMI to the risk of neurodegenerative disease. The health benefits are emphasized of maintaining mitochondrial competence high particularly with progressive age, as achieved by a physically active and nutritionally balanced life style.  


[[MitoCom#Acknowledgment|Contribution to K-Regio]] ''[[MitoCom_K-Regio|MitoCom Tyrol]]''.
Contribution to K-Regio ''[[MitoCom_O2k-Fluorometer|MitoCom Tyrol]]''.
|mipnetlab=AT Innsbruck Gnaiger E,
|mipnetlab=AT Innsbruck Oroboros
}}
}}
{{Labeling
{{Labeling
|instruments=Oxygraph-2k
|injuries=Mitochondrial disease
|injuries=Mitochondrial Disease; Degenerative Disease and Defect
|organism=Human
|organism=Human
|tissues=Skeletal muscle
|tissues=Skeletal muscle
|preparations=Permeabilized tissue
|preparations=Permeabilized tissue
|couplingstates=OXPHOS
|couplingstates=OXPHOS
|instruments=Oxygraph-2k
|additional=BMI,
}}
}}

Latest revision as of 18:28, 10 January 2022

Gnaiger E (2013) Body mass index and the risk of neurodegeneration: from mitochondrial fitness to brain function. Abstract Neurocon 2013, Kolkata, India. Symposium: Neurocon 2013. January 17-20.

Link: Neurocon

Gnaiger E (2013)

Event: Neurocon 2013

Persistence of being overweight decreases the quality of life and increases the risk of developing early signs of neurodegeneration. Obesity and overweight are an emerging epidemic indicated by high body mass indexes, BMI>30 and >25 kg/m2. BMI is a lifestyle accumulator integrating the imbalance between daily deficits of physical exercise and unmatched caloric intake. In addition, regional distributions of BMI correlate with chronic exposure to persistent organic pollutants in the environment and food chains, and pharmacological accumulation in post-industrial societies. Whereas correlations between high BMI and reduced cognitive function are well established, the underlying mechanisms remain elusive. The present analysis provides a turning point for finding the mechanistic basis to explain how BMI is related to neurological and brain function. Three previously disparate lines of study substantiate the hypothesis that preservation of mental health with age is related to maintenance of mitochondrial competence expressed as the capacity of oxidative phosphorylation (OXPHOS). (i) OXPHOS capacity in vastus lateralis declines significantly with BMI increasing from normal to overweight in healthy young and middle-aged men and women. Diminished mitochondrial density in muscle fibres is the main cause for low OXPHOS capacity. (ii) OXPHOS capacity in skeletal muscle is a potential marker for mitochondrial function in other highly aerobic tissues such as heart and brain. (iii) Low OXPHOS capacity in all or specific areas of the brain is causally related to impaired cognitive function and neurodegenerative diseases. Taken together, declining OXPHOS capacity in skeletal muscle with increasing BMI is suggested to indicate systemic ‘mitochondrial fever’ in a pro-inflammatory state of oxidative stress and reduced mitochondrial biogenesis. This translates high BMI to the risk of neurodegenerative disease. The health benefits are emphasized of maintaining mitochondrial competence high particularly with progressive age, as achieved by a physically active and nutritionally balanced life style.

Contribution to K-Regio MitoCom Tyrol.


O2k-Network Lab: AT Innsbruck Oroboros


Labels:

Stress:Mitochondrial disease  Organism: Human  Tissue;cell: Skeletal muscle  Preparation: Permeabilized tissue 


Coupling state: OXPHOS 

HRR: Oxygraph-2k 

BMI