Category:BME and mitObesity: Difference between revisions
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Β | == Executive abstract == | ||
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Β ''Work in progress'' by [[Gnaiger E]] 2020-01-20 linked to a preprint in preparation on [[body mass excess |'''body mass excess, BME''']] and mitObesity. | |||
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:::: The decline of muscular mitochondrial fitness in overweight states is a biomarker of the systemic '''mitObesity''' syndrome: Compromised mitochondrial fitness across metabolically active organs provides the mechanistic link between obesity and comorbidities such as diabetes, cardiovascular and neurodegenerative diseases and various types of cancer bound to redox imbalance, inflammation, oxidative stress and insulin resistance. Today mitObesity is the world-wide leading cause of deaths and early aging, which can be prevented by an active lifestyle and improvement of the quality of life by exercise and caloric balance. | :::: The decline of muscular mitochondrial fitness in overweight states is a biomarker of the systemic '''mitObesity''' syndrome: Compromised mitochondrial fitness across metabolically active organs provides the mechanistic link between obesity and comorbidities such as diabetes, cardiovascular and neurodegenerative diseases and various types of cancer bound to redox imbalance, inflammation, oxidative stress and insulin resistance. Today mitObesity is the world-wide leading cause of deaths and early aging, which can be prevented by an active lifestyle and improvement of the quality of life by exercise and caloric balance. | ||
Revision as of 22:26, 19 January 2020
Executive abstract
Work in progress by Gnaiger E 2020-01-20 linked to a preprint in preparation on body mass excess, BME and mitObesity.
- The decline of muscular mitochondrial fitness in overweight states is a biomarker of the systemic mitObesity syndrome: Compromised mitochondrial fitness across metabolically active organs provides the mechanistic link between obesity and comorbidities such as diabetes, cardiovascular and neurodegenerative diseases and various types of cancer bound to redox imbalance, inflammation, oxidative stress and insulin resistance. Today mitObesity is the world-wide leading cause of deaths and early aging, which can be prevented by an active lifestyle and improvement of the quality of life by exercise and caloric balance.
- Obesity is defined by convention of the WHO as a body mass index, BMI, equal or above 30 kgΒ·m-2. The BMI has been critizised, however, as an indicator of obesity due to its poor correlation with body fat expressed as percent body fat mass per total body mass, BF%. Another fundamental limitation of the BMI as a general index of obesity is the fact that BMI cutoff points which have been evaluated in adult Caucasian populations are not generally applicable and have to be adjusted for Asian populations, where different BMI cutoff points are discussed for women and men, as well as for children and adolescents. A superior index of obesity is provided by the concept of body mass excess, BME, with respect to the healthy reference population: The BME (1) correlates linearly and tightly with body fat excess equally in women and men, (2) with BME cutoff points for overweight and obesity which are identical in a wide range of evolutionary (ethnic) background including European and American white Caucasians, American blacks, and Asian populations, and (3) with BME cutoff points that apply equally to adults, adolescents and children. The BME cutoff points for overweight and obese are easily understood by non-experts, as 20 % and 40 %, respectively, in excess of the reference body mass at a given height. In contrast, only specialists are familiar with the meaning of age-adjusted values of the BMI.
- The decline of mitochondrial fitness in skeletal muscle is tightly associated with the body mass excess, BME, in healthy populations in the succession from the reference BME to overweight and obese BME-cutoff values. The decline of mitochondrial fitness is quantitatively related to the progressive loss of cariorespiratory fitness with increasing BME, measured as maximum ergometric aerobic capacity per total body mass, VO2max/M. The systemic decline of mitochondrial respiratory fitness is a hallmark of mitObesity.
- Several drugst and nutraceuticals, which yield some promising results in the treatment of a diverse range of preventable degenerative diseases implicated in comorbidities, have common mechanisms of action targeting mitochondria. These drugs and neutraceuticals - such as metformin, melatonin, flavonoids, curcumin, and resveratrol - may be classified as anti-mitObesity bioactive compounds, providing strong evidence for the common mechanisms of action underlying the mitObesity syndrome.
Further details - MitoPedia: BME
Labels: MiParea: Respiration, mt-Biogenesis;mt-density, Gender, Exercise physiology;nutrition;life style, mt-Medicine Pathology: Obesity
Organism: Human
MitoPedia:BME
Pages in category "BME and mitObesity"
The following 13 pages are in this category, out of 13 total.