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• W2895787502 abstract "Aging is characterized by a progressive loss of skeletal muscle mass and function (sarcopenia). Obesity exacerbates age-related decline and lead to frailty. Skeletal muscle fat infiltration increases with aging and seems to be crucial for the progression of sarcopenia. Additionally, skeletal muscle plasticity modulates metabolic adaptation to different pathophysiological situations. Thus, cellular bioenergetics and mitochondrial profile were studied in the skeletal muscle of overweight aged people without reaching obesity to prevent this extreme situation. Overweight aged muscle lacked ATP production, as indicated by defects in the phosphagen system, glycolysis and especially mostly by oxidative phosphorylation metabolic pathway. Overweight subjects exhibited an inhibition of mitophagy that was linked to an increase in mitochondrial biogenesis that underlies the accumulation of dysfunctional mitochondria and encourages the onset of sarcopenia. As a strategy to maintain cellular homeostasis, overweight subjects experienced a metabolic switch from oxidative to lactic acid fermentation metabolism, which allows continued ATP production under mitochondrial dysfunction, but without reaching physiological aged basal levels. This ATP depletion induced early signs of impaired contractile function and a decline in skeletal muscle structural integrity, evidenced by lower levels of filamin C. Our findings reveal the main effector pathways at an early stage of obesity and highlight the importance of mitochondrial metabolism in overweight and obese individuals. Exploiting mitochondrial profiles for therapeutic purposes in humans is an ambitious strategy for treating muscle impairment diseases." @default.
• W2895787502 created "2018-10-26" @default.
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• W2895787502 date "2019-01-01" @default.
• W2895787502 modified "2023-10-18" @default.
• W2895787502 title "Overweight in the Elderly Induces a Switch in Energy Metabolism that Undermines Muscle Integrity" @default.
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• W2895787502 doi "https://doi.org/10.14336/ad.2018.0430" @default.
• W2895787502 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6457058" @default.
• W2895787502 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31011474" @default.
• W2895787502 hasPublicationYear "2019" @default.
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