Difference between revisions of "Joseph 2012 Aging Cell"
Bader Helga (talk | contribs) Β |
|||
| (One intermediate revision by the same user not shown) | |||
| Line 1: | Line 1: | ||
{{Publication | {{Publication | ||
|title=Joseph AM, Adhihetty PJ, Buford TW, Wohlgemuth SE, Lees HA, Nguyen LM, Aranda JM, Sandesara BD, Pahor M, Manini TM, Marzetti E, Leeuwenburgh C (2012) The impact of aging on mitochondrial function and biogenesis pathways in skeletal muscle of sedentary high- and low-functioning elderly individuals. Aging Cell 11: 801- | |title=Joseph AM, Adhihetty PJ, Buford TW, Wohlgemuth SE, Lees HA, Nguyen LM, Aranda JM, Sandesara BD, Pahor M, Manini TM, Marzetti E, Leeuwenburgh C (2012) The impact of aging on mitochondrial function and biogenesis pathways in skeletal muscle of sedentary high- and low-functioning elderly individuals. Aging Cell 11:801-9. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed?term=PMID%3A%2022681576)%20%20Joseph%20AM%2C%20Adhihetty%20PJ%2C%20Buford%20TW%2C%20Wohlgemuth%20SE%2C%20Lees%20HA%2C%20Nguyen%20LMD%2C%20Aranda%20JM%2C%20Sandesara%20BD%2C%20Pahor%20M%2C%20Manini%20TM%2C%20Marzetti%20E%2C%20Leeuwenburgh%20C%20(2012)%20The%20Impact%20of%20Aging%20on%20Mitochondrial%20Function%20and%20Biogenesis%20Pathways%20in%20Skeletal%20Muscle%20of%20Sedentary%20High-%20and%20Low-Functioning%20Elderly%20Individuals.%20Aging%20Cell%2C%20%5BEpub%20ahead%20of%20print%5D PMID: 22681576] | |info=[http://www.ncbi.nlm.nih.gov/pubmed?term=PMID%3A%2022681576)%20%20Joseph%20AM%2C%20Adhihetty%20PJ%2C%20Buford%20TW%2C%20Wohlgemuth%20SE%2C%20Lees%20HA%2C%20Nguyen%20LMD%2C%20Aranda%20JM%2C%20Sandesara%20BD%2C%20Pahor%20M%2C%20Manini%20TM%2C%20Marzetti%20E%2C%20Leeuwenburgh%20C%20(2012)%20The%20Impact%20of%20Aging%20on%20Mitochondrial%20Function%20and%20Biogenesis%20Pathways%20in%20Skeletal%20Muscle%20of%20Sedentary%20High-%20and%20Low-Functioning%20Elderly%20Individuals.%20Aging%20Cell%2C%20%5BEpub%20ahead%20of%20print%5D PMID: 22681576] | ||
|authors=Joseph AM, Adhihetty PJ, Buford TW, Wohlgemuth SE, Lees HA, Nguyen LM, Aranda JM, Sandesara BD, Pahor M, Manini TM, Marzetti E, Leeuwenburgh C | |authors=Joseph AM, Adhihetty PJ, Buford TW, Wohlgemuth SE, Lees HA, Nguyen LM, Aranda JM, Sandesara BD, Pahor M, Manini TM, Marzetti E, Leeuwenburgh C | ||
| Line 6: | Line 6: | ||
|journal=Aging Cell | |journal=Aging Cell | ||
|abstract=Age-related loss of muscle mass and strength (sarcopenia) leads to a decline in physical function and frailty in the elderly. Among the many proposed underlying causes of sarcopenia, mitochondrial dysfunction is inherent in a variety of aged tissues. The intent of this study was to examine the effect of aging on key groups of regulatory proteins involved in mitochondrial biogenesis and how this relates to physical performance in two groups of sedentary elderly participants, classified as high- and low-functioning based on the Short Physical Performance Battery test. Muscle mass was decreased by 38% and 30% in low-functioning elderly (LFE) participants when compared to young and high-functioning elderly (HFE) participants, respectively, and positively correlated to physical performance. Mitochondrial respiration in permeabilized muscle fibers was reduced (41%) in the LFE group when compared to the young, and this was associated with a 30% decline in COX activity. Levels of key metabolic regulators, SIRT3 and [[PGC-1Ξ±]] were significantly reduced (50%) in both groups of elderly participants when compared to young. Similarly, the fusion protein OPA1 was lower in muscle from elderly subjects, however no changes were detected in Mfn2, Drp1 or Fis1 among the groups. In contrast, protein import machinery (PIM) components Tom22 and cHsp70 were increased in the LFE group when compared to the young. This study suggests that aging in skeletal muscle is associated with impaired mitochondrial function and altered biogenesis pathways, and that this may contribute to muscle atrophy and the decline in muscle performance observed in the elderly population. | |abstract=Age-related loss of muscle mass and strength (sarcopenia) leads to a decline in physical function and frailty in the elderly. Among the many proposed underlying causes of sarcopenia, mitochondrial dysfunction is inherent in a variety of aged tissues. The intent of this study was to examine the effect of aging on key groups of regulatory proteins involved in mitochondrial biogenesis and how this relates to physical performance in two groups of sedentary elderly participants, classified as high- and low-functioning based on the Short Physical Performance Battery test. Muscle mass was decreased by 38% and 30% in low-functioning elderly (LFE) participants when compared to young and high-functioning elderly (HFE) participants, respectively, and positively correlated to physical performance. Mitochondrial respiration in permeabilized muscle fibers was reduced (41%) in the LFE group when compared to the young, and this was associated with a 30% decline in COX activity. Levels of key metabolic regulators, SIRT3 and [[PGC-1Ξ±]] were significantly reduced (50%) in both groups of elderly participants when compared to young. Similarly, the fusion protein OPA1 was lower in muscle from elderly subjects, however no changes were detected in Mfn2, Drp1 or Fis1 among the groups. In contrast, protein import machinery (PIM) components Tom22 and cHsp70 were increased in the LFE group when compared to the young. This study suggests that aging in skeletal muscle is associated with impaired mitochondrial function and altered biogenesis pathways, and that this may contribute to muscle atrophy and the decline in muscle performance observed in the elderly population. | ||
|keywords=Aging, | |keywords=Aging, Mitochondrial function, Biogenesis pathways, Short Physical Performance Battery test, Muscle mass | ||
|mipnetlab= | |mipnetlab=US FL Gainesville Wohlgemuth SE, US FL Gainesville Leeuwenburgh C | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
| Line 14: | Line 14: | ||
|tissues=Skeletal muscle | |tissues=Skeletal muscle | ||
|preparations=Permeabilized tissue | |preparations=Permeabilized tissue | ||
|diseases=Aging; senescence | |diseases=Aging;senescence | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
}} | }} | ||
Latest revision as of 15:13, 12 March 2015
| Joseph AM, Adhihetty PJ, Buford TW, Wohlgemuth SE, Lees HA, Nguyen LM, Aranda JM, Sandesara BD, Pahor M, Manini TM, Marzetti E, Leeuwenburgh C (2012) The impact of aging on mitochondrial function and biogenesis pathways in skeletal muscle of sedentary high- and low-functioning elderly individuals. Aging Cell 11:801-9. |
Joseph AM, Adhihetty PJ, Buford TW, Wohlgemuth SE, Lees HA, Nguyen LM, Aranda JM, Sandesara BD, Pahor M, Manini TM, Marzetti E, Leeuwenburgh C (2012) Aging Cell
Abstract: Age-related loss of muscle mass and strength (sarcopenia) leads to a decline in physical function and frailty in the elderly. Among the many proposed underlying causes of sarcopenia, mitochondrial dysfunction is inherent in a variety of aged tissues. The intent of this study was to examine the effect of aging on key groups of regulatory proteins involved in mitochondrial biogenesis and how this relates to physical performance in two groups of sedentary elderly participants, classified as high- and low-functioning based on the Short Physical Performance Battery test. Muscle mass was decreased by 38% and 30% in low-functioning elderly (LFE) participants when compared to young and high-functioning elderly (HFE) participants, respectively, and positively correlated to physical performance. Mitochondrial respiration in permeabilized muscle fibers was reduced (41%) in the LFE group when compared to the young, and this was associated with a 30% decline in COX activity. Levels of key metabolic regulators, SIRT3 and PGC-1Ξ± were significantly reduced (50%) in both groups of elderly participants when compared to young. Similarly, the fusion protein OPA1 was lower in muscle from elderly subjects, however no changes were detected in Mfn2, Drp1 or Fis1 among the groups. In contrast, protein import machinery (PIM) components Tom22 and cHsp70 were increased in the LFE group when compared to the young. This study suggests that aging in skeletal muscle is associated with impaired mitochondrial function and altered biogenesis pathways, and that this may contribute to muscle atrophy and the decline in muscle performance observed in the elderly population. β’ Keywords: Aging, Mitochondrial function, Biogenesis pathways, Short Physical Performance Battery test, Muscle mass
β’ O2k-Network Lab: US FL Gainesville Wohlgemuth SE, US FL Gainesville Leeuwenburgh C
Labels: MiParea: Respiration, mt-Biogenesis;mt-density, Exercise physiology;nutrition;life style, mt-Medicine
Pathology: Aging;senescence
Organism: Human Tissue;cell: Skeletal muscle Preparation: Permeabilized tissue
HRR: Oxygraph-2k
