scholarly journals Subpopulation-specific differences in skeletal muscle mitochondria in humans with obesity: insights from studies employing acute nutritional and exercise stimuli

2020 ◽  
Vol 318 (4) ◽  
pp. E538-E553
Author(s):  
Nisreen Wahwah ◽  
Katon A. Kras ◽  
Lori R. Roust ◽  
Christos S. Katsanos

Mitochondria from skeletal muscle of humans with obesity often display alterations with respect to their morphology, proteome, biogenesis, and function. These changes in muscle mitochondria are considered to contribute to metabolic abnormalities observed in humans with obesity. Most of the evidence describing alterations in muscle mitochondria in humans with obesity, however, lacks reference to a specific subcellular location. This is despite data over the years showing differences in the morphology and function of subsarcolemmal (found near the plasma membrane) and intermyofibrillar (nested between the myofibrils) mitochondria in skeletal muscle. Recent studies reveal that impairments in mitochondrial function in obesity with respect to the subcellular location of the mitochondria in muscle are more readily evident following exposure of the skeletal muscle to physiological stimuli. In this review, we highlight the need to understand skeletal muscle mitochondria metabolism in obesity in a subpopulation-specific manner and in the presence of physiological stimuli that modify mitochondrial function in vivo. Experimental approaches employed under these conditions will allow for more precise characterization of impairments in skeletal muscle mitochondria and their implications in inducing metabolic dysfunction in human obesity.


2005 ◽  
Vol 59 (4) ◽  
pp. 163-168 ◽  
Author(s):  
Alexey P. Kudin ◽  
Grazyna Debska-Vielhaber ◽  
Wolfram S. Kunz


2014 ◽  
Vol 10 (1) ◽  
Author(s):  
T. M. Henagan ◽  
W. T. Cefalu ◽  
D. M. Ribnicky ◽  
R. C. Noland ◽  
K. Dunville ◽  
...  






2014 ◽  
Vol 2 (10) ◽  
pp. e12154 ◽  
Author(s):  
Sofhia V. Ramos ◽  
Rebecca E. K. MacPherson ◽  
Patrick C. Turnbull ◽  
Kirsten N. Bott ◽  
Paul LeBlanc ◽  
...  


2019 ◽  
Vol 81 (1) ◽  
pp. 19-41 ◽  
Author(s):  
David A. Hood ◽  
Jonathan M. Memme ◽  
Ashley N. Oliveira ◽  
Matthew Triolo

Mitochondria are critical organelles responsible for regulating the metabolic status of skeletal muscle. These organelles exhibit remarkable plasticity by adapting their volume, structure, and function in response to chronic exercise, disuse, aging, and disease. A single bout of exercise initiates signaling to provoke increases in mitochondrial biogenesis, balanced by the onset of organelle turnover carried out by the mitophagy pathway. This accelerated turnover ensures the presence of a high functioning network of mitochondria designed for optimal ATP supply, with the consequence of favoring lipid metabolism, maintaining muscle mass, and reducing apoptotic susceptibility over the longer term. Conversely, aging and disuse are associated with reductions in muscle mass that are in part attributable to dysregulation of the mitochondrial network and impaired mitochondrial function. Therefore, exercise represents a viable, nonpharmaceutical therapy with the potential to reverse and enhance the impaired mitochondrial function observed with aging and chronic muscle disuse.



2021 ◽  
Author(s):  
Christian J Elliehausen ◽  
Dennis M Minton ◽  
Alexander D Nichol ◽  
Adam R Konopka

A decline in skeletal muscle mitochondrial function is associated with the loss of skeletal muscle size and function during knee osteoarthritis (OA). We have recently reported that the 12-weeks of dietary rapamycin (Rap, 14ppm), with or without metformin (Met, 1000ppm), increased plasma glucose and OA severity in male Dunkin Hartley (DH) guinea pigs, a model of naturally occurring, age-related OA. The purpose of the current study was to determine if increased OA severity after dietary Rap and Rap+Met was accompanied by impaired skeletal muscle mitochondrial function. Mitochondrial respiration and hydrogen peroxide (H2O2) emissions were evaluated in permeabilized muscle fibers via high-resolution respirometry and fluorometry using either a saturating bolus or titration of ADP. Rap and Rap+Met decreased complex I (CI)-linked respiration and increased ADP sensitivity, consistent with previous findings in patients with end-stage OA. Rap also tended to decrease mitochondrial H2O2 emissions, however, this was no longer apparent after normalizing to respiration. The decrease in CI-linked respiration was accompanied with lower CI protein abundance. This is the first inquiry into how lifespan extending treatments Rap and Rap+Met can influence skeletal muscle mitochondria in a model of age-related OA. Collectively, our data suggest that Rap with or without Met inhibits CI-linked capacity and increases ADP sensitivity in DH guinea pigs that have greater OA severity.



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