Reply to “Discussion of ‘Interleukin-15 as a myokine: mechanistic insight into its effect on skeletal muscle metabolism’ – Interleukin-15 and interleukin-15Rα-dependent/-independent functions in human skeletal muscle are largely unknown”

2019 ◽  
Vol 44 (3) ◽  
pp. 338-339
Author(s):  
Lucien Nadeau ◽  
Céline Aguer
1993 ◽  
Vol 84 (s28) ◽  
pp. 38P-38P ◽  
Author(s):  
CH Thompson ◽  
GJ Kemp ◽  
DJ Taylor ◽  
GK Radda ◽  
B Rajagopalan

2020 ◽  
Vol 45 (1) ◽  
pp. 11-23 ◽  
Author(s):  
Hashim Islam ◽  
David A. Hood ◽  
Brendon J. Gurd

Despite its widespread acceptance as the “master regulator” of mitochondrial biogenesis (i.e., the expansion of the mitochondrial reticulum), peroxisome proliferator-activated receptor (PPAR) gamma coactivator-1 alpha (PGC-1α) appears to be dispensable for the training-induced augmentation of skeletal muscle mitochondrial content and respiratory function. In fact, a number of regulatory proteins have emerged as important players in skeletal muscle mitochondrial biogenesis and many of these proteins share key attributes with PGC-1α. In an effort to move past the simplistic notion of a “master regulator” of mitochondrial biogenesis, we highlight the regulatory mechanisms by which nuclear factor erythroid 2-related factor 2 (Nrf2), estrogen-related receptor gamma (ERRγ), PPARβ, and leucine-rich pentatricopeptide repeat-containing protein (LRP130) may contribute to the control of skeletal muscle mitochondrial biogenesis. We also present evidence supporting/refuting the ability of sulforaphane, quercetin, and epicatechin to promote skeletal muscle mitochondrial biogenesis and their potential to augment mitochondrial training adaptations. Targeted activation of specific pathways by these compounds may allow for greater mechanistic insight into the molecular pathways controlling mitochondrial biogenesis in human skeletal muscle. Dietary activation of mitochondrial biogenesis may also be useful in clinical populations with basal reductions in mitochondrial protein content, enzyme activities, and/or respiratory function as well as individuals who exhibit a blunted skeletal muscle responsiveness to contractile activity. Novelty The existence of redundant pathways leading to mitochondrial biogenesis refutes the simplistic notion of a “master regulator” of mitochondrial biogenesis. Dietary activation of specific pathways may provide greater mechanistic insight into the exercise-induced mitochondrial biogenesis in human skeletal muscle.


1999 ◽  
Vol 84 (3) ◽  
pp. 1007-1010
Author(s):  
Linda A. Jahn ◽  
Eugene J. Barrett ◽  
Michael L. Genco ◽  
Liping Wei ◽  
Thomas A. Spraggins ◽  
...  

2014 ◽  
Vol 39 (9) ◽  
pp. 1083-1091 ◽  
Author(s):  
Christopher J. Gerling ◽  
Jamie Whitfield ◽  
Kazutaka Mukai ◽  
Lawrence L. Spriet

Omega-3 supplementation has been purported to improve the function of several organs in the body, including reports of increased resting metabolic rate (RMR) and reliance on fat oxidation. However, the potential for omega-3s to modulate human skeletal muscle metabolism has received little attention. This study examined the effects of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) supplementation on whole-body RMR and the content of proteins involved in fat metabolism in human skeletal muscle. Recreationally active males supplemented with 3.0 g/day of EPA and DHA (n = 21) or olive oil (n = 9) for 12 weeks. Resting muscle biopsies were sampled in a subset of 10 subjects before (pre) and after (post) omega-3 supplementation. RMR significantly increased (5.3%, p = 0.040) following omega-3 supplementation (Pre, 1.33 ±0.05; Post, 1.40 ±0.04 kcal/min) with variable individual responses. When normalizing for body mass, this effect was lost (5.2%, p = 0.058). Omega-3s did not affect whole-body fat oxidation, and olive oil did not alter any parameter assessed. Omega-3 supplementation did not affect whole muscle, sarcolemmal, or mitochondrial FAT/CD36, FABPpm, FATP1 or FATP4 contents or mitochondrial electron chain and PDH proteins, but did increase the long form of UCP3 by 11%. In conclusion, supplementation with a high dose of omega-3s for 12 weeks increased RMR in a small and variable manner in a group of healthy young men. Omega-3 supplementation also had no effect on several proteins involved in skeletal muscle fat metabolism and did not cause mitochondrial biogenesis.


Sign in / Sign up

Export Citation Format

Share Document