scholarly journals Constitutive activation of AMP-activated protein kinase (AMPK) propel mitochondrial biogenesis

2014 ◽  
Vol 4 (2) ◽  
pp. 15-26 ◽  
Author(s):  
B. Bokko Paul ◽  
U. Ahmed Afsar ◽  
R. Fisher Paul
Keyword(s):  
Protein Kinase ◽  
Mitochondrial Biogenesis ◽  
Constitutive Activation ◽  
Amp Activated Protein Kinase

scholarly journals Effect of Quercetin Treatment on Mitochondrial Biogenesis and Exercise-Induced AMP-Activated Protein Kinase Activation in Rat Skeletal Muscle

Nutrients ◽  
2020 ◽  
Vol 12 (3) ◽  
pp. 729 ◽  
Author(s):  
Keiichi Koshinaka ◽  
Asuka Honda ◽  
Hiroyuki Masuda ◽  
Akiko Sato
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase ◽  
Endurance Exercise ◽  
Mitochondrial Biogenesis ◽  
Exercise Performance ◽  
Term Therapy ◽  
High Dose ◽  
Rat Skeletal Muscle ◽  
Amp Activated Protein Kinase ◽  
Quercetin Treatment

The purpose of this study was to evaluate the effect of chronic quercetin treatment on mitochondrial biogenesis, endurance exercise performance and activation levels of AMP-activated protein kinase (AMPK) in rat skeletal muscle. Rats were assigned to a control or quercetin group and were fed for 7 days. Rats treated with quercetin showed no changes in the protein levels of citrate synthase or cytochrome C oxidase IV or those of sirtuin 1, peroxisome proliferator-activated receptor gamma coactivator-1α or phosphorylated AMPK. After endurance swimming exercise, quercetin-treated rats demonstrated no differences in blood and muscle lactate levels or glycogen utilization speed compared to control rats. These results indicate that quercetin treatment does not stimulate mitochondrial biogenesis in skeletal muscle and does not influence metabolism in a way that might enhance endurance exercise capacity. On the other hand, the AMPK phosphorylation level immediately after exercise was significantly lower in quercetin-treated muscles, suggesting that quercetin treatment might provide a disadvantage to muscle adaptation when administered with exercise training. The molecular results of this study indicate that quercetin treatment may not be advantageous for improving endurance exercise performance, at least after high-dose and short-term therapy.

Apolipoprotein a1 increases mitochondrial biogenesis through AMP-activated protein kinase

2015 ◽  
Vol 27 (9) ◽  
pp. 1873-1881 ◽  
Author(s):  
Parkyong Song ◽  
Yonghoon Kwon ◽  
Kyungmoo Yea ◽  
Hyo-Youl Moon ◽  
Jong Hyuk Yoon ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Mitochondrial Biogenesis ◽  
Apolipoprotein A1 ◽  
Amp Activated Protein Kinase

Puerarin Attenuates Osteoarthritis via Upregulating AMP-Activated Protein Kinase/Proliferator-Activated Receptor-γ Coactivator-1 Signaling Pathway in Osteoarthritis Rats

Pharmacology ◽  
2018 ◽  
Vol 102 (3-4) ◽  
pp. 117-125 ◽  
Author(s):  
Luyao Wang ◽  
Haojie Shan ◽  
Bin Wang ◽  
Nan Wang ◽  
Zubin Zhou ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Signaling Pathway ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Function ◽  
Cartilage Damage ◽  
Joint Disease ◽  
Mitochondrial Dysfunctions ◽  
Compound C ◽  
Amp Activated Protein Kinase ◽  
And Cartilage

Background/Aims: Osteoarthritis is the most common degenerative joint disease and causes major pain and disability in adults. It has been reported that mitochondrial dysfunction in chondrocytes was associated with osteoarthritis. Puerarin has multiple effects including restoring mitochondrial function. In this study, the potential effects of puerarin on osteoarthritis and osteoarthritis associated mitochondrial dysfunctions were evaluated. Methods: Osteoarthritis rats were treated with puerarin and the severity of osteoarthritis and cartilage damages was evaluated. The mitochondrial biogenesis and functions were analyzed by measuring related proteins expression, mitochondrial DNA content, ATP production, and oxygen consumption. The dependence of AMP-activated protein kinase (AMPK) pathway on puerarin-regulated mitochondrial function was analyzed by applying AMPK inhibitor Compound C. Results: Puerarin treatment alleviated mechanical hyperalgesia and cartilage damage in osteoarthritis rats. Puerarin increased mitochondrial biogenesis and attenuated mitochondrial dysfunctions in osteoarthritis rats. AMPK inhibitor Compound C abolished puerarin’s effects. Conclusion: Puerarin attenuates osteoarthritis by upregulating the AMPK/proliferator-activated receptor-γ coactivator signaling pathway in osteoarthritis rats.

scholarly journals Critical role of AMP-activated protein kinase in the balance between mitophagy and mitochondrial biogenesis in MELAS disease

2015 ◽  
Vol 1852 (11) ◽  
pp. 2535-2553 ◽  
Author(s):  
Juan Garrido-Maraver ◽  
Marina Villanueva Paz ◽  
Mario D. Cordero ◽  
Juan Bautista-Lorite ◽  
Manuel Oropesa-Ávila ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Mitochondrial Biogenesis ◽  
Critical Role ◽  
Amp Activated Protein Kinase

Strawberry consumption improves aging-associated impairments, mitochondrial biogenesis and functionality through the AMP-activated protein kinase signaling cascade

2017 ◽  
Vol 234 ◽  
pp. 464-471 ◽  
Author(s):  
Francesca Giampieri ◽  
Josè M. Alvarez-Suarez ◽  
Mario D. Cordero ◽  
Massimiliano Gasparrini ◽  
Tamara Y. Forbes-Hernandez ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Mitochondrial Biogenesis ◽  
Signaling Cascade ◽  
Kinase Signaling ◽  
Amp Activated Protein Kinase ◽  
Protein Kinase Signaling

Molecular responses to high-intensity interval exerciseThis paper is one of a selection of papers published in this Special Issue, entitled 14th International Biochemistry of Exercise Conference – Muscles as Molecular and Metabolic Machines, and has undergone the Journal’s usual peer review process.

2009 ◽  
Vol 34 (3) ◽  
pp. 428-432 ◽  
Author(s):  
Martin Gibala
Keyword(s):  
Protein Kinase ◽  
Endurance Training ◽  
Signaling Pathways ◽  
Mitochondrial Biogenesis ◽  
High Intensity ◽  
Mitogen Activated Protein Kinase ◽  
Interval Exercise ◽  
Mitogen Activated Protein ◽  
High Intensity Interval ◽  
Amp Activated Protein Kinase

From a cell-signaling perspective, short-duration intense muscular work is typically associated with resistance training and linked to pathways that stimulate growth. However, brief repeated sessions of high-intensity interval exercise training (HIT) induce rapid phenotypic changes that resemble traditional endurance training. Given the oxidative phenotype that is rapidly upregulated by HIT, it is plausible that metabolic adaptations to this type of exercise could be mediated in part through signaling pathways normally associated with endurance training. A key controller of oxidative enzyme expression in skeletal muscle is peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), a transcriptional coactivator that serves to coordinate mitochondrial biogenesis. Most studies of acute PGC-1α regulation in humans have used very prolonged exercise interventions; however, it was recently shown that a surprisingly small dose of very intense interval exercise, equivalent to only 2 min of all-out cycling, was sufficient to increase PGC-1α mRNA during recovery. Intense interval exercise has also been shown to acutely increase the activity of signaling pathways linked to PGC-1α and mitochondrial biogenesis, including AMP-activated protein kinase (α1 and α2 subunits) and the p38 mitogen-activated protein kinase. In contrast, signaling pathways linked to muscle growth, including protein kinase B/Akt and downstream targets p70 ribosomal S6 kinase and 4E binding protein 1, are generally unchanged after acute interval exercise. Signaling through AMP-activated protein kinase and p38 mitogen-activated protein kinase to PGC-1α may therefore explain, in part, the metabolic remodeling induced by HIT, including mitochondrial biogenesis and an increased capacity for glucose and fatty acid oxidation.

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