Effect of epicatechin on skeletal muscle

2021 ◽  
Vol 29 ◽  
Author(s):  
Hermann Zbinden-Foncea ◽  
Mauricio Castro-Sepulveda ◽  
Jocelyn Fuentes ◽  
Hernan Speisky
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Structure Function ◽  
Mass Loss ◽  
Mitochondrial Biogenesis ◽  
Myogenic Differentiation ◽  
Naturally Occurring ◽  
Muscle Mass Loss ◽  
Clinical Conditions ◽  
Stimulation Of

: Loss of skeletal muscle (SkM) quality is associated with different clinical conditions such as aging, diabetes, obesity, cancer and heart failure. Nutritional research has focused on identifying naturally occurring molecules that mitigate the loss of SkM quality induced by a pathology or syndrome. In this context, although few human studies have been conducted, Epicatechin (Epi) is a prime candidate that may positively affect SkM quality by its potential ability to mitigate muscle mass loss. This seems to be a consequence of its antioxidant, anti-inflammatory properties, and its stimulation of mitochondrial biogenesis to increase myogenic differentiation, as well as its modulation of key proteins involved in SkM structure, function, metabolism, and growth. In conclusion, the Epi could prevent, mitigate, delay, and even treat muscle-related disorders caused by aging and diseases, however, studies in humans are needed.

scholarly journals Racial Differences in Relative Skeletal Muscle Mass Loss During Diet-Induced Weight Loss in Women

Obesity ◽  
2018 ◽  
Vol 26 (8) ◽  
pp. 1255-1260 ◽  
Author(s):  
Gary R. Hunter ◽  
David R. Bryan ◽  
Juliano H. Borges ◽  
M. David Diggs ◽  
Stephen J. Carter
Keyword(s):  
Skeletal Muscle ◽  
Weight Loss ◽  
Mass Loss ◽  
Racial Differences ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Muscle Mass Loss

scholarly journals Thyroid Hormone Stimulation of Autophagy Is Essential for Mitochondrial Biogenesis and Activity in Skeletal Muscle

Endocrinology ◽  
2016 ◽  
Vol 157 (1) ◽  
pp. 23-38 ◽  
Author(s):  
Ronny Lesmana ◽  
Rohit A. Sinha ◽  
Brijesh K. Singh ◽  
Jin Zhou ◽  
Kenji Ohba ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Thyroid Hormone ◽  
Protein Kinase ◽  
Mitochondrial Biogenesis ◽  
Mitochondrial Protein ◽  
Adenosine Monophosphate ◽  
Mitochondrial Activity ◽  
Dependent Manner ◽  
In Vivo Models ◽  
Stimulation Of

Abstract Thyroid hormone (TH) and autophagy share similar functions in regulating skeletal muscle growth, regeneration, and differentiation. Although TH recently has been shown to increase autophagy in liver, the regulation and role of autophagy by this hormone in skeletal muscle is not known. Here, using both in vitro and in vivo models, we demonstrated that TH induces autophagy in a dose- and time-dependent manner in skeletal muscle. TH induction of autophagy involved reactive oxygen species (ROS) stimulation of 5′adenosine monophosphate-activated protein kinase (AMPK)-Mammalian target of rapamycin (mTOR)- Unc-51-like kinase 1 (Ulk1) signaling. TH also increased mRNA and protein expression of key autophagy genes, microtubule-associated protein light chain 3 (LC3), Sequestosome 1 (p62), and Ulk1, as well as genes that modulated autophagy and Forkhead box O (FOXO) 1/3a. TH increased mitochondrial protein synthesis and number as well as basal mitochondrial O2 consumption, ATP turnover, and maximal respiratory capacity. Surprisingly, mitochondrial activity and biogenesis were blunted when autophagy was blocked in muscle cells by Autophagy-related gene (Atg)5 short hairpin RNA (shRNA). Induction of ROS and 5′adenosine monophosphate-activated protein kinase (AMPK) by TH played a significant role in the up-regulation of Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PPARGC1A), the key regulator of mitochondrial synthesis. In summary, our findings showed that TH-mediated autophagy was essential for stimulation of mitochondrial biogenesis and activity in skeletal muscle. Moreover, autophagy and mitochondrial biogenesis were coupled in skeletal muscle via TH induction of mitochondrial activity and ROS generation.

scholarly journals Loss of Skeletal Muscle Mass Affects the Incidence of Minimal Hepatic Encephalopathy: A Case Control Study

2020 ◽  
Author(s):  
Masakuni Tateyama ◽  
Hideaki Naoe ◽  
Motohiko Tanaka ◽  
Kentaro Tanaka ◽  
Satoshi Narahara ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Liver Cirrhosis ◽  
Hepatic Encephalopathy ◽  
Mass Loss ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Lumbar Vertebra ◽  
Minimal Hepatic Encephalopathy ◽  
Skeletal Muscle Index ◽  
Muscle Mass Loss

Abstract Background: Sarcopenia is a syndrome characterized by progressive and systemic decreases in skeletal muscle mass and muscle strength. The influence or prognosis of various liver diseases in this condition have been widely investigated, but little is known about whether sarcopenia and/or muscle mass loss are related to minimal hepatic encephalopathy.Methods: To clarify the relationship between minimal hepatic encephalopathy and sarcopenia and/or muscle mass loss in patients with liver cirrhosis. Ninety-nine patients with liver cirrhosis were enrolled. Minimal hepatic encephalopathy was diagnosed by a neuropsychiatric test. Skeletal mass index was calculated by dividing muscle area at the third lumbar vertebra by the square of height in meters.Results: MHE was detected in 48 cases (48.5%) and sarcopenia in 6 cases (6.1%). Patients were divided into two groups, with or without MHE. Comparing groups, no significant differences were seen in serum ammonia concentration or rate of sarcopenia. Skeletal muscle index was smaller in patients with minimal hepatic encephalopathy (46.4 cm2/m2) than in those without (51.2 cm2/m2, P = 0.027). Skeletal muscle index represented a predictive factor related to minimal hepatic encephalopathy (<50 cm2/m2; odds ratio 0.300, P = 0.002).Conclusions: Muscle mass loss was related to minimal hepatic encephalopathy, although sarcopenia was not. Measurement of muscle mass loss might be useful to predict MHE.

scholarly journals Loss of skeletal muscle mass affects the incidence of minimal hepatic encephalopathy: A case control study

2020 ◽  
Author(s):  
Masakuni Tateyama ◽  
Hideaki Naoe ◽  
Motohiko Tanaka ◽  
Kentaro Tanaka ◽  
Satoshi Narahara ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Hepatic Encephalopathy ◽  
Mass Loss ◽  
Muscle Mass ◽  
Odds Ratio ◽  
Skeletal Muscle Mass ◽  
Psoas Muscle ◽  
Minimal Hepatic Encephalopathy ◽  
Muscle Area ◽  
Muscle Mass Loss

Abstract Background: Sarcopenia is a syndrome characterized by progressive and systemic decreases in skeletal muscle mass and muscle strength. The influence or prognosis of various liver diseases in this condition have been widely investigated, but little is known about whether sarcopenia and/or muscle mass loss are related to minimal hepatic encephalopathy (MHE).Methods: To clarify the relationship between MHE and sarcopenia and/or muscle mass loss in patients with liver cirrhosis.Methods: Ninety-nine patients with liver cirrhosis were enrolled. MHE was diagnosed by a neuropsychiatric test. Skeletal mass index (SMI) and Psoas muscle index (PMI) were calculated by dividing skeletal muscle area and psoas muscle area at the third lumbar vertebra by the square of height in meters, respectively, to evaluate muscle volume.Results: This study enrolled 99 patients (61 males, 38 females). MHE was detected in 48 cases (48.5%) and sarcopenia in 6 cases (6.1%). Patients were divided into two groups, with or without MHE. Comparing groups, no significant differences were seen in serum ammonia concentration or rate of sarcopenia. SMI was smaller in patients with MHE (46.4 cm2/m2) than in those without (51.2 cm2/m2, P = 0.027). Similarly, PMI was smaller in patients with MHE (4.24 cm2/m2) than in those without (5.53 cm2/m2, P = 0.003). Skeletal muscle volume, which is represented by SMI or PMI was a predictive factor related to MHE (SMI ≥ 50 cm2/m2; odds ratio 0.300, P = 0.002, PMI ≥ 4.3 cm2/m2; odds ratio 0.192, P = 0.001).Conclusions: Muscle mass loss was related to minimal hepatic encephalopathy, although sarcopenia was not. Measurement of muscle mass loss might be useful to predict MHE.

scholarly journals Skeletal muscle mass loss and dose‐limiting toxicities in metastatic colorectal cancer patients

2019 ◽  
Vol 10 (4) ◽  
pp. 803-813 ◽  
Author(s):  
Sophie Kurk ◽  
Petra Peeters ◽  
Rebecca Stellato ◽  
B. Dorresteijn ◽  
Pim Jong ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Skeletal Muscle ◽  
Mass Loss ◽  
Metastatic Colorectal Cancer ◽  
Cancer Patients ◽  
Muscle Mass ◽  
Skeletal Muscle Mass ◽  
Muscle Mass Loss ◽  
Colorectal Cancer Patients

scholarly journals Red Ginseng Improves Exercise Endurance by Promoting Mitochondrial Biogenesis and Myoblast Differentiation

Molecules ◽  
2020 ◽  
Vol 25 (4) ◽  
pp. 865 ◽  
Author(s):  
Eun Ju Shin ◽  
Seongin Jo ◽  
Sungbin Choi ◽  
Chang-Won Cho ◽  
Won-Chul Lim ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mitochondrial Biogenesis ◽  
Muscle Function ◽  
Myogenic Differentiation ◽  
Myoblast Differentiation ◽  
Time To Exhaustion ◽  
Therapeutic Effects ◽  
Red Ginseng ◽  
Skeletal Muscle Function ◽  
Exercise Endurance

Red ginseng has been reported to elicit various therapeutic effects relevant to cancer, diabetes, neurodegenerative diseases, and inflammatory diseases. However, the effect of red ginseng on exercise endurance and skeletal muscle function remains unclear. Herein, we sought to investigate whether red ginseng could affect exercise endurance and examined its molecular mechanism. Mice were fed with red ginseng extract (RG) and undertook swimming exercises to determine the time to exhaustion. Animals fed with RG had significantly longer swimming endurance. RG treatment was also observed to enhance ATP production levels in myoblasts. RG increased mRNA expressions of mitochondrial biogenesis regulators, NRF-1, TFAM, and PGC-1α, which was accompanied by an elevation in mitochondrial DNA, suggesting an enhancement in mitochondrial energy-generating capacity. Importantly, RG treatment induced phosphorylation of p38 and AMPK and upregulated PGC1α expression in both myoblasts and in vivo muscle tissue. In addition, RG treatment also stimulated C2C12 myogenic differentiation. Our findings show that red ginseng improves exercise endurance, suggesting that it may have applications in supporting skeletal muscle function and exercise performance.

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