Melatonin as a Potential Agent in the Treatment of Sarcopenia

Coto‐Montes, Ana; Boga, José Antonio; Tan, Dun Xian; Reíter, Russel J.

doi:10.3390/ijms17101771

Cited by 43 publications

(24 citation statements)

References 138 publications

(166 reference statements)

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“…Under these conditions, the endogenous antioxidative defense capacity is weakened in CMT1A patients. The elevated GSSG/GSH ratio here reported in these patients is consistent with an elevated intracellular hyperoxidative status [ 35 ]. GSH can also act as a direct free radical scavenger through electron donation [ 50 ].…”

Section: Discussionsupporting

confidence: 80%

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Melatonin Treatment Reduces Oxidative Damage and Normalizes Plasma Pro-Inflammatory Cytokines in Patients Suffering from Charcot-Marie-Tooth Neuropathy: A Pilot Study in Three Children

et al. 2017

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Charcot-Marie-Tooth neuropathy (CMT) is a motor and sensory neuropathy comprising a heterogeneous group of inherited diseases. The CMT1A phenotype is predominant in the 70% of CMT patients, with nerve conduction velocity reduction and hypertrophic demyelination. These patients have elevated oxidative stress and chronic inflammation. Currently, there is no effective cure for CMT; herein, we investigated whether melatonin treatment may reduce the inflammatory and oxidative damage in CMT1A patients. Three patients, aged 8–10 years, were treated with melatonin (60 mg at 21:00 h plus 10 mg at 09:00 h), and plasma levels of lipid peroxidation (LPO), nitrites (NOx), IL-1β, IL-2, IL-6, TNF-α, INF-γ, oxidized to reduced glutathione (GSSG/GSH) ratio, and the activities of superoxide dismutase (SOD), glutathione-S transferase (GST), glutathione peroxidase (GPx), and reductase (GRd), were determined in erythrocytes at 3 and 6 months of treatment. Healthy age- and sex-matched subjects were used as controls. The results showed increased activities of SOD, GST, GPx, and GRd in CMT1A patients, which were reduced at 3 and 6 months of treatment. The GSSG/GSH ratio significantly increased in the patients, returning to control values after melatonin treatment. The inflammatory process was confirmed by the elevation of all proinflammatory cytokines measured, which were also normalized by melatonin. LPO and NOx, which also were elevated in the patients, were normalized by melatonin. The results document beneficial effects of the use of melatonin in CMT1A patients to reduce the hyperoxidative and inflammatory condition, which may correlate with a reduction of the degenerative process.

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Section: Discussionsupporting

confidence: 80%

“…Collectively, the data support trophic effects of melatonin on skeletal muscle [ 33 , 34 , 35 ]. With these considerations, we evaluated whether melatonin administration could reduce the oxidative stress and inflammation in CMT patients.…”

Section: Introductionsupporting

confidence: 57%

Melatonin Treatment Reduces Oxidative Damage and Normalizes Plasma Pro-Inflammatory Cytokines in Patients Suffering from Charcot-Marie-Tooth Neuropathy: A Pilot Study in Three Children

et al. 2017

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“…Coto-Montes and co-workers reviewed the promising utility of safe melatonin dietary intake in sarcopenia, even if its therapeutic potential in patients is still controversial [98,99]. Recent evidence in different sarcopenic mice models obtained by single or double KO (DKO) of mitochondrial shaping proteins (DRP1-KO and Opa1-Drp1 DKO) definitively indicated how, in skeletal muscles mitohormesis, the mitochondrial size balance was essential [100,101].…”

Section: Melatonin Alleviates Skeletal Muscle Disorders In Vitro and mentioning

confidence: 99%

Impact of Melatonin on Skeletal Muscle and Exercise

Stacchiotti

Favero

Rodella

2020

Cells

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Skeletal muscle disorders are dramatically increasing with human aging with enormous sanitary costs and impact on the quality of life. Preventive and therapeutic tools to limit onset and progression of muscle frailty include nutrition and physical training. Melatonin, the indole produced at nighttime in pineal and extra-pineal sites in mammalians, has recognized anti-aging, anti-inflammatory, and anti-oxidant properties. Mitochondria are the favorite target of melatonin, which maintains them efficiently, scavenging free radicals and reducing oxidative damage. Here, we discuss the most recent evidence of dietary melatonin efficacy in age-related skeletal muscle disorders in cellular, preclinical, and clinical studies. Furthermore, we analyze the emerging impact of melatonin on physical activity. Finally, we consider the newest evidence of the gut–muscle axis and the influence of exercise and probably melatonin on the microbiota. In our opinion, this review reinforces the relevance of melatonin as a safe nutraceutical that limits skeletal muscle frailty and prolongs physical performance.

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“…Although the mechanisms are not completely understood, the synthesis and actions of melatonin and leptin seem to regulate each other. Moreover, the role of melatonin in protein synthesis regulation is well documented (36,37). We conclude that melatonin drives dosedependent effects in tissues and strongly suggests the use of melatonin in obesity management since it is implicated in the regulation of adipokine secretion.…”

Section: Figure 2 Illustration Of the Effect Of Leptin Deficiency Anmentioning

confidence: 66%

Dose-dependent beneficial effect of melatonin on obesity; interaction of melatonin and leptin

et al. 2019

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Although numerous studies have noted leptin’s role in obesity, there are still important mechanisms insights that need to be elucidated. Disturbed leptin production is associated with eating disorders, leading to alter food intake and energy expenditure. Proper regulation of protein homeostasis is critical for metabolic diseases such as obesity. Thus, the purpose of the present work was to study the unfolded protein response, which is implicated in the alleviation of endoplasmic reticulum stress-dependent dysregulation of nutritional status. We studied the effect of leptin deficiency on liver, brain and skeletal muscle tissues in obese (ob/ob) mice and the actions of a daily melatonin administration, as a possible treatment. Our findings showed that the leptin-deficient mice presented tissue-specific alterations of the three adaptive unfolded protein responses. ATF6α arm is strongly activated in all of them, indicating a deregulated lipid metabolism by the lack of leptin. Likewise, melatonin also alleviates unfolded protein response in a tissue-specific manner, acting mainly in the restoration of this disturbed ATF6α pathway. These findings support the use of melatonin as a potential therapeutic treatment against leptin-associated disorders.

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Melatonin as a Potential Agent in the Treatment of Sarcopenia

Cited by 43 publications

References 138 publications

Melatonin Treatment Reduces Oxidative Damage and Normalizes Plasma Pro-Inflammatory Cytokines in Patients Suffering from Charcot-Marie-Tooth Neuropathy: A Pilot Study in Three Children

Melatonin Treatment Reduces Oxidative Damage and Normalizes Plasma Pro-Inflammatory Cytokines in Patients Suffering from Charcot-Marie-Tooth Neuropathy: A Pilot Study in Three Children

Impact of Melatonin on Skeletal Muscle and Exercise

Dose-dependent beneficial effect of melatonin on obesity; interaction of melatonin and leptin

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