l -Carnitine enhances exercise endurance capacity by promoting muscle oxidative metabolism in mice

Kim, Jun Ho; Pan, Jeong Hoon; Lee, Eui Seop; Kim, Young Jun

doi:10.1016/j.bbrc.2015.07.009

Cited by 38 publications

(27 citation statements)

References 31 publications

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“…Several reports have indicated that the L‐carnitine can exert a pleiotropic effect. For example, the administration of L‐carnitine to exercise‐loaded mice increased their exercise endurance via the up‐regulation of mitochondrial biosynthesis factors such as PGC‐1α 28. L‐carnitine also decreased the levels of markers for oxidative stress, such as 8‐OHdG and 4‐hydroxynonenal and TNF‐α in livers of non‐alcoholic steatohepatitis model mice,29 suggesting that L‐carnitine exhibits anti‐oxidative and anti‐inflammatory actions.…”

Section: Discussionmentioning

confidence: 99%

Potential therapeutic interventions for chronic kidney disease‐associated sarcopenia via indoxyl sulfate‐induced mitochondrial dysfunction

Enoki

Watanabe

Arake

et al. 2017

J cachexia sarcopenia muscle

131

132

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BackgroundChronic kidney disease (CKD) patients experience skeletal muscle wasting and decreased exercise endurance. Our previous study demonstrated that indoxyl sulfate (IS), a uremic toxin, accelerates skeletal muscle atrophy. The purpose of this study was to examine the issue of whether IS causes mitochondria dysfunction and IS‐targeted intervention using AST‐120, which inhibits IS accumulation, or mitochondria‐targeted intervention using L‐carnitine or teneligliptin, a dipeptidyl peptidase‐4 inhibitor which retains mitochondria function and alleviates skeletal muscle atrophy and muscle endurance in chronic kidney disease mice.MethodsThe in vitro effect of IS on mitochondrial status was evaluated using mouse myofibroblast cells (C2C12 cell). The mice were divided into sham or 5/6‐nephrectomized (CKD) mice group. Chronic kidney disease mice were also randomly assigned to non‐treatment group and AST‐120, L‐carnitine, or teneligliptin treatment groups.ResultsIn C2C12 cells, IS induced mitochondrial dysfunction by decreasing the expression of PGC‐1α and inducing autophagy in addition to decreasing mitochondrial membrane potential. Co‐incubation with an anti‐oxidant, ascorbic acid, L‐carnitine, or teneligliptine restored the values to their original state. In CKD mice, the body and skeletal muscle weights were decreased compared with sham mice. Compared with sham mice, the expression of interleukin‐6 and atrophy‐related factors such as myostatin and atrogin‐1 was increased in the skeletal muscle of CKD mice, whereas muscular Akt phosphorylation was decreased. In addition, a reduced exercise capacity was observed for the CKD mice, which was accompanied by a decreased expression of muscular PCG‐1α and increased muscular autophagy, as reflected by decreased mitochondria‐rich type I fibres. An AST‐120 treatment significantly restored these changes including skeletal muscle weight observed in CKD mice to the sham levels accompanied by a reduction in IS levels. An L‐carnitine or teneligliptin treatment also restored them to the sham levels without changing IS level.ConclusionsOur results indicate that IS induces mitochondrial dysfunction in skeletal muscle cells and provides a potential therapeutic strategy such as IS‐targeted and mitochondria‐targeted interventions for treating CKD‐induced muscle atrophy and decreased exercise endurance.

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Section: Discussionmentioning

confidence: 99%

Potential therapeutic interventions for chronic kidney disease‐associated sarcopenia via indoxyl sulfate‐induced mitochondrial dysfunction

Enoki

Watanabe

Arake

et al. 2017

J cachexia sarcopenia muscle

131

132

View full text Add to dashboard Cite

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“…Thus, the weight gain in l-Carnitinetreated hyperuricemic rats was unreasonable and hard to be explained herein. However, the anti-adiposity effects of l-Carnitine in fructose-supplemented hyperuricemic rats could be attributed to its lipolytic and antioxidant effects according to Flanagan et al (2010) and Derosa et al (2011), in addition to eliciting more energy expenditure (Kim, Pan, Lee, & Kim, 2015).…”

Section: Discussionmentioning

confidence: 99%

Possible role ofl‐carnitine in improvement of metabolic and hepatic changes in hyperuricemic and hyperuricemic—Fructose‐supplemented rats

et al. 2019

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Hyperuricemia was linked to diabetes mellitus, metabolic syndrome, and oxidative stress, and could be induced by higher fructose consumption through altering energy status in liver. l‐Carnitine is an antioxidant, affecting mitochondria and cellular energetics; however, little is known about its effects in hyperuricemic states. This study investigated metabolic and hepatic effects of hyperuricemia and fructose feeding, and demonstrated the role of l‐Carnitine in such states. Fifty adult male Wistar rats were randomly divided into control, untreated hyperuricemic, fructose‐supplemented hyperuricemic, l‐Carnitine‐treated hyperuricemic, and l‐Carnitine‐treated fructose‐supplemented hyperuricemic groups. The separated plasma was used for determination of the glycemic control, lipid profile, liver function tests, uric acid level, and oxidative stress markers. Atherogenic index, HOMA‐IR, and body mass index (BMI) were calculated. Left liver lobe and left kidney specimen from all groups were used for histopathological studies. Hyperuricemic rats exhibited significantly hypoalbuminemia, dyslipidemia, insulin resistance, and oxidative stress compared to the controls. Fructose‐supplemented hyperuricemic group showed obesity and more deleterious effects, as well as, steatosis, and renal tubular damage compared to the hyperuricemic rats. Concomitant l‐Carnitine treatment with hyperuricemia improved such effects, despite causing adiposity. While combined l‐Carnitine treatment and fructose supplementation in hyperuricemia limited the aggressive hyperuricemic picture of fructose supplementation. It is concluded that hyperuricemia has detrimental metabolic and hepatic effects. Artificial fructose supplementation worsened such effects, while l‐Carnitine was efficient in ameliorating these hyperuricemia and/or excess fructose‐induced hyperuricemia effects, through its anti‐inflammatory, antisteatotic, and antioxidant properties.

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“…Carbohydrate oxidation is less oxygen demanding per molecule of ATP produced than fatty-acid oxidation,69 but it is limited to the carbohydrate storage. However, during prolonged exercise, lipids might be the more important source of energy, and a high capability for lipid oxidation delays carbohydrate depletion and increases endurance capacity 70. L-carnitine is suggested to be the major direct regulator of fatty-acid oxidation in the transition from moderate to higher exercise intensities 66.…”

Section: Introductionmentioning

confidence: 99%

Story behind meldonium–from pharmacology to performance enhancement: a narrative review

et al. 2016

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Recent reports from the World Anti-Doping Agency (WADA) indicate an alarming prevalence in the use of meldonium among elite athletes. Therefore, in January 2016, meldonium was added to WADA's prohibited list after being monitored since 2015. Meldonium has been shown to have beneficial effects in cardiovascular, neurological and metabolic diseases due to its anti-ischaemic and cardioprotective properties, which are ascribed mainly to its inhibition of ß-oxidation and its activation of glycolysis. Despite its widespread use, there are only a few clinical studies or clinical trials available. Meldonium is registered in most Baltic countries and is easily accessible through the internet with no serious adverse effects reported by the manufacturer so far. Among athletes, meldonium is used with the purpose of increasing recovery rate or exercise performance. The benefit of taking meldonium in view of performance enhancement in athletes is quite speculative and is discussed without sound scientific evidence. This narrative review provides a detailed overview of the drug meldonium, focusing on the main topics pharmacology and biochemical actions, clinical applications, pharmacokinetics, methods of detection and potential for performance enhancement in athletes.

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l -Carnitine enhances exercise endurance capacity by promoting muscle oxidative metabolism in mice

Cited by 38 publications

References 31 publications

Potential therapeutic interventions for chronic kidney disease‐associated sarcopenia via indoxyl sulfate‐induced mitochondrial dysfunction

Potential therapeutic interventions for chronic kidney disease‐associated sarcopenia via indoxyl sulfate‐induced mitochondrial dysfunction

Possible role ofl‐carnitine in improvement of metabolic and hepatic changes in hyperuricemic and hyperuricemic—Fructose‐supplemented rats

Story behind meldonium–from pharmacology to performance enhancement: a narrative review

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