Leucine as a treatment for muscle wasting: A critical review

Ham, Daniel J.; Caldow, Marissa K.; Lynch, Gordon S.; Koopman, René

doi:10.1016/j.clnu.2014.09.016

Cited by 70 publications

(63 citation statements)

References 72 publications

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“…Indeed, numerous studies reveal that inactivation of the IGF1 receptor impairs muscle growth whereas activation of the IGF1 receptor promotes hypertrophy (reviewed in [36]). The activation of the IGF1-Akt pathway promotes protein synthesis by increasing mRNA translation of specific proteins [37]. …”

Section: Redox Regulation Of Muscle Atrophymentioning

confidence: 99%

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Redox control of skeletal muscle atrophy

Powers

Morton

Ahn

et al. 2016

Free Radical Biology and Medicine

149

157

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Skeletal muscles comprise the largest organ system in the body and play an essential role in body movement, breathing, and glucose homeostasis. Skeletal muscle is also an important endocrine organ that contributes to the health of numerous body organs. Therefore, maintaining healthy skeletal muscles is important to support overall health of the body. Prolonged periods of muscle inactivity (e.g., bed rest or limb immobilization) or chronic inflammatory diseases (i.e., cancer, kidney failure, etc.) result in skeletal muscle atrophy. An excessive loss of muscle mass is associated with a poor prognosis in several diseases and significant muscle weakness impairs the quality of life. The skeletal muscle atrophy that occurs in response to inflammatory diseases or prolonged inactivity is often associated with both oxidative and nitrosative stress. In this report, we critically review the experimental evidence that provides support for a causative link between oxidants and muscle atrophy. More specifically, this review will debate the sources of oxidant production in skeletal muscle undergoing atrophy as well as provide a detailed discussion on how reactive oxygen species and reactive nitrogen species modulate the signaling pathways that regulate both protein synthesis and protein breakdown.

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Section: Redox Regulation Of Muscle Atrophymentioning

confidence: 99%

“…Abundant evidence indicates that mTORC1 is the primary mediator of protein synthesis in skeletal muscle [36]. Upon activation, the two main effectors phosphorylated by mTORC1 that promote protein synthesis are ribosomal protein S6 kinase 1 (S6K1) and eukaryotic initiation factor 4E (4E-BP1) [36, 37]. …”

Section: Redox Regulation Of Muscle Atrophymentioning

confidence: 99%

Redox control of skeletal muscle atrophy

Powers

Morton

Ahn

et al. 2016

Free Radical Biology and Medicine

149

157

View full text Add to dashboard Cite

show abstract

“…Although essential amino acid intake enhances muscle protein synthesis 48,49) , it cannot maintain a positive net balance in the long run 31) ; not even leucine-rich amino acid supplements, which are known to increases protein synthesis 50) , can do such. Moreover, a recent review concluded that leucine, as a stand-alone nutritional intervention, is not effective in the prevention of muscle wasting and sarcopenia 51) . Also, many other intervention studies have shown that nutritional supplementation alone does not increase muscle mass [52][53][54][55] .…”

Section: Loss Of Skeletal Muscle Mass With Agingmentioning

confidence: 99%

Link between blood flow and muscle protein metabolism in elderly adults

Zempo

Isobe

Naito

2017

JPFSM

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The mechanism which causes sarcopenia, a loss of muscle mass and strength with aging, remains unclear. Muscle mass is controlled by the net balance between protein synthesis and breakdown; however, net balance differences in the basal state do not contribute to sarcopenia. On the other hand, anabolic resistance, a reduction in muscle protein synthesis in response to protein intake, does seem to be involved in sarcopenia. Muscles which are subject to anabolic resistance do not show incremental blood flow volume during the fed-state. Because the vascular system transports amino acids and other nutrients that are essential for muscle protein synthesis, blood flow volume may be a regulator of anabolic resistance. There is some evidence of a link between blood flow and muscle protein metabolism. In addition, a combination of resistance training and amino acid supplementation promotes a positive net protein balance. Resistance training improves, and detraining reduces blood flow volume; therefore, blood flow volume may be involved as a background mechanism for sarcopenia. Moreover, previous studies have shown that sodium nitroprusside, a vasodilatory nitric oxide donor, enhances muscle protein synthesis. Conversely, angiotensin II, a major vasoconstrictive peptide, induces skeletal muscle protein breakdown. In this review, we discuss a possible role for blood flow in skeletal muscle protein metabolism in elderly adults. The regulation of blood flow may prove to be a beneficial treatment for sarcopenia.

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“…Eine Steigerung der Muskelkraft durch die verzweigtkettigen Aminosäuren ist bislang jedoch nicht gesichert [11,206]. Ham et al bewerteten Leuzin als alleinige Ernährungsintervention zur Prä-vention eines Muskelverlusts als wirkungslos [207]. dass es in Kombination mit parenteraler Ernährung die Muskelproteinsynthese und die Eiweißbilanz bei postoperativen Tumorpatienten verbessern kann [208].…”

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2015

Aktuel Ernahrungsmed

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Leucine as a treatment for muscle wasting: A critical review

Cited by 70 publications

References 72 publications

Redox control of skeletal muscle atrophy

Redox control of skeletal muscle atrophy

Link between blood flow and muscle protein metabolism in elderly adults

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