Short-term nicotinamide riboside treatment improves muscle quality and function in mice and increases cellular energetics and differentiating capacity of myogenic progenitors.
Short-term nicotinamide riboside treatment improves muscle quality and function in mice and increases cellular energetics and differentiating capacity of myogenic progenitors.
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DOI：
10.1016/j.nut.2021.111189
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发表时间：
2021-07
期刊：
影响因子：
--
通讯作者：
Troen BR
中科院分区：
文献类型：
--
作者：
Seldeen KL;Shahini A;Thiyagarajan R;Redae Y;Leiker M;Rajabian N;Dynka A;Andreadis ST;Troen BR
Nicotinamide adenine dinucleotide (NAD+), an essential co-factor for mitochondrial function, declines with aging, which may lead to impaired physical performance. Nicotinamide riboside (NR), a NAD+ precursor, restores cellular NAD+ levels. Here we examined the impacts of short term NR supplementation on physical performance in middle-aged mice and impacts on mouse and human muscle stem cells. We treated fifteen-month-old male C57BL/6J mice with NR at 300 mg/kg/day (NR3), 600 mg/kg/day (NR6), or placebo (PLB), n=8 per group, and assessed changes in physical performance, muscle histology, and NAD+ content after 4 weeks of treatment. We found that NR increased total NAD+ in muscle tissue (NR3 p=0.01; NR6 p=0.004, both versus PLB), enhanced treadmill endurance and open field activity, and prevented decline in grip strength. Histologic analysis revealed NR treated mice exhibited enlarged slow twitch fibers (NR6 versus PLB p=0.014; NR3 p=0.16) and a trend towards more slow fibers (NR3 p=0.14; NR6 p=0.22). We next carried out experiments to characterize NR impacts on mitochondrial activity and cellular energetics in vitro. We observed that NR boosted basal and maximal cellular aerobic and anaerobic respiration in both mouse and human myoblasts and human myotubes. Additionally, NR treatment improved the differentiating capacity of myoblasts and increased myotube size and fusion index upon stimulation of these progenitors to form multinucleated myotubes. These findings support a role for NR in improving cellular energetics and functional capacity in mice, which support the translation of this work into clinical settings as a strategy for improving and/or maintaining healthspan during aging.
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影响因子：
4.9
作者：
Goody MF;Henry CA
通讯作者：
Henry CA
血浆NAD（+）代谢组在“正常”衰老中失调。
影响因子：
2.6
作者：
Clement J;Wong M;Poljak A;Sachdev P;Braidy N
通讯作者：
Braidy N
影响因子：
4.2
作者：
Gong B;Pan Y;Vempati P;Zhao W;Knable L;Ho L;Wang J;Sastre M;Ono K;Sauve AA;Pasinetti GM
通讯作者：
Pasinetti GM
影响因子：
29
作者：
Frederick DW;Loro E;Liu L;Davila A Jr;Chellappa K;Silverman IM;Quinn WJ 3rd;Gosai SJ;Tichy ED;Davis JG;Mourkioti F;Gregory BD;Dellinger RW;Redpath P;Migaud ME;Nakamaru-Ogiso E;Rabinowitz JD;Khurana TS;Baur JA
通讯作者：
Baur JA
影响因子：
6.1
作者：
Crisol, Barbara M.;Veiga, Camilla B.;Ropelle, Eduardo R.
通讯作者：
Ropelle, Eduardo R.