Kourtzidis I A, Dolopikou C F, Tsiftsis A N, Margaritelis N V, Theodorou A A, Zervos I A, Tsantarliotou M P, Veskoukis A S, Vrabas I S, Paschalis V, Kyparos A, Nikolaidis M G
School of Physical Education and Sport Science at Serres, Aristotle University of Thessaloniki, Serres, Greece.
Intensive Care Unit, 424 General Military Hospital of Thessaloniki, Thessaloniki, Greece.
Exp Physiol. 2018 Oct;103(10):1357-1366. doi: 10.1113/EP086964. Epub 2018 Aug 28.
What is the central question of this study? The aim was to investigate the potential metabolic and redox mechanisms that impaired exercise performance after 21 days of supplementation with 300 mg (kg body weight) of nicotinamide riboside in rats. What is the main finding and its importance? Nicotinamide riboside disturbed energy and redox metabolism and impaired exercise performance in heathy rats. Exogenously administered redox agents in heathy populations might lead to adverse effects.
Nicotinamide riboside is a recently discovered form of vitamin B that can increase NAD(P) levels. NAD(P) plays key roles in energy metabolism, and its main function is the transfer of electrons in various cellular reactions. Research in aged or diseased mice reported that nicotinamide riboside increases NAD(H) levels, reduces morbidity and improves health and muscle function. We have recently shown that in healthy young rats, chronic administration of nicotinamide riboside marginally non-significantly decreased exercise performance by 35% (P = 0.071). As a follow-up to this finding, we analysed samples from these animals, in an attempt to reveal the potential mechanisms driving this adverse effect, focusing on redox homeostasis and bioenergetics. Thirty-eight Wistar rats were divided into four groups: control (n = 10), exercise (n = 9), nicotinamide riboside (n = 10) and exercise plus nicotinamide riboside (n = 9). Nicotinamide riboside was administered for 21 days [300 mg (kg body weight) daily]. At the end of administration, the exercise and the exercise plus nicotinamide riboside groups performed an incremental swimming performance test until exhaustion. Nicotinamide riboside supplementation increased the levels of NADPH in the liver (P = 0.050), increased the levels of F -isoprostanes in plasma (P = 0.047), decreased the activity of glutathione peroxidase (P = 0.017), glutathione reductase (P < 0.001) and catalase (P = 0.024) in erythrocytes, increased the level of glycogen in the liver (P < 0.001) and decreased the concentration of glucose (P = 0.016) and maximal lactate accumulation in plasma (P = 0.084). These findings support the prevailing idea that exogenously administered redox agents in heathy populations might lead to adverse effects and not necessarily to beneficial or neutral effects.
本研究的核心问题是什么？目的是研究在大鼠中补充300毫克/（千克体重）烟酰胺核糖21天后损害运动能力的潜在代谢和氧化还原机制。主要发现及其重要性是什么？烟酰胺核糖扰乱了健康大鼠的能量和氧化还原代谢并损害了运动能力。在健康人群中外部施用氧化还原剂可能会导致不良反应。
烟酰胺核糖是最近发现的一种维生素B形式，可提高NAD(P)水平。NAD(P)在能量代谢中起关键作用，其主要功能是在各种细胞反应中传递电子。对老年或患病小鼠的研究报告称，烟酰胺核糖可提高NAD(H)水平、降低发病率并改善健康和肌肉功能。我们最近发现，在健康的年轻大鼠中，长期施用烟酰胺核糖会使运动能力略有下降但无统计学意义，下降了35%（P = 0.071）。作为这一发现的后续研究，我们分析了这些动物的样本，试图揭示导致这种不良反应的潜在机制，重点关注氧化还原稳态和生物能量学。38只Wistar大鼠分为四组：对照组（n = 10）、运动组（n = 9）、烟酰胺核糖组（n = 10）和运动加烟酰胺核糖组（n = 9）。烟酰胺核糖连续施用21天[每天300毫克/（千克体重）]。给药结束时，运动组和运动加烟酰胺核糖组进行递增游泳耐力测试直至精疲力竭。补充烟酰胺核糖可提高肝脏中NADPH水平（P = 0.050），提高血浆中F -异前列腺素水平（P = 0.047），降低红细胞中谷胱甘肽过氧化物酶（P = 0.017）、谷胱甘肽还原酶（P < 0.001）和过氧化氢酶（P = 0.024）的活性，提高肝脏中糖原水平（P < 0.001），降低血浆中葡萄糖浓度（P = 0.016）和最大乳酸积累量（P = 0.084）。这些发现支持了一种普遍观点，即在健康人群中外部施用氧化还原剂可能会导致不良反应，而不一定是有益或中性作用。
