神奇源 ReMage-Power 600mg / 30粒 -金装瓶

制造商: Merion Inc
UPC/SKU: p_remage_400_30
$1,200.00
梯度价-买得越多,省得越多
数量 3+
价格 $999.98
ReMage-Power 神奇源 金装瓶
如何保持年轻态?
β-烟酰胺单核苷酸(β-Nicotinamide mononucleotide,NMN),NMN 在人体细胞能量生成中扮演重 要角色,它参与细胞内烟酰胺腺嘌呤二核苷酸(NAD)的合成,而 NAD 是细胞能量转化的重要辅酶。

ReMage Power   神奇源  金装瓶 

β-烟酰胺单核苷酸(β-Nicotinamide mononucleotide,NMN),NMN 在人体细胞能量生成中扮演重 要角色,它参与细胞内烟酰胺腺嘌呤二核苷酸(NAD)的合成,而 NAD 是细胞能量转化的重要辅 酶。 

看哈佛大学的科学家们对NMN的功效怎么说:

 

 

 

(一)产品描述:

神奇源含有高浓度高酶活性的β-Nicotinamide mononucleotide, NMN 。

其中NMN 是由核糖和烟酰胺衍生的核苷酸, 它是一种天然存在的化合物,在细胞能量代谢中发挥重要作用。β-烟酰胺单核苷酸(“NMN”)参与烟酰胺腺嘌呤二核苷酸(NAD )的合成,它本身是没有活性的,直到在人体内被转化成了 NAD 才有真正的生理效果。

NAD 全名烟酰胺腺嘌呤双核苷酸, 又称辅酶 I 或者诺加因子。参与人体内 200 种氧化还原的酶反应,而其中最重要的莫过于乙酰化酶 Sirtuin1-7 和 1 型多聚 ADP 核糖聚合酶 PARP1。NAD 是参与氧化还原反应的辅酶,对于将营养物质的能量转化为细胞能够使用的人体必需酶。 它由两个磷酸基连接的核苷酸组成。 一个核苷酸含有腺嘌呤,另一个是烟酰胺。 它有助于酶在氧化还原反应过程中转移电子形成 ATP,从而帮助提供能量。
然而,水平随着年龄的增长而下降 - 老年人细胞中的 NAD 会下降超过 60%。 如果 NAD 的水平增加, 细胞内能量机制可能恢复正常。

从新南威尔士大学和哈佛大学的科学家David Sinclair团队研究发现了这种β-烟酰胺单核苷酸(β-Nicotinamide mononucleotideNMN),可以让60岁的小鼠身体指标回到20岁的状态,定期摄入NMN,可以有效地增加 NAD+在体内的含量, 从而帮助人类自身修复细胞的损伤,延缓老年化现象的发生!

 

(二)科研报道:

以下是各大顶级学术期刊相续发表过基于NAD+的抗衰老研究:


上个世纪的诺贝尔获得者 Linus Pauline 坚持服用 NAD+前体 40 年,一直活到93 岁。 加拿大第二长寿的老人在70 岁的时候开始服用 NAD+前体,活到了 111 岁,还去参加滑雪比赛。 

在英国多达 8000 人,长达 15 年的 CDP 临床实验中,服用 NAD+的组比其他所有组减少了11%的全死亡率!

新南威尔士大学和哈佛大学的研究发现,定期摄入 NMN,可以有效地增加 NAD+在体内的含量,从而帮助人类自身修复细胞的损伤,修复神经元,减少老年化的发生!

如此强大的天然营养物质,在 2016 年 12 月获得了美国航空局 NASA 颁布了 iTech 奖。NAD+将作为保护宇航员的 DNA 不受到辐射伤害的专用抗氧化补充剂。该物质将列入 2025 年与人类一同登 陆火星计划。

 

(三)试验显示: β-Nicotinamide mononucleotide, NMN 的作用示意图:

 

(四)神奇功效: “神奇源”的主要成分NMN功效:能改善体力下降、缺乏精力、智力退化、代谢紊乱、睡眠质量低下等。

 

(五)适用人群: 

适用工作生活压力大感觉自己精力不足的人群;工作与生活在高辐射或者高化学物质环境人群,例如空乘,科研人员和户外工作者等

“神奇源”还有一个广大女性梦寐以求的效果:增加皮肤的微循环,抗氧化。

众所周知,随着年龄的增加,人体的皮肤下的毛细血管会被代谢物逐渐堵塞。而被堵塞的毛细血管无法提供足够的营养给皮肤细胞就会导致皮肤细胞逐渐死亡,于是产生了各种皮肤干燥,发黄,粗糙等结果。 

在服用“神奇源”以后(特别是空腹食用的情况下)可以切实体会到皮肤有刺痒感,有些服用者会有皮肤泛红的现象,这些就是因为人体皮下毛细血管被疏通,细胞得到了额外的血液供应的结果。但我们仍然建议,饭后服用以减少不适感。

(六)服用反馈:

白天精力明显变好了,一点都不犯困,好神奇。 

空腹服用全身一下变得好红,一开始有点害怕但后来知道是在疏通血管就放心了,这段时间每天 以肉眼可见的速度变美呢? 

给妈妈买了服用,她晚上睡眠好了很多,大便也成型了,这个药怎么能同时做到这两点的? 刚开始脸和头皮有点刺痒感,但确实感觉最近皮肤比以前润了 老爸每天去打羽毛球,他感觉体力比以前好了,体力恢复速度也快了很多 感觉专注力提高了啊,每天的时间都好短,晚上上床秒睡,早上起来就可以直接工作了 为什么酒量感觉比以前提升了?你们的产品还有这个效果吗?

 

(七)有效成分:

β-Nicotinamide mononucleotide, NMN 。

 

(八)服用方法: 一天一次,一次一粒。空腹服用,效果更好。科学研究证实,摄入 NMN 是安全和有效的。

【産地】USA

【有效期】3 年

【注意事项】本品不能替代药物的治疗作用。孕妇禁用

【储存】密封,置阴凉干燥处。

【制造商】:MERION,INC. USA

NMNNAD性能对比

品名

原料价格

分子量大小

氧化型

还原型

非氧化/还原

前体

辅酶型

干扰性

NMN

(β-煙酰胺單核苷酸

/ β-nicotinamide mononucleotide)

$6000.00-$16000.00/kg

 

分子量334.2192 g/mol-2个NMN结合在一起形成一个NAD+分子,NMN分子很容易透过细胞膜,进入细胞内部。

 

 

 

非氧化还原型

 

 

口服NMN途径不影响其它酶的活性

 

 

 

 

 

 

 

 

 

NAD+辅酶I,全称烟酰胺腺嘌呤二核苷酸,又称二磷酸烟苷

$1900.00/kg

分子量663.43 g/mol- NAD+分子,不能透过细胞膜,进入细胞内部。服用NAD+没有功效的原因之所在。

 

氧化型

 

 

 

NMN是NAD前体

 

辅酶I

干扰其它酶的活性

 

 

 

 

 

 

 

 

 

NADH(Nicotinamide adenine dinucleotide)是脱氢酶一种化学物质,是烟酰胺腺嘌呤二核苷酸的还原态,还原型辅酶Ⅰ。

N指烟酰胺,

A指腺嘌呤,

D是二核苷酸。

$4230.00/kg

分子量663.43 g/mol-

NADH分子是线粒体中能量产生链中的控制标志物。

经过的途径不一样。

用于糖酵解和细胞呼吸作用中的柠檬酸循环。

 

还原型

 

 

辅酶I

干扰其它酶的活性

 

说明:当2个NMN结合在一起形成一个NAD+分子,此时NAD+辅酶I消耗酶的唯一底物,即DNA修复酶PARP的唯一底物、长寿蛋白Sirtuins1-7的唯一底物、环ADP核糖合成酶CD38/157的唯一底物。所以,NMN物质+矿物质+微量元素+载体才能起到修复神经元细胞,延长神经元寿命,才能逆转长寿基因Sirtuins1-7,才能延长长寿基因Sirtuins1-7寿命,让你年轻30岁的不是梦!

 

 

富含NMN的食物NMN是人体内固有的物质,一些水果和蔬菜也富含,Cell杂志统计了一些常见食物的NMN含量

食物中NMN含量

食物类型

名称

Mg/100g食物

蔬菜

毛豆

0.47–1.88

蔬菜

西兰花

0.25–1.12

蔬菜

黄瓜种子

0.56

黄瓜皮

0.65

蔬菜

卷心菜

0.0–0.90

水果

鳄梨

0.36–1.60

水果

番茄

0.26–0.30

菌类

蘑菇

0.0–1.01

牛肉(生)

0.06–0.42

海鲜

0.22

 

 

70公斤(Kg)左右的65岁以上的,每天补充600mg;45岁左右的,每天补充300mg。NMN服用量:

 

注:

(1)一千克(公斤)=2.2046226218488磅,那么70公斤就是154.323584磅 

(2)如果要吃食物补充NMN这个量600mg,吃毛豆32公斤/每天;吃西兰花54公斤/每天。

 


参考文献

Nicotinamide adenine dinucleotide is transported into mammalian mitochondria

Antonio Davila, Ling Liu, Karthikeyani Chellappa, Philip Redpath, Eiko Nakamaru-Ogiso, Lauren M Paolella, Zhigang Zhang, Marie E Migaud, Joshua D Rabinowitz

Institute for Diabetes, Obesity, and Metabolism, Perelman School of Medicine, University of Pennsylvania, United States; University of Pennsylvania, United States;Princeton University, United States; Queen’s University Belfast, United Kingdom; Perelman School of Medicine, University of Pennsylvania, United States; Northeast Agricultural University, China; University of South Alabama, United States

Abstract

Mitochondrial NAD levels influence fuel selection, circadian rhythms, and cell survival under stress. It has alternately been argued that NAD in mammalian mitochondria arises from import of cytosolic nicotinamide (NAM), nicotinamide mononucleotide (NMN), or NAD itself. We provide evidence that murine and human mitochondria take up intact NAD. Isolated mitochondria preparations cannot make NAD from NAM, and while NAD is synthesized from NMN, it does not localize to the mitochondrial matrix or effectively support oxidative phosphorylation. Treating cells with nicotinamide riboside that is isotopically labeled on the nicotinamide and ribose moieties results in the appearance of doubly labeled NAD within mitochondria. Analogous experiments with doubly labeled nicotinic acid riboside (labeling cytosolic NAD without labeling NMN) demonstrate that NAD(H) is the imported species. Our results challenge the long-held view that the mitochondrial inner membrane is impermeable to pyridine nucleotides and suggest the existence of an unrecognized mammalian NAD (or NADH) transporter.

https://elifesciences.org/articles/33246

 

 

β-Nicotinamide Mononucleotide, an Anti-Aging Candidate Compound, Is Retained in the Body for Longer than Nicotinamide in Rats.

 Kawamura T1, Mori N, Shibata K.

Abstract

The turnover of the oxidized form of nicotinamide adenine dinucleotide (NAD+) has attracted interest in regard to longevity. Thus, compounds that can rapidly increase the cellular NAD+ concentration have been surveyed by many researchers. Of those, β-nicotinamide mononucleotide (β-NMN) has been focused on. Studies on the biosynthesis of NAD+ from β-NMN have been reported at the cellular level, but not at the whole animal level. In the present study, we investigated whether β-NMN is superior to nicotinamide (Nam) as a precursor of NAD+ in whole animal experiments. To this end we compared the NAD+ concentration in the blood and the urinary excretion amounts of NAD+ catabolites. Rats were intraperitoneally injected with β-NMN or Nam. After the injection, blood samples and urine samples were collected at 3-h intervals. The concentration of blood total NAD (NAD11NADH) in each sample showed no significant differences between the two groups. The urinary excretion amounts of NAD+ catabolites in the urine samples collected at 3-6 h after the injection were lower in the β-NMN group than in the Nam group. These results suggest that β-NMN is retained in the body for longer than Nam.

https://www.ncbi.nlm.nih.gov/pubmed/27725413

 

 

Long-term administration of nicotinamide mononucleotide mitigates age-associated physiological decline in mice

Kathryn F. Mills,1 Shohei Yoshida,2 Liana R. Stein,1,§ Alessia Grozio,1 Shunsuke Kubota,3 Yo Sasaki,4Philip Redpath,5 Marie E. Migaud,5 Rajendra S. Apte,1,3 Koji Uchida,2 Jun Yoshino,6,* and Shin-ichiro Imai1,*

Summary

NAD+ availability decreases with age and in certain disease conditions. Nicotinamide mononucleotide (NMN), a key NAD+ intermediate, has been shown to enhance NAD+ biosynthesis and ameliorate various pathologies in mouse disease models. In this study, we conducted a 12 month-long NMN administration to regular chow-fed wild-type C57BL/6N mice during their normal aging. Orally administered NMN was quickly utilized to synthesize NAD+ in tissues. Remarkably, NMN effectively mitigates age-associated physiological decline in mice. Without any obvious toxicity or deleterious effects, NMN suppressed age-associated body weight gain, enhanced energy metabolism, promoted physical activity, improved insulin sensitivity and plasma lipid profile, and ameliorated eye function and other pathophysiologies. Consistent with these phenotypes, NMN prevented age-associated gene expression changes in key metabolic organs and enhanced mitochondrial oxidative metabolism and mitonuclear protein imbalance in skeletal muscle. These effects of NMN highlight the preventive and therapeutic potential of NAD+

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5668137/

 

 

Nicotinamide Mononucleotide: Exploration of Diverse Therapeutic Applications of a Potential Molecule

Saikat Kumar Poddar 1,*,Ali Ehsan Sifat 1,Sanjana Haque 1,Noor Ahmed Nahid 1,Sabiha Chowdhury 1 andImtias Mehedi 2

1.Department of Clinical Pharmacy and Pharmacology, Faculty of Pharmacy, University of Dhaka, Dhaka 1000, Bangladesh

2.Department of Pharmaceutical Chemistry, Faculty of Pharmacy, University of Dhaka, Dhaka 1000, Bangladesh

Abstract

Nicotinamide mononucleotide (NMN) is a nucleotide that is most recognized for its role as an intermediate of nicotinamide adenine dinucleotide (NAD+) biosynthesis. Although the biosynthetic pathway of NMN varies between eukaryote and prokaryote, two pathways are mainly followed in case of eukaryotic human—one is through the salvage pathway using nicotinamide while the other follows phosphorylation of nicotinamide riboside. Due to the unavailability of a suitable transporter, NMN enters inside the mammalian cell in the form of nicotinamide riboside followed by its subsequent conversion to NMN and NAD+. This particular molecule has demonstrated several beneficial pharmacological activities in preclinical studies, which suggest its potential therapeutic use. Mostly mediated by its involvement in NAD+ biosynthesis, the pharmacological activities of NMN include its role in cellular biochemical functions, cardioprotection, diabetes, Alzheimer’s disease, and complications associated with obesity. The recent groundbreaking discovery of anti-ageing activities of this chemical moiety has added a valuable essence in the research involving this molecule. This review focuses on the biosynthesis of NMN in mammalian and prokaryotic cells and mechanism of absorption along with the reported pharmacological activities in murine model. View Full-Text

Keywords: ageing; Alzheimer’s disease; diabetes; ischemic preconditioning; nicotinamide mononucleotide; obesity

https://www.mdpi.com/2218-273X/9/1/34

 

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