M-Power 600mg / 120Capsules

Manufacturer: Merion Inc
$3,700.00
M-Power
The life limit of human beings is around 120 years old. How can we keep our lives fresh?
β-Nicotinamide mononucleotide (NMN), NMN plays an important role in human cell energy production, it is involved in the synthesis of nicotinamide adenine dinucleotide (NAD), and NAD is a cell. An important coenzyme for energy conversion. Scientists have a very good effect on the study of NMN to prevent and treat aging diseases associated with aging.

M-Power 

  • Anti-Aging NAD+ Support

  • Promotes Energy Metabolism

The life limit of human beings is around 120 years old. How can we keep our lives fresh?

β-Nicotinamide mononucleotide (NMN), NMN plays an important role in human cell energy production, it is involved in the synthesis of nicotinamide adenine dinucleotide (NAD), and NAD is a cell. An important coenzyme for energy conversion. Scientists have a very good effect on the study of NMN to prevent and treat aging diseases associated with aging.

 

Product description:

M-Power contains Vitamin A, Vitamin C, Vitamin D3, Zinc citrate, L-Carnitine, beta Nicotinamide mononucleotide (NMN), and other substances.

The -nicotinamide mononucleotide (" NMN ") is involved in the synthesis of nicotinamide adenine dinucleotide (NAD +). NAD + is a coenzyme in the cell that is necessary to convert nutrient energy into enzymes that the cell can use. NMN is a nucleotide derived from ribose and nicotinamide. NMN is a naturally occurring compound that plays an important role in cellular energy metabolism.

From scientists at the university of new south wales and Harvard University team found the beta Nicotinamide single nucleotide (beta Nicotinamide mononucleotide, NMN), can prolong the aging of Nicotinamide single nucleotide (NMN) material, to repair DNA and nerve yuan cell. It stops the production of cancer cells, increases energy efficiency, and can even activate 'autophagy' (as mentioned in the 2016 Nobel Prize for cell autophagy). It's amazing and it's powerful.

NAD + is a coenzyme involved in the REDOX reaction. It consists of two nucleotides joined by phosphate groups. One nucleotide contains adenosine and the other is nicotinamide.

It helps the enzyme transfer electrons during the REDOX reaction to form ATP, which helps provide energy. However, levels decline with age - NAD + levels in older cells drop by more than 60%.

At this time, many senile diseases and senility occur. Mitochondria then produce less energy and cell age. This process may not be irreversible, and if NAD + levels increase, the cellular energy mechanism may return to normal.

Function:

The NMN of "M-power" can improve physical decline, lack of energy, mental degradation, metabolic disorders, poor sleep quality and other symptoms.

For people:

People who want to reduce their risk of chronic disease in the future; People who feel low energy due to stress in work and life; People who work and live in environments with high levels of radiation or chemicals, such as flight attendants, scientists and outdoor workers, and anyone who wants to fight aging and disease.

Dosage:

Take two capsules twice a day. Scientific studies confirm that ingestion of NMN is safe and effective.

 

【#1 Serving Size】600mg/120 capsules

【Shelf Life】3years

【Store】Keep bottle closed and store at room temperature.

【Distributed By】 Merion, Inc.

【Manufacturer】 USA

【Warning】Not for pregnant and kid

 

 

 

 

 

 

 

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




Short-term administration of Nicotinamide Mononucleotide preserves cardiac mitochondrial homeostasis and prevents heart failure

 

Rongli Zhang,Yuyan Shen,Lin Zhou, Panjamaporn Sangwung, Hisashi Fujioka, Lilei Zhang,Xudong Liao

 

a.Case Cardiovascular Research Institute, Case Western Reserve University School of Medicine, University Hospitals Cleveland Medical Center, Cleveland, OH 44106, USA

b.Department of Cardiology, Tongji Hospital, Tongji University, Shanghai 20065, China

c.Department of Physiology and Biophysics, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA

D. Electron Microscopy Core Facility, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA

E. Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, TX 77030, USA

Received 14 April 2017, Revised 31 August 2017, Accepted 1 September 2017, Available online 5 September 2017.

 

https://www.sciencedirect.com/science/article/pii/S0022282817303036





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

 

Received: 4 January 2019 / Revised: 15 January 2019 / Accepted: 15 January 2019 / Published: 21 January 2019

 

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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