Nicotinamide Riboside

Avatar de Usuario
Dalamar
Site Admin
Mensajes: 8867
Registrado: 09 May 2012 01:38

Nicotinamide Riboside

Mensajepor Dalamar » 05 Nov 2014 18:26

Un suplemento que se está haciendo muy famoso por los estudios de Sinclair, rejuvenecimiento en ratones vía Sirtuinas...
Adjuntos
uploadfromtaptalk1415204775973.jpg
uploadfromtaptalk1415204764076.jpg
¿Te ha gustado este hilo? Compartelo en las redes sociales para que se sume mas gente a la conversacion!

Vigilantexx
Especulador Sabelotodo
Mensajes: 697
Registrado: 24 Jul 2012 00:26

Re: Nicotinamide Riboside

Mensajepor Vigilantexx » 11 Ene 2015 19:05

Sinclair es un cientifico prestigioso pero muchas veces no sabes donde esta el limite entre ciencia y avaricia-ego

yo de los comentarios de los yanquis no me fio mucho, se emocionan con cualquier cosa pero el feedback parece en general positivo

http://www.reddit.com/r/Nootropics/comm ... de_niagen/
http://www.longecity.org/forum/topic/75 ... d-updates/

y aunque sea de Perogrullo decirlo, que algo funcione con ratas no quiere decir que lo haga en humanos...veremos, pero la empresa que saque algo aquí va a pegar el super pelotazo

Avatar de Usuario
Dalamar
Site Admin
Mensajes: 8867
Registrado: 09 May 2012 01:38

Re: Nicotinamide Riboside

Mensajepor Dalamar » 11 Ene 2015 19:18

Hay muchos comentarios de gente que la ha probado en longecity... Yo diria que no he notado super poderes y llevo un par de semanas tomando, pero mi mujer si que me dijo que habia notado beneficios sobre todo en la piel... no se!
¿Te ha gustado este hilo? Compartelo en las redes sociales para que se sume mas gente a la conversacion!

Avatar de Usuario
Dalamar
Site Admin
Mensajes: 8867
Registrado: 09 May 2012 01:38

Re: Nicotinamide Riboside

Mensajepor Dalamar » 13 Feb 2015 18:17

Three-Parent Babies or a Failure to Communicate

You’ve probably noticed the raging debate about three-parent babies in the media. Personally, I think this term is incredibly irresponsible and misleading. What is really happening is that the gametes from the father and mother (sperm and ovum) join to form the new genome in the zygote. That doesn’t change at all. The genetic makeup of a child’s genome comes from the father and mother. Period.

Mitochondria, however, are not produced by the genome. They exist in the mother’s oocyte, the egg cell, just as they do in all cells. These mitochondria are integrated into the developing fetus and reproduce over the time. The so-called three-parent babies are actually a zygotic nucleus, made of the two parents’ gametes, transplanted into the egg of a woman with healthy mitochondria. In this way, mitochondria with genetic defects from the mother are not passed on to the baby.

So how do potentially fatal mutations in mitochondrial DNA appear in the first place? One way is directly related to NAD+. Mitochondria don’t have the sophisticated genetic repair mechanisms that our genomes do. With only 37 coding genes, compared to the tens of thousands in the genome, they deal with mutations differently.

In healthy, young individuals, mitochondrial DNA repair takes place, we now believe, by replicating intact plasmids to make new mitochondria and abandoning the bad plasmids. It’s a system that works well, but it deteriorates as we age. If, for some reason, communication between mitochondria and the master genome isn’t efficient, mutated plasmids can replicate to the point that they replace healthy versions.

Until recently, we didn’t understand how this failure to communicate happened. Now, it’s become clear that NAD+ levels fall as we age. This has two primary impacts. One is that our ability to convert food into ATP is compromised. One result of this is increased storage of food as fat, but the more important impact is that our cells lack the energy they need to perform optimally. Critical cellular maintenance function declines, which can hurt the genome itself.

Even worse, it has become apparent only recently that NAD+ is the energy substrate that genes rely on to perform remote functions. This means that genes can makes their incredible protein machines, but those machines fail to perform their intended function.

It’s not a great metaphor, but you can think of a gene protein as a robotic ambulance created to find and fix a problem. Without sufficient NAD+, that robotic ambulance is created but finds that the roads and phone system are in such a bad state of disrepair that they often can’t get to their targets.

In an advanced state of failure, it becomes a vicious circle. Low NAD+ levels cause cellular problems that result in even lower NAD+ levels. Our mitochondria are stranded and alone, lacking the ability to communicate with the central dispatcher, the genome. They do their best but, isolated, they degrade further.

Sometimes, mutated mitochondria may be passed on in the germ line of the mother. This can cause mitochondrial diseases associated with diabetes, deafness, blindness, multiple sclerosis-type diseases and a lot of other really awful disorders. Not only can they be passed down, they can worsen over subsequent generations.

An interesting thing about mitochondrial disease is that many of the same disorders occur with increasing frequency in older people as NAD+ levels fall. Diseases that are not caused by mitochondrial mutation can also be provoked by low NAD+ levels as well. Many neurodegenerative diseases are currently being investigated by major universities for treatment with NR. Animal studies have been extremely promising. For example, NR has been used to effectively treat animals with the accelerated aging disease Cockayne syndrome (CS). In those studies, NAD+ levels in the mitochondria of animals were restored. NR and another NAD+ precursor, a form of oxaloacetate, have also yielded significantly increased life spans in lower animal forms.

Obviously, we therefore want to know if NR increases NAD+ levels in humans. Now we know that it does. Read the entire press release here. The study also showed a very strong safety profile.

Will NR prove to be as effective in humans as it is in animals? We may never have proof, for two reasons. One is that different people live very different lives and aren’t subject to controlled double-blind tests. It’s conceivable that we could control for various lifestyle factors for a while, but the final data point in a longevity study is death. You don’t really know how something affects a life span until the test subject dies. Since humans are among the longest living species, any valid controlled study would take decades and necessarily include a lot of people.

Some top scientists, however, believe for reasons that I explained at the start of this article that we already know enough to warrant use of the molecule for purposes of life extension. MIT biologist Leonard Guarente is best known for his research into the sirtuin genes, which are activated via calorie restriction with optimal nutrition (CRON). This article, about his decision to formulate a nutraceuticals product line featuring NR got a lot of attention.

As I’ve explained previously, the incredible interest and excitement about resveratrol, the grape skin extract, was based on sirtuin activation. Resveratrol does activate the sirtuin genes associated with life extension. Unfortunately, the proteins produced by the sirtuin genes did not act strongly enough to produce health benefits in humans.

Guarente, along with other scientists, has concluded that the failure is connected to an insufficient energy substrate: NAD+. This is really interesting research and may mean that normal sirtuin activation is sufficient in a cellular environment with enough NAD+. Since Guarente is including pterostilbene, a phytochemical from blueberries known to activate the sirtuins, he is evidently hedging his bets. According to the MIT Technology Review article, he expects a synergistic effect with NR.

We don’t yet know if NR is going to be the kind of marketing success that resveratrol was, but it’s more likely, given Guarente’s entry to the market. Others in the same article believe so.

“NAD replacement is one of the most exciting things happening in the biology of aging,” says Nir Barzilai, director of the Institute for Aging Research at the Albert Einstein College of Medicine in New York, who has coauthored scientific papers with Guarente but is not involved in Elysium. “The frustration in our field is that we have shown we can target aging, but the FDA does not [recognize it] as an indication.”

Even skeptics quoted in the article are only partially so.

“There is enough evidence to be excited, but not completely compelling evidence,” said Brian K. Kennedy, CEO of the California-based Buck Institute for Research on Aging.

Personally, I’m about the same age as Guarente so I may not have time for “completely compelling evidence,” so I take both of the molecules in his product, as does the boss, John Mauldin. Guarente is absolutely correct when he complains about the lack of a regulatory path for extending health spans. The Japanese are much further along the way to solving this problem, by the way.

Unlike anatabine citrate, which was pressured off the market by the FDA, NR and pterostilbene do not usually cause immediate physiological changes noticeable to most people, though the recent study shows that important changes are taking place on the cellular level. This makes sense, however, as they work from opposite directions. Anatabine citrate shuts down the autoimmune feedback loop of inflammation caused by excess activation of the NF kappa B transcription factor. Based on animal tests, human trials, and the anecdotal reports of many thousands of people, it appears to help in conditions ranging from arthritis to IBS and Parkinson’s. I believe, based on current research into the inflammation-related causes of cancer, it will also reduce risk of that disease.
¿Te ha gustado este hilo? Compartelo en las redes sociales para que se sume mas gente a la conversacion!

Avatar de Usuario
Dalamar
Site Admin
Mensajes: 8867
Registrado: 09 May 2012 01:38

Re: Nicotinamide Riboside

Mensajepor Dalamar » 27 Mar 2015 15:57

In early February, Elysium Health, a startup cofounded by Sinclair’s former mentor, MIT biologist Lenny Guarente, jumped into the NAD game by unveiling another supplement with NR. Dubbed Basis, it’s only offered online by the company. Elysium is taking no chances when it comes to scientific credibility. Its website lists a dream team of advising scientists, including five Nobel laureates and other big names such as the Mayo Clinic’s Jim Kirkland, a leader in geroscience, and biotech pioneer Lee Hood. I can’t remember a startup with more stars in its firmament.

A few days later, ChromaDex reasserted its first-comer status in the NAD game by announcing that it had conducted a clinical trial demonstrating that “a single dose of NR resulted in statistically significant increases” in NAD in humans—the first evidence that supplements could really boost NAD levels in people. Details of the study won’t be out until it’s reported in a peer-reviewed journal, the company said. (ChromaDex also brandishes Nobel credentials: Roger Kornberg, a Stanford professor who won the Chemistry prize in 2006, chairs its scientific advisory board. He’s the son of Nobel laureate Arthur Kornberg, who, ChromaDex proudly notes, was among the first scientists to study NR some 60 years ago.)
¿Te ha gustado este hilo? Compartelo en las redes sociales para que se sume mas gente a la conversacion!

Avatar de Usuario
Dalamar
Site Admin
Mensajes: 8867
Registrado: 09 May 2012 01:38

Re: Nicotinamide Riboside

Mensajepor Dalamar » 21 Oct 2016 06:14

Los estudios animales han mostrado que aumentar los niveles de NAD+ (que descienden con la edad) pueden hacer más difícil el sobrepeso, mejora los niveles de glucosa y colesterol, reduce daños nervioso y puede suponer una mayor esperanza de vida.

Desde hace relativamente poco tiempo existe la nicotinamida ribósido como compuesto para aumentar los niveles de NAD+, pero hasta ahora no existían estudios en seres humanos. Una nueva investigación aparecida en Nature Communications supone el primer ensayo publicado con humanos, en el que 6 varones y 6 mujeres recibieron dosis de 100, 300 y 1000 mg de nicotinamida ribósido. Se analizaron muestras de sangre y de orina de los participantes y se corroboró que los niveles de NAD+ aumentaron en correlación con las dosis suplementadas. "Este ensayo muestra que la nicotinamida ribósido aumenta el metabolismo del NAD+ en humanos" dijeron los autores.

- Charles Brenner y el NAD+

En la historia, aunque reciente, de la investigación sobre el NAD+ y formas para impulsarlo, destaca el doctor Charles Brenner que ha participado en estudios como el arriba mencionado.

De hecho puede decirse que el primer ensayo con nicotinamida ribósido lo hizo con él mismo allá por 2004. Así que decidió tomar 1000 mg una vez al día de esta sustancia durante una semana, tras lo cual su sangre arrojaba valores de NAD+ 2,7 superiores a los de la semana previa. Y él fue quien desubrió que más sencillo que medir el NAD+ era hacerlo a través de un metabolito suyo llamado NAAD, algo que demostró consigo mismo y en ratones y que se ha empleado en este último ensayo con humanos. Brenner es profesor de medicina interna y director del Obesity Research and Education Initiative en la Universidad de Iowa.

- Y otro nuevo estudio animal

Pero las novedades publicadas sobre la nicotinamida ribósido no acaban aquí. Un nuevo estudio animal muestra que el NAD+ en el organismo frena el daño mitocondrial y el envejecimiento. En concreto los investigadores estaban estudiando sus efectos en ratones susceptibles de desarrollar enfermedades neurodegenerativas, por lo que se cree que el NAD+ podría contribuir a combatir el Parkinson o el Alzheimer.
¿Te ha gustado este hilo? Compartelo en las redes sociales para que se sume mas gente a la conversacion!

Avatar de Usuario
Dalamar
Site Admin
Mensajes: 8867
Registrado: 09 May 2012 01:38

Re: Nicotinamide Riboside

Mensajepor Dalamar » 20 Ene 2017 12:47

Nicotinamide riboside (or NR for short) is a form of vitamin B3. So, before delving into the depths of NR, let us first take a short look at vitamin B3 in general.

Our history starts in 1735 when the Spanish doctor Gasper Casal described a disease in poor farmers characterised by sun-sensitive Dermatitis (inflammation of the skin), Diarrhea, Dementia and eventually Death (the four ‘Ds’). This same disease became an epidemic in the southern states of the US around the turn of the 20th century. It is estimated that at least 100,000 Americans died from this disease between 1907 and 1940. This disease was pellagra and is common in people whose diet consists nearly completely out of corn and are low in meat. While the role of diet in the development of pellagra was already suspected by Casal and the French had successfully eradicated pellagra by limiting the cultivation of corn many continued to believe that pellagra was an infectious disease.

The American physician and epidemiologist Joseph Goldberger definitively proved that pellagra was caused by a deficient diet in the early 20th century after conducting dietary experiments on inmates. When the inmates were placed on a corn-rich diet with little other food sources they started to develop pellagra. Eventually researchers were able to figure out that pellagra was caused by a deficiency of two nutrients vitamin B3 and tryptophan (see below to find out the role of tryptophan) (Wan et al., 2011; Yang and Sauve, 2016).

There are several different forms of vitamin B3 which all have slightly different properties but share the fact that the body can use them equally to produce the vitamin B3 analogs that we need to stay alive. Nicotinic acid is a form of vitamin B3 that in high dosages is used as a drug to lower blood lipids but its use has been mostly replaced by statin drugs, although recently there’s a resurgence of interest in nicotinic acid due to its wide effect on many blood lipids. Of all drugs used to lower blood lipids nicotinic acid remains unique in the fact that it positively influences a large array of blood lipids (it lowers LDL, Lp(a) and triglycerides while increasing HDL) hence it is sometimes called a “broad-spectrum lipid drug”. Interestingly, nicotinamide, while very similar to nicotinic acid in chemical structure (see image 1), does not have blood lipid lowering properties (Ballantyne, 2009; Carlson, 2005; Jacobson et al., 2012). A major problem with the use of high dose nicotinic acid therapy is that it causes flushing leading to low compliance. Hence extended-release forms that cause less severe flushing have been developed. In shops one may also find “flush-free” niacin, this is inositol hexanicotinate but this molecule does not improve lipid levels. Researchers are working on the development of newer non-flush nicotinic acid derivatives against cardiovascular disease including transdermal (through the skin) delivery (Jacobson et al., 2012). NR is a form of vitamin B3 found in low amounts in milk and yeast products (Chi and Sauve, 2013) and NR together with pterostilbene are the major components of “Basic”, the supplement produced by the biotech company Elysium Health. NR is a very recent supplement as the production of this molecule remained difficult until recently. This also made studies with NR difficult. In July 2013 the first NR supplement, NIAGEN, hit the market (Chi and Sauve, 2013). Today NR is available as capsules or as bulk powder from many supplement companies.

Different forms of vitamin B3.png

Image 1: Different forms of vitamin B3. Image generated using ACD/ChemSketch®.

Our bodies need vitamin B3 as precursor for NAD+, an electron transfer molecule that has a crucial role to play in energy production. In addition NAD+ is needed in certain signaling pathways and is also converted into NADPH which is involved in detoxification of reactive oxygen species (ROS). The amino acid tryptophan can also be converted into NAD+ explaining why tryptophan deficiency can cause pellagra (image 2).

NR appears to be very safe with a safety profile similar to that of nicotinamide. No adverse effects were observed in rats for doses below 300 mg/kg/day (Conze et al., 2016). Supplement companies typically advice 100-300mg a day.

Recently, several animal studies have been published that show the effectiveness of NR against several diseases. Supplementation of mice with NR prevented weight gain in animals fed a high fat diet despite the fact that NR supplemented animals tended to eat more. Blood sugar levels were similar in NR supplemented animals compared to control animals but insulin levels are lower indicating increased insulin sensitivity in the NR supplemented animals. The researchers next performed a battery of standard diabetes tests and found that the NR-supplemented animals performed better compared to the control animals (Cantó et al., 2012). Similarly, Charles Brenner and colleagues treated pre-diabetic and diabetic mice with NR and found improvements in glucose tolerance, reduced weight gain, improved protection against liver damage from diabetes and protection against diabetic neuropathy (nerve damage caused by diabetes) (Trammell et al., 2016b). Levels of amyloid-beta were decreased and cognitive function was improved in a mouse-model of Alzheimer’s disease treated with NR for three months (Gong et al., 2013). NR supplementation improved mitochondrial function in a mouse model of mitochondrial disease (Cerutti et al., 2014). NR also protected mice from noise-induced hearing loss (Brown et al., 2014) and improves liver regeneration in mice (Mukherjee et al., 2016). Johan Auwerx and colleagues demonstrated that NR supplementation delayed disease progression in a mice model of mitochondrial myopathy (muscle disease) (Khan et al., 2014). NR supplementation improved muscle function and heart problems in a mouse model of muscular dystrophy (Ryu et al., 2016). Furthermore, NR supplementation reversed muscle fiber degeneration in mice missing the Nampt enzyme involved in NAD+ recycling (see image 2) (Frederick et al., 2016). However, it should be pointed out that one study found that NR supplementation decreased exercise performance in normal rats by 35% (Kourtzidis et al., 2016).

In 2007 it was discovered that NR increases replicative lifespan in yeast (Belenky et al., 2007). Replicative lifespan is the number of times that a cell, referred to as the mother cell, can bud of daughter cells before it permanently stops dividing. Uptake of endogenous NR is also needed for calorie restriction-induced lifespan extension (Lu et al., 2009). More recently, it was shown that NR supplementation is able to slightly increase the lifespan of mice (Zhang et al., 2016). Mean lifespan was increased by 4.7% and maximum lifespan was also increased (as illustrated by the graph in the paper) but the authors did not calculate the statistical significance for the maximum lifespan data (Zhang et al., 2016). Supplementation of the roundworm C. elegans with NAD+ (Hashimoto et al., 2010), nicotinamide or 1-methylnicotinamide (Schmeisser et al., 2013) has also been found to increase lifespan.

While NR supplementation seems to have multiple benefits in laboratory animals we should notice that research in this area has only started. To the best of our knowledge no human data on the health effects of NR has been published so far. Also the reduced exercise performance in rats fed NR is a warning that we shouldn’t implement NR supplementation in healthy humans as of yet (Kourtzidis et al., 2016). In a few years more data about NR should be available allowing us to make a much more informed decision.

Sirt1 is a well-known enzyme that removes a chemical group known as an acetyl group from proteins, most notably from histones (the proteins around which DNA is wrapped). By chemically modifying the histone proteins, Sirt1 is able to regulate the expression of genes. Multiple studies have found that overexpression of Sirt1 (or its homologs) increases lifespan in yeast, fruit flies, and the roundworm C. elegans. However, a 2011 Nature paper found that the lifespan extending effects in fruit flies and C. elegans were caused by unrelated background mutations (Burnett et al., 2011). Sirt1 is also famous as the reputed target of the geroprotector resveratrol. However, multiple studies have found that resveratrol does not bind Sirt1 (Calamini et al., 2010). In the original Sirt1 studies a fluorescent peptide was used to measure the Sirt1 activity and this peptide induced a binding of resveratrol to Sirt1 while no such binding takes place in the absence of this ‘artificial measuring tool’. However resveratrol may also work through other mechanisms such as mTOR inhibition (Park et al., 2016) or inhibition of phosphodiesterases leading to AMPK activation (Park et al., 2012).

Yang et al. (2007) has shown that NR increases NAD+ levels by up to 270% in cultured mammalian cells.

Interestingly, a recent human study showed that oral administration of 1,000 mg NR increases human blood NAD+ levels by 270% (Trammell et al., 2016a). Johan Auwerx and colleagues have demonstrated that administration of NR to mice increased NAD+ concentrations and activates Sirt1 (Cantó et al., 2012). Sirt1 needs NAD+ to dump the acetyl group on that it removes from its targets. Hence without NAD+, Sirt1 cannot do its enzymatic function. In the process the NAD+ molecule splits in two parts, one of which is nicotinamide (NAM). As you might remember nicotinamide is one form of vitamin B3. Nicotinamide can then be converted back in NAD+. Because nicotinamide is the end product of the reaction catalysed by Sirt1 it is expected that the presence of nicotinamide will inhibit Sirt1 activity. Indeed, nicotinamide is a well known inhibitor of Sirt1. In addition to Sirt1, NR also activates Sirt3 and mitochondrial biogenesis (Brown et al., 2014; Cantó et al., 2012; Gong et al., 2013).

Sirt1 enzymatic activity.png

Image 2: Sirt1 removes acetyl groups (round circle) from substrates (such as proteins). On the left is the circular mechanism in which NAD+ is regenerated from the end products of the Sirt1-catalysed reaction. In green are the two ways in which new molecules can enter in this cycle. Nicotinic acid and tryptophan are direct precursors of NAD+ while nicotinamide riboside enters this cycle by conversion into NMN.
Overexpression of NAMPT, an enzyme involved in recycling the end products from the Sirt1 reaction back to NAD+, extends replicative lifespan of human cells in culture (van der Veer et al., 2007; Ho et al., 2009). Restricting glucose in the medium used to grow cells in leads to an upregulation of NAMPT and increased NAD+ levels leading to an increase in replicative lifespan (Yang et al., 2015). Furthermore, overexpression of NAMPT in human endothelial cells (cells that line the blood vessels) is able to protect these cells from the harmful consequences of high glucose levels (Borradaile and Pickering, 2009). Similar results have been obtained in yeast. Yeast has an enzyme called Pnc1 that converts nicotinamide into nicotinic acid and thereby removes the inhibitory effect of nicotinamide on Sir2 (the yeast equivalent of Sirt1). Indeed, overexpression of Pnc1 was found to stimulate Sir2 activity (Gallo et al., 2004).

Mechanisms NR longevity.png

Image 3: Mechanisms by which NR promotes longevity. The color of the arrows refers to decreases (red) or increases (green) and does not reflect if these changes or beneficial or harmful.
References
Ballantyne CM (ed.) (2009). Clinical Lipidology: A Companion to Braunwald's Heart Disease, 1st edition. Saunders Elsevier, Philadelphia.
Belenky P et al. (2007). Nicotinamide riboside promotes Sir2 silencing and extends lifespan via Nrk and Urh1/Pnp1/Meu1 pathways to NAD+. Cell 129(3): 473-484.
Borradaile NM, and Pickering JG (2009). Nicotinamide phosphoribosyltransferase imparts human endothelial cells with extended replicative lifespan and enhanced angiogenic capacity in a high glucose environment. Aging Cell 8: 100-112.
Brown KD et al. (2014). Activation of SIRT3 by the NAD⁺ precursor nicotinamide riboside protects from noise-induced hearing loss. Cell Metab 20(6): 1059-1068.
Burnett C et al. (2011). Absence of effects of Sir2 overexpression on lifespan
in C. elegans and Drosophila. Nature 477: 482-485.
Calamini B et al. (2010). Pleiotropic mechanisms facilitated by resveratrol and its metabolites. Biochemical J 429(2): 273-282.
Cantó C et al. (2012). The NAD(+) precursor nicotinamide riboside enhances oxidative metabolism and protects against high-fat diet-induced obesity. Cell Metab 15(6): 838-847.
Carlson LA (2005). Nicotinic acid: the broad-spectrum lipid drug: a 50th anniversary review. J Intern Med 258(2): 94-114.
Cerutti R et al. (2014). NAD(+)-dependent activation of Sirt1 corrects the phenotype in a mouse model of mitochondrial disease. Cell Metab 19(6): 1042-1049.
Chi Y, Sauve AA (2013). Nicotinamide riboside, a trace nutrient in foods, is a vitamin B3 with effects on energy metabolism and neuroprotection. Curr Opin Clin Nutr Metab Care 16(6): 657-661.
Conze DB et al. (2016). Safety assessment of nicotinamide riboside, a form of vitamin B3. Hum Exp Toxicol [Epub ahead of print].
Frederick DW et al. (2016). Loss of NAD homeostasis leads to progressive and reversible degeneration of skeletal muscle. Cell Metab 24(2): 269-282.
Gong B et al. (2013). Nicotinamide riboside restores cognition through an upregulation of proliferator-activated receptor-γ coactivator 1α regulated β-secretase 1 degradation and mitochondrial gene expression in Alzheimer's mouse models. Neurobiol Aging 34(6): 1581-1588.
Hashimoto T et al. (2010). Nicotinamide adenine dinucleotide extends the lifespan of Caenorhabditis elegans mediated by sir-2.1 and daf-16. Biogerontology 11(1): 31-43.
Ho C et al. (2009). SIRT1 markedly extends replicative lifespan if the NAD+ salvage pathway is enhanced. FEBS Lett 583(18): 3081-3085.
Jacobson EL et al. (2012). Niacin: Vitamin and antidyslipidemic drug. In: Stranger O (ed.). Water soluble vitamins: Clinical research and future application. Subcellular Biochemistry 56. Springer, Dordrecht.
Khan NA et al. (2014). Effective treatment of mitochondrial myopathy by nicotinamide riboside, a vitamin B3. EMBO Mol Med 6(6): 721-731.
Kourtzidis IA et al. (2016). The NAD(+) precursor nicotinamide riboside decreases exercise performance in rats. J Int Soc Sports Nutr 13: 32.
Lu SP et al. (2009). Assimilation of endogenous nicotinamide riboside is essential for calorie restriction-mediated life span extension in Saccharomyces cerevisiae. J Biol Chem 284(25): 17110-17119.
Mukherjee S et al. (2016). Nicotinamide adenine dinucleotide biosynthesis promotes liver regeneration. Hepatology [Epub Ahead of Print].
Park SJ et al. (2012). Resveratrol ameliorates aging-related metabolic phenotypes by inhibiting cAMP phosphodiesterases. Cell 148(3): 421-433.
Park D et al. (2016). Resveratrol induces autophagy by directly inhibiting mTOR through ATP competition. Scientific Reports 6: 21772.
Schmeisser K et al. (2013). Role of sirtuins in lifespan regulation is linked to methylation of nicotinamide. Nat Chem Biol 9(11): 693-700.
Trammell SAJ et al. (2016a). Nicotinamide riboside is uniquely and orally bioavailable in mice and humans. Nature Communications 7: 12948.
Trammell SA et al. (2016b). Nicotinamide Riboside Opposes Type 2 Diabetes and Neuropathy in Mice. Sci Rep 6: 26933.
van der Veer E et al. (2007). Extension of human cell lifespan by nicotinamide phosphoribosyltransferase. J Biol Chem 282: 10841-10845.
Wan P et al. (2011). Pellagra: a review with emphasis on photosensitivity. Br J Dermatol 164: 1188-1200.
Yang T et al. (2007). Syntheses of nicotinamide riboside and derivatives: effective agents for increasing nicotinamide adenine dinucleotide concentrations in mammalian cells. J Med Chem 50(26): 6458-6461.
Yang NC et al. (2015). Up-regulation of nicotinamide phosphoribosyltransferase and increase of NAD+ levels by glucose restriction extend replicative lifespan of human fibroblast Hs68 cells. Biogerontology 16(1): 31-42.
Yang Y, Sauve AA (2016). NAD+ metabolism: Bioenergetics, signaling and manipulation for therapy. Biochim Biophys Acta 1864(12): 1787-1800.
Zhang H et al. (2016). NAD⁺ repletion improves mitochondrial and stem cell function and enhances life span in mice. Science 352(6292): 1436-1443.
Adjuntos
image03.png
image02.png
image01.png
¿Te ha gustado este hilo? Compartelo en las redes sociales para que se sume mas gente a la conversacion!

Avatar de Usuario
Dalamar
Site Admin
Mensajes: 8867
Registrado: 09 May 2012 01:38

Re: Nicotinamide Riboside

Mensajepor Dalamar » 29 Abr 2017 05:48

Niagen tiene la patente de Nicotinamide Riboside:

Richest man in Asia invests in Chromadex (Niagen), will own 20% of company

ChromaDex announced yesterday that it has entered into a stock purchase agreement for the sale of up to $25 million of its common stock to Horizons Ventures an entity owned by Mr. Li Ka-shing.

With Chromadex cash position now dramatically improved and that combined with the networking clout of Horizon Ventures it is fair to expect that Nicotinamide Riboside will receive more attention and attract more research. In a wider context it would seem that anti-aging is gaining credibility, so good news all around.


Ver: https://finance.yahoo.com/news/chromade ... 00158.html
¿Te ha gustado este hilo? Compartelo en las redes sociales para que se sume mas gente a la conversacion!

Avatar de Usuario
Dalamar
Site Admin
Mensajes: 8867
Registrado: 09 May 2012 01:38

Re: Nicotinamide Riboside

Mensajepor Dalamar » 03 Nov 2017 18:00

From the paper--

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.

And the dosing from the supplemental material--

(A) NMN concentrations in freshly prepared NMN-containing drinking water and the leftover of used NMNcontaining
drinking water were periodically measured by HPLC throughout the entire period of NMN
treatment. Percentages of NMN concentrations after 7-10 days in both 100 and 300 mg/kg/day groups were
calculated ...


Ver: https://sci-hub.ac/http://www.sciencedi ... 3116304958
¿Te ha gustado este hilo? Compartelo en las redes sociales para que se sume mas gente a la conversacion!


Volver a “Suplementos y vitaminas”

Ingresar