High Dose of Dietary Nicotinamide Riboside Induces Glucose Intolerance and White Adipose Tissue Dysfunction in Mice Fed a Mildly Obesogenic Diet https://www.mdpi.com/2072-6643/11/10/2439/htm
Nicotinamide mononucleotide ameliorates the depression-like behaviors and is associated with attenuating the disruption of mitochondrial bioenergetics in depressed mice. https://www.ncbi.nlm.nih.gov/pubmed/31818774/
The Lifespan Extension Ability of Nicotinic Acid Depends on Whether the Intracellular NAD+ Level Is Lower than the Sirtuin-Saturating Concentrations. https://www.mdpi.com/1422-0067/21/1/142/htm
NAD+ Repletion Rescues Female Fertility during Reproductive Aging
Summary
Reproductive aging in female mammals is an irreversible process associated with declining oocyte quality, which is the rate-limiting factor to fertility. Here, we show that this loss of oocyte quality with age accompanies declining levels of the prominent metabolic cofactor nicotinamide adenine dinucleotide (NAD+). Treatment with the NAD+ metabolic precursor nicotinamide mononucleotide (NMN) rejuvenates oocyte quality in aged animals, leading to restoration in fertility, and this can be recapitulated by transgenic overexpression of the NAD+-dependent deacylase SIRT2, though deletion of this enzyme does not impair oocyte quality. These benefits of NMN extend to the developing embryo, where supplementation reverses the adverse effect of maternal age on developmental milestones. These findings suggest that late-life restoration of NAD+ levels represents an opportunity to rescue female reproductive function in mammals.
Vitamin B3 revitalizes energy metabolism in muscle disease 1 day ago University of Helsinki
An international team of scientists, led by University of Helsinki reported that vitamin B3, niacin, has therapeutic effects in progressive muscle disease. Niacin delayed disease progression in patients with mitochondrial myopathy, a progressive disease with no previous curative treatments.
Vitamin B3 forms have recently emerged as potent boosters of energy metabolism in rodents. These vitamins are precursors for NAD+, a molecular switch of metabolism between fasting and growth modes.
As fasting has been shown promote health and longevity in for example mice, a variety of "NAD boosters" are being developed. However, whether actual NAD+ deficiency exists in human disease, and whether NAD+ boosters could have curative effects in patients with degenerative diseases, has remained elusive.
In the current publication, a collaborative team of investigators led by academy professor Anu Suomalainen-Wartiovaara and academy research fellow Eija Pirinen report lowered NAD+ levels in both blood and muscle of mitochondrial myopathy patients.
"The disease is characterized by progressive muscle weakness, exercise intolerance and cramps. Currently, no treatments that would slow down disease progression exist," says Suomalainen-Wartiovaara.
Niacin—a promising treatment option
Pirinen and colleagues report that niacin treatment efficiently increased blood NAD+ both in patients and healthy subjects. Niacin restored NAD+ in the muscle of the patients to the normal level and improved strength of large muscles and mitochondrial oxidative capacity. Overall metabolism shifted towards that of normal subjects.
The results of this open pilot study revealed that niacin is a promising treatment option for mitochondrial myopathy. The authors emphasize, however, that niacin and NAD+ are efficient metabolic modifiers and niacin treatment should be cautiously applied only, when NAD deficiency is detected for example in the patient's blood.
"Our results are a proof-of-principle that NAD+ deficiency exists in humans and that NAD+ boosters can delay progression of mitochondrial muscle disease," Suomalainen-Wartiovaara comments.
"The study is a significant leap in the development of targeted therapy options for energy metabolic diseases," Suomalainen-Wartiovaara continues.
im Moment nehme ich 500 mg NMN zyklisch ein (z.B. 1 - 2 mal wöchentlich). Die tägliche Gabe von 500 mg NMN reduziert bei mir die Zahl der Mitochondrien (Energiemangel).