Discussion in 'Other Health News and Research' started by Ema, Apr 16, 2015.
Some info I'd previously come across :
Peroxisome proliferator-activated receptors (PPARs) are important regulators of mitochondrial function and may provide neuroprotection. Watt et al (2004) demonstrated that nicotinic acid could induce the production of mitochondrial regulating PPARs as effectively as exercise.
(possibly mediated by increased epinephrine).
Has anyone tried nicotinic acid for ME?
I was a happy ex-smoker until ME/CFS. Hasn't cured me though (cured as in made better rather than made brown and smelly).
Nicotinic acid is plain old B3.
About B3 forms and NAD synthesis pathways
"NAD+ levels decline with mitochondrial dysfunction and reduced NAD+/NADH ratio is implicated in mitochondrial disorders, various age-related pathologies as well as during aging."
"Recent studies have demonstrated that NAD levels are limiting, making the availability of NAD critical for mitochondrial function [9–11]. It has also been shown that the biosynthesis, subcellular localization, and systemic transport of NAD and its intermediates, play an important role in the regulation of various biological processes, with significant impact on mitochondrial functionality"
"A growing body of evidence also suggests that mitochondria have their own NAD biosynthetic machinery which appears to play an important role in maintaining the mitochondrial NAD pool, in response to environmental and nutritional stresses"
"In mammals, NAD biosynthesis can proceed via four different routes:
-de novo synthesis from tryptophan (TRP),
-synthesis from either form of vitamin B3, nicotinamide (NAM)
-or nicotinic acid (NA),
-or conversion of nicotinamide riboside (NR) (Figure I) .
Together, these pathways generate a cellular NAD concentration of 300 to 800 μM, depending upon the tissue/organ [8, 16, 25, 26]. In mammals, NAM has the better capability of stimulating NAD biosynthesis than NA in multiple organs [27, 28]. Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the NAD biosynthetic pathway from NAM, converts NAM and 5-phosphoribosyl-pyrophosphate to a key NAD intermediate, nicotinamide mononucleotide (NMN). NMN is adenylated to NAD by nicotinamide mononucleotide adenylyl transferase (NMNAT) [8, 14, 29]. Accordingly, increased gene dosage of NAMPT but not NMNAT, increases NAD levels [16, 30–33]."
good content! thanks
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