This topic is lockedInteresting review / editorial of effects of NR supplementation in Heart Failure and why.
http://circ.ahajourn...7/21/2274.short
Emerging evidence suggests that derangements in the myocardial NAD pool are causally linked to metabolic remodeling and mitochondrial dysfunction in the failing heart. Stabilizing the intracellular NAD+ level represents a promising therapeutic strategy to improve myocardial bioenergetics and cardiac function.1,3,4 In this issue of Circulation, Diguet et al5 report exciting data suggesting that supplementation with a NAD+ precursor, nicotinamide riboside (NR), reduces cardiac dysfunction in preclinical models of heart failure.
In the study there was also this interesting comment. We have often discussed whether NR leads to increases in NAM but appearently only metabolities or at least it not enough to raise NAM levels. NAM inhibits SIRT1, does anybody know whether those metabolities do as well? If not then this I think is an interesting observation. Also wonder if high dosing NR would be more beneficial if its combined with a ROS antioxidant.
Diguet et al5 found substantial increases
of Methyl-nicotinamide (MeNAM) and N1-Methyl-4-pyridone-
5-carboxamide (Me4PY) after NR supplementation,
although nicotinamide levels were unchanged. The finding
seems to indicate that feeding the NAD pool with
NR without salvage nicotinamide may lead to overflow of
downstream metabolites of nicotinamide (Figure). It is important
to note that the conversion of MeNAM to Me4PY
is accompanied by reactive oxygen species generation.
The biological significance of these reactions has not
been fully investigated, but it is important for therapeutic
application and should be addressed in future studies.
Edited by stefan_001, 27 May 2018 - 07:19 AM.
