"The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome–mediated inflammatory disease"
http://www.nature.com/nm/journal/vaop/ncurrent/full/nm.3804.htmlVery nice. This adds ANOTHER mechanism by which time-restricted feeding / intermittent fasting is anti-inflammatory and thus more-so beneficial.
The NLRs initiate synthesis of pro-inflammatory cytokine, IL-1 beta, which is part of the acute phase response and mediates a rapid inflammatory response and fever. This represses that.
Just to point this out in case anyone is curious, that makes a third or fourth mechanism by which time-restricted feeding is/can be anti-inflammatory:
* mTOR repression - this one is obvious as rapamycin causes severe immuno- compromisation. Essentially, the cytokine IL-2 pretty much requires mTOR signaling to cause clonal expansion of the T-cell pool.
* Increases in circulating glucagon and norepinephrine upregulate cAMP/PKA pathways, which can directly impede activation of and DNA binding of NFkB and NFAT slightly
* HDAC4 activation which also represses NFkB. I think this also may be mediated via a PKA dependent mechanism though, so it may fall into the former group. IIRC, PKA phosphorylates and represses salt-inducible kinases, which normally sequesters the HDAC4 inactive in the cytosol, but this disinhibition allows nuclear translocation/activation.