Table 1.
type | mechanism | physiological processes | references |
---|---|---|---|
direct | HDACs inhibition | gene expression | (60–62) |
BHB-ylation | gene expression | (63–65) | |
FFAR inhibition | sympathetic system | (66, 67) | |
HCAR2 activation | lipid metabolism | (68–70) | |
plasma member K+ channel expansion | NLRP3-induced inflammation | (71, 72) | |
VGLUT inhibition | epilepsy | (73, 74) | |
indirect | feedback inhibition of Ac-CoA | glucose metabolism | (52, 75) |
inhibition of protein succinylation | lipid metabolism | (76, 77) | |
NAD+ sparing | sirtuin activity | (78–80) | |
GABA synthesis | epilepsy | (81, 82) |
HDACs, histone deacetylases; BHB-ylation, β-hydroxybutyrylation; FFAR3, free fatty acid receptor 3; HCAR2, hydroxycarboxylic acid receptor 2; NLRP3, NOD-like receptor protein 3; VGLUT, vesicular glutamate transporter; Ac-CoA, acetyl-CoA; NAD+, nicotinamide adenine dinucleotide; GABA, gamma-aminobutyric acid.