The potential for modification of epigenetic mechanisms,
by their nature potentially reversible, by metabolic products of
resistant starch also holds promise for dietary prevention of
colorectal cancer. Butyrate is well known as an inhibitor of histone deacetylase, an enzyme that modifies wrapping of strands
of DNA around nuclear histone proteins and thereby regulates
gene transcription. Inhibitors of histone deacetylation, such as
butyrate, have the ability to modify expression of genes that
control cell cycle and apoptosis and function to suppress the
development of pre-neoplastic and neoplastic phenotypes in
vitro (150). Furthermore, butyrate exerts protective effects
against intestinal mucosal inflammation, a component of
inflammation-mediated colorectal cancer, through apoptosis of T lymphocytes and inhibition of inducible nitric
oxide synthase in colonic epithelium (151).