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| Microbial substrates | Metabolites produced | Epigenetic changes | Cancer activity |
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Carbohydrates | Nonstarch carbohydrates, resistant starch, and oligosaccharides from plants | SCFA such as acetate, butyrate, and propionate | Butyrate inhibits the activity of histone deacetylase (HDAC) activity, thus inducing apoptosis and inhibiting cell proliferation. | Anticancer activity |
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Phytochemicals | Polyphenols such as curcuminoids, lignans, polyphenol ellagitannins, flavonoids, anthocyanins, and epigallocatechin-3-gallate | Ellagic acid, urolithins, and valerolactone | Ellagic acid and urolithins inhibit the activity of histone acetyltransferase (HAT) activity. Valerolactone modulates DNA methylation and histone modifications resulting in anti-inflammatory activities. | Anticancer activity |
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Fats | Polyunsaturated fatty acids (PUFA) | Linoleic acids | Inhibit fatty acid synthase. Inhibit cancer cell metastasis. It also induces DNA methylation and histone modifications to induce apoptosis and anti-inflammatory activities. | Anticancer activity |
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Fats | Undigested fats and unabsorbed bile | Ursodeoxycholate (UDCA) and deoxycholate (DCA) | Modulation of expression of several genes at mRNA levels and the production of reactive oxygen species (ROS), resulting in DNA damage and alteration in the expression of chromosomal maintenance and mitosis genes. Moreover, DCA induces apoptosis through HDAC. | Cancer and anticancer activity |
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Fats | Alcohol | Acetaldehyde | Distort DNA repair system causes chromosomal damage and hence alters gene expression. | Cancer activity |
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Proteins | Valine, leucine, and isoleucine | SCFA such as acetate, butyrate, and propionate | Butyrate inhibits the activity of histone deacetylase (HDAC) activity, thus inducing apoptosis and inhibiting cell proliferation. | Anticancer activity |
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Proteins | Undigested amino acids such as methionine, arginine, phenylalanine, and tryptophan | Polyamines, phenols, and indoles | Cocarcinogens | Cancer activity |
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