When ingested along the diet, genistin is readily converted to its aglycone form, genistein. It is hydrolyzed by removing the covalently boundglucose to form genistein and that genistein is the form of the compound that is absorbed in the intestine and is the form responsible for the biological activities of the isoflavone. The digestive metabolism was first demonstrated in 2002 that the gut microflora played a large role in the conversion of genistin to genistein.[2] It was later found that enzymes present in the human small intestine and liver also have the ability to convert the isoflavone. Hydrolysis actually starts very quickly in the digestive system once genistin is ingested, conversion begins in the mouth and then continues in the small intestine. Moreover, both human saliva and the intestinal cell-free extract from mice can cause the complete conversion.[2]
Genistin and other isoflavones are demonstrated to be bioactive within the neonatal intestine and may reduce the severity of rotavirus infections; genistin alone shows inhibition of the viral infectivity by 40-60%.[4]
In vitro study have shown that both genistin and genistein are capable of enhancing bonemetabolism in the femoral-metaphyseal tissues of elderly rats.[5] The presence of genistein or genistin in the tissue culture caused a significant increase in alkaline phosphatase activity, deoxyribonucleic acid (DNA) and calcium contents. The effect of genistein was greater than that of genistin. It is also revealed that genistin has a strong bone loss preventive activity on experimental rats, and is especially enhanced by combination with fructooligosaccharides.[6] The amount of new bone produced by grafting genistin in collagen matrix was compared to the bone produced by collagen matrix alone in New Zealand white rabbits, and was observed that genistin caused significant increase in bone formation.[7]
^Walter ED (1941). "Genistin (an isoflavone glucoside) and its aglucone, genistein, from soybeans". J Am Chem Soc. 62 (12): 3273–3276. doi:10.1021/ja01857a013.
^ abColdham NG, Darby C, Hows M, King LJ, Zhang AQ, Sauer MJ (2001). "Comparative metabolism of genistin by human and rat gut microflora: detection and identification of the end-products of metabolism". Xenobiotica. 32 (10): 45–62. doi:10.1080/00498250110085809. PMID11820509.
^Donovan SM, Andres A, Mathai RA, Kuhlenschmidt TB, Kuhlenschmidt MS (2009). "Soy formula and isoflavones and the developing intestine". Nutr. Rev. 67 (S2): 192–200. doi:10.1111/j.1753-4887.2009.00240.x. PMID19906223.
^Yamaguchi M, Gao YH (January 1998). "Anabolic effect of genistein and genistin on bone metabolism in the femoral-metaphyseal tissues of elderly rats: the genistein effect is enhanced by zinc". Mol. Cell. Biochem. 178 (1–2): 377–82. doi:10.1023/A:1006809031836. PMID9546622.
^Hooshmand S, Juma S, Arjmandi BH (2010). "Combination of Genistin and Fructooligosaccharides Prevents Bone Loss in Ovarian Hormone Deficiency". J Med Food. 13 (2): 320–5. doi:10.1089/jmf.2009.0059. PMID20132047.
^Wong RW, Rabie AB (2010). "Effect of genistin on bone formation". Front Biosci. 2 (1): 764–770. PMID20036920.
