Hormonal Actions

The evidence for a hormonal action of wild yam varies. Wild yam extract may enhance oestradiol binding to oestrogen receptors and induce transcription activity in Wild yam 1359

oestrogen-responsive cells (NMCD 2003) and diosgenin has been observed to have an © 2007 Elsevier Australia

oestrogenic action on mouse mammary epithelium (Aradhana & Kale 1992). Alternatively, in an oestrogen competition assay using human breast cancer cell, diosgenin was found to cause an acute, endothelium-independent coronary artery relaxation, but did not interact with oestrogen or progesterone receptors (Au et al 2004) and extracts with an upper limit of 3.5% diosgenin have been found to have no oestrogenic activity (Hooker 2004).

One study looking at steroid hormone-regulated gene expression using an in vitro tissue culture indicator system suggests that wild yam extract does not have significant oestrogenic or progesteronal activity, but rather weak anti-oestrogenic and/or anti-androgenic activities (Rosenberg Zand et al 2001). A further study suggests that wild yam extract suppresses progesterone synthesis without direct effects on oestrogen or progesterone receptors (Zava 1998). In an in vivo study, supplementation with diosgenin protected the kidney from morphological changes associated with ovariectomy (Tucci & Benghuzzi 2003) and produced a significant decrease in the cortical and medullary adrenal areas of the ovariectomised rats (Benghuzzi etal 2003).

There is in vitro evidence that diosgenin up-regulates vascular endothelial growth factor-A and promotes angiogenesis in preosteoblast-like cells via pathways involving oestrogen receptors (Men et al 2005).

cholagogue

There appears to be more consistent evidence for wild yam's effect on bile flow. Diosgenin has been shown to increase biliary secretion of cholesterol (Accatino et al 1998; Yamada et al 1997) and prevent oestrogen-induced bile flow suppression in rats (Accatino et al 1998), as well as increase elimination of indomethacin and reduce indomethacin-induced intestinal inflammation (Yamada etal 1997).

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