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Anderson P.H.,Endocrine Bone Research Laboratory | Anderson P.H.,University of South Australia | Anderson P.H.,Hanson Institute | Atkins G.J.,University of Adelaide | And 9 more authors.
Molecular and Cellular Endocrinology | Year: 2011

The endocrine activity of 1,25-dihydroxyvitamin D (1,25(OH) 2D 3) contributes to maintaining plasma calcium and phosphate homeostasis through actions on the intestine, kidney and bone. A significant body of evidence has been published over the last 10years indicating that all major bone cells have the capacity to metabolise 25-hydroxyvitamin D (25(OH)D 3) to 1,25(OH) 2D 3, which in turn exerts autocrine/paracrine actions to regulate bone cell proliferation and maturation as well as bone mineralisation and resorption. In vivo and in vitro studies indicate that these autocrine/paracrine activities of 1,25(OH) 2D 3 in bone tissue contribute to maintaining bone mineral homeostasis and enhancing skeletal health. © 2011 Elsevier Ireland Ltd.

Suetani R.J.,University of Adelaide | Ho K.,University of Adelaide | Jindal S.,University of Adelaide | Manavis J.,Center for Neurological Diseases | And 8 more authors.
Molecular and Cellular Endocrinology | Year: 2012

Links between a low vitamin D status and an increased risk of breast cancer have been observed in epidemiological studies. These links have been investigated in human tissue homogenates and cultured cell lines. We have used non-malignant, malignant and normal reduction mammoplasty breast tissues to investigate the biological and metabolic consequences of the application of vitamin D to intact ex vivo human breast tissue. Tissues were exposed to 1α,25(OH)2D3 (1,25D; active metabolite) and 25(OH)D (25D; pre-metabolite). Changes in mRNA expression and protein expression after vitamin D exposure were analysed. Results indicate that while responses in normal and non-malignant breast tissues are similar between individuals, different tumour tissues are highly variable with regards to their gene expression and biological response. Collectively, malignant breast tissue responds well to active 1,25D, but not to the inactive pre-metabolite 25D. This may have consequences for the recommendation of vitamin D supplementation in breast cancer patients. © 2012 Elsevier Ireland Ltd.

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