Vitamin D metabolism in growing pigs: influence of UVB irradiation and dietary vitamin D supply on calcium homeostasis, its regulation and bone metabolism

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Vitamin D (vitD, here representing vitD2, ergocalciferol and vitD3, cholecalciferol) requirements of humans and animals can be met either by supply from dietary sources or by cutaneous synthesis of vitD3. The synthesis of vitD in the skin was demonstrated for many species such as human (Holick et al., 1980; Adams et al., 1982), rat (Holick et al., 1979), cattle (Hymoller and Jensen, 2010), sheep, goat (Kohler et al., 2013; Kovacs et al., 2015), guinea pig (Watson et al., 2014), rabbit (Emerson et al., 2014) and recently for pig (Burild et al., 2015) and hen (Kuehn et al., 2015). Ultraviolet B irradiation (UVB, 290–315 nm) changes 7‐dehydrocholesterol (7‐DHC, provitamin D3) in the skin to pre‐vitamin D3 (pre‐vitD3) which is instable and converts heat‐dependent (faster at warmer temperatures) into vitD3. Under further irradiation, pre‐vitD3 is changed into lumisterol and tachysterol (Webb and Holick, 1988). However, different factors influence the vitD status: either the UVB irradiation reaching (latitude, season, time, clothes, sun blocker – humans) or penetrating (pigmentation) the skin as well as the 7‐DHC content in the skin which is age‐dependent (Holick, 1995). Because the livestock husbandry systems restrict the access to sunlight for farm animals, they are mainly dependent on dietary vitD sources (Dittmer and Thompson, 2011).
Vitamin D is bound to vitamin D‐binding protein (DBP; Haddad et al., 1993) and transported to the liver where it is transformed to 25‐hydroxyvitamin D (25‐OH‐D, calcidiol). This is the main metabolite in the blood and the most suitable to evaluate the vitD status (Adams et al., 1982; Watson et al., 2014), because of its good correlation with vitD supply and its long half‐life time (10 days for swine; Flohr et al., 2014). Transferred to different tissues (primarily fat, muscle and liver), it can be stored in the body (Heaney et al., 2009; Arnold et al., 2015). In the kidneys, 25‐OH‐D is metabolized to 1,25‐dihydroxyvitamin D (1,25‐(OH)2‐D, calcitriol), the most active metabolite, by the 1α‐hydroxylase (CYP27B1). This enzyme is stimulated in the kidney by parathyroid hormone (PTH) and inhibited by calcium (Ca), phosphorus (P) and 1,25‐(OH)2‐D (Lips, 2006; Dittmer and Thompson, 2011; Bikle, 2012). Both metabolites (25‐OH‐D and 1,25‐(OH)2‐D) are degraded by 24‐hydroxylase (CYP24A1) in the kidney and skin (Holick, 2007), stimulated by high serum levels of themselves and P and inhibited by PTH (Dittmer and Thompson, 2011). The main function of 1,25‐(OH)2‐D is the maintenance of Ca homeostasis, although it is also involved in cell differentiation and immunomodulatory functions (Dittmer and Thompson, 2011).
In the intestines and kidney, 1,25‐(OH)2‐D is responsible for active Ca absorption and reabsorption respectively. Binding to the cellular vitamin D receptor (VDR), it stimulates the expression of different proteins involved in Ca transport (Bronner, 2003). In bone, 1,25‐(OH)2‐D mobilizes Ca to maintain the Ca concentration in the blood (Dittmer and Thompson, 2011). This effect depends on PTH (stimulated by low Ca in the blood; Lips and van Schoor, 2011).
In humans, two levels of lack of vitD are defined as vitD deficiency and ‘insufficiency’: vitD deficiency means 25‐OH‐D levels below 12.5 nmol/l and is accompanied by hypocalcaemia and rickets. Levels of 25‐OH‐D between 13 and 50 nmol/l indicate a vitD ‘insufficiency’ and are accompanied with increase in PTH, bone loss and risk of fractures (Chapuy et al., 1997; Need, 2006), but no clinical signs can be observed.
The aim of this study was to show the ability of pigs to produce vitD in the skin, the influence of the vitD source on vitD status in blood and its effect on intestinal Ca absorption, renal Ca excretion and bone metabolism in growing pigs.
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