Around parturition, many dairy cows experience varying degrees of hypocalcemia, which increases the incidence of several diseases in early lactation. In the current study, an established concept of feeding a diet negative in cation-anion difference (DCAD) was combined with oral supplementation of 25-hydroxyvitamin D(3) (25-OHD(3)) from d 270 of gestation until parturition. Fifty-six dairy cows were divided into 2 feeding groups (low DCAD and control). Fourteen animals of each group received a daily dosage of 3mg of 25-OHD(3). From the beginning of the treatment to d 10 after parturition, plasma samples for analysis of 25-OHD(3), 1,25-dihydroxyvitamin D(3), parathyroid hormone (PTH), Ca(2+), phosphate, the bone resorption marker CrossLaps, and osteocalcin were collected every other day, at calving, and at 6, 12, and 24h after calving. Urine samples for determination of macrominerals and measures of acid-base status were collected on d 6 of treatment and on d 6 after calving. The induction of a compensated metabolic acidosis by the animals on the DCAD diet could be demonstrated by decreased urinary pH. A linear correlation between treatment duration and the plasma concentration of 25-OHD(3) indicated effective absorption of 25-OHD(3) in supplemented animals. The mean plasma concentrations of Ca(2+) from d -4 prepartum to d 4 postpartum were significantly higher in animals treated with the combination of the low DCAD diet and 25-OHD(3) supplementation (1.24±0.02 mmol/mL) compared with the 3 other groups (low DCAD: 1.17±0.02 mmol/mL; control diet plus 25-OHD(3): 1.16±0.02 mmol/mL; control diet: 1.18±0.02 mmol/mL). We postulate that the increased tissue responsiveness to parathyroid hormone induced by the low DCAD is crucial for the observed positive effects of the 25-OHD(3) treatment.

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The effects of subclinical hypocalcemia have been explored in numerous observational and mechanistic studies in recent years. Besides obvious, well-known effects on muscle contractility, the role of Ca with respect to immune function and intermediary metabolism explains the contribution of subclinical hypocalcemia to the development of several diseases observed in early lactation and underlines its importance in highperforming dairy cows. The present review aims at integrating recent scientific progress, such as discoveries about the role of the mammary gland in regulating bone mobilization, into generally accepted aspects of the endocrine control of Ca homeostasis. We will discuss Ca transport mechanisms through absorption, resorption, secretion, and mobilization, as well as the physiological regulation of Ca through parathyroid hormone, 1,25-dihydroxyvitamin D, fibroblast growth factor 23, and serotonin, in addition to dietary mineral requirements. To improve hypocalcemia prevention strategies, our knowledge of the physiological mechanisms necessary to maintain normocalcemia and their endogenous regulation should be combined with data derived from herd-level studies. Using such studies, we will discuss prepartum nutritional strategies aimed at reducing the incidence of subclinical hypocalcemia, as well as options for postpartum Ca supplementation and their effects on early-lactation health and production. Especially in respect to approaches that might interfere with endogenous adaptation processes, such as supple-mentation with vitamin D metabolites or large doses of Ca, a thorough understanding of the underlying mechanisms that might induce unwanted hypocalcemia rebound effects will be crucial to ameliorate our future management of transition cows. Continued efforts by researchers to understand the interaction of Ca homeostasis with prevention strategies is necessary to optimize cow health and support copious milk production.