practitioners often examine Vitamin D status if someone
experiences an unexpected fracture (for example, a 32 year female
presents to the primary care physician with an appendicular
fracture suffered from an accident while running). The general idea
is that inappropriately low Vitamin D levels will fail to repress
PTH secretion. In order to test this, an experiment was done using
freshly isolated bovine parathyroid cells. In the study referenced
below, these primary parathyroid cells were grown under normal
conditions containing supplementary calcium. After 24 hr, the cell
media was replaced with fresh media containing either 100 nM
1,25(OH)₂D₃ or ethanol (vehicular control).
Total RNA was extracted at baseline, 24 hr, 48 hr, 72 hr, and 96
hr. The abundance of preproPTH mRNA was assessed and the results
plotted below. FYI: A higher number along the Y-axis indicates
higher density and reflects an increase in mRNA being
examined.

Part A (4 Points): Why might
the cells be supplemented with calcium 24 hr prior to being treated
with 1,25(OH)₂D₃? How would increasing the
calcium concentration be predicted to affect baseline levels of
preproPTH mRNA?

Part B (6 Points): How might
the results shown in Figure 1 above support (or refute) the
rationale that supplementing patients with either ergocalciferol or
cholecalciferol is osteoprotective through the regulation of PTH.
Please explain your answer with as much detail as possible (as well
as a proposed model for the regulation).