title: Regulation of serum calcitriol by serum ionized calcium in rats during pregnancy and lactation.
abstract: Serum calcitriol concentrations in rats follow a biphasic pattern during reproduction, with elevated levels during late pregnancy, a decline after parturition, and a rise to even higher levels during peak lactation. We have previously shown that serum calcitriol in rats at peak lactation correlates significantly with, and appears to be regulated by, serum ionized Ca (Ca2+), with parathyroid hormone (PTH) serving a permissive role. We have extended this study by determining if serum calcitriol also correlates with serum Ca2+ during late pregnancy, when calcitriol levels are clearly elevated, and during early lactation, when only modest increases in serum calcitriol are observed. Analyses of data combined from nonmated, 21-day pregnant (P), and 1-day lactating rats (L) revealed a significant regression (p < 0.001) of calcitriol on Ca2+, but a nonsignificant regression (p = 0.34) of calcitriol on serum PTH. An even stronger correlation (p < 0.001) between calcitriol and Ca2+ was found for the combined data for 5-, 8-, and 14-day L rats. The partial correlation coefficient for calcitriol versus Ca2+, with PTH as the independent variable, was highly significant (p < 0.01) for the data from both combined groups. However, the coefficient for calcitriol versus PTH, with Ca2+ as the independent variable, was not significant (p > 0.05). Fetal weights (uterus and contents) correlated significantly with both maternal calcitriol and Ca2+ concentrations (p < 0.01), but not with maternal PTH levels. Litter weights for 14-day-old pups likewise correlated significantly with maternal calcitriol and Ca2+ (p < 0.001). We conclude that hypocalcemia, induced by the demands for Ca for fetal calcification and milk production, appears to be a controlling factor in serum calcitriol elevation in late pregnancy and throughout lactation, whereas PTH may be important for calcitriol synthesis without playing a direct regulatory role.
authors.affiliation: Department of Pharmacology, School of Medicine, University of North Carolina at Chapel Hill, USA.
authors.forename: A
authors.initials: A
authors.lastname: Boass
authors.forename: S C
authors.initials: SC
authors.lastname: Garner
authors.forename: V L
authors.initials: VL
authors.lastname: Schultz
authors.forename: S U
authors.initials: SU
authors.lastname: Toverud
mesh_terms: D000818:Animals; D001835:Body Weight; D002117:Calcitriol / Q000097:blood*; D002118:Calcium / Q000097:blood*; D005260:Female; D005333:Fetus / Q000033:anatomy & histology; D006706:Homeostasis; D007774:Lactation / Q000097:blood*; D010281:Parathyroid Hormone / Q000097:blood; D011247:Pregnancy; D011270:Pregnancy, Animal / Q000097:blood*; D051381:Rats; D013997:Time Factors
chemical_list: D010281:Parathyroid Hormone; D002117:Calcitriol; D002118:Calcium