The possible effects of magnesium on the vitamin D-dependent renal and
intestinal calbindin-D were investigated. In a low magnesium model 70
Wistar rats were allocated to either a normomagnesemic diet (Mg 3.2 g
/kg) or a Mg-deficient diet (Mg 0.18 g/kg) for 10 or 24 days. The rats
had intraperitoneal injections of 1,25-(OH)(2) vitamin D-3 0.2 mu g,
MgSO4 100 mu mol or placebo daily for the last 4 days. In a high magne
sium model 60 Wistar rats were allocated to three groups on a normomag
nesemic diet supplied with intraperitoneal MgSO4 20 mu mol, 100 mu mol
or placebo daily. Half of the animals in each group were further supp
lied with intraperitoneal 1,25-(OH)(2) vitamin D-3 0.2 mu g daily. The
concentrations of intestinal calbindin-D-9k increased on the low Mg d
iet from 1.6 (1.1-2.0) to 2.7 (2.0-2.9) mu g/mg protein (p < 0.02), bu
t were unchanged in the high Mg groups. Vitamin D treatment raised the
levels of calbindin-Dg, in the normomagnesemic group (p < 0.01), but
not significantly in the low Mg group. Administration of MgSO4 to the
low Mg rats normalized the elevated levels of intestinal calbindin-D-9
k (p < 0.05). The concentrations of renal calbindin-D-28k were not cha
nged by the low Mg diet, but were lower in the high Mg group [0.8 (0.6
-1.1) mu g/mg protein] than in the control group [1.5 (1.1-1.8) mu g/m
g protein; p < 0.05]. Animals in the low, high and normal magnesium gr
oup showed no differences in plasma concentrations of 1,25-(OH)(2) vit
amin D. Thus, in the present study we found that a high Mg load decrea
sed renal calbindin-D-28k whereas a low Mg load increased intestinal c
albindin-D-9k. This indicates the existence of a not previously descri
bed relationship between magnesium load and renal and intestinal calbi
ndin-D in rats and suggests that these proteins may be involved in the
active absorption of magnesium.