Ra. Mason et Ha. Morris, INCREASED URINARY CALCIUM EXCRETION POTENTIATES BONE TURNOVER IN OOPHORECTOMIZED RATS, Mineral and electrolyte metabolism, 23(1), 1997, pp. 38-42
The differential effects of sodium-induced renal hypercalciuria on the
biochemical markers of bone metabolism and calcium homeostasis were s
tudied in oophorectomized (Oophx) and sham-operated rats. The rats con
suming a normal (0.4%) calcium semisynthetic diet were randomly alloca
ted to either 0, 0.4, 0.6, 0.9, or 1.25% NaCl in their drinking water
for 7 days, At that time fasting blood and urine specimens were collec
ted and analyzed for bone-related biochemical variables. The urinary c
alcium/creatinine ratio was increased with increasing urinary sodium (
p < 0.01) in both sham and Oophx animals. The hydroxyproline/creatinin
e ratio was elevated as a result of Oophx (p < 0.001) and was raised w
ith increasing urinary sodium In both sham (p = 0.012) and Oophx anima
ls (p = 0.007). Serum osteocalcin and alkaline phosphatase were elevat
ed in Oophx rats (p <0.02). While serum osteocalcin was raised with in
creasing urinary sodium in Oophx rats (p = 0.035), there was no effect
on osteocalcin levels in sham-operated rats. This study demonstrates
that sodium-induced renal hypercalciuria potentiates bone turnover in
Oophx rats as compared with ovary-intact rats and indicates important
implications for the effect of dietary salt on bone turnover with ovar
ian hormone deficiency.