Restoration of Parathyroid Responsiveness in Vitamin D—Deficient Rats by Parenteral Calcium or Dietary Lactose*

Abstract

Abstract. The effects of treatment with vitamin D, calcium, or lactose on the responsiveness of vitamin D-deficient rats to parathyroid hormone were compared. In the absence of vitamin D, parenteral calcium or dietary lactose administration resulted in increases in serum calcium concentration although not to the normal values obtained in animals given vitamin D. Dietary lactose also partially restored the low bone calcium content of vitamin D-deficient rats. Untreated vitamin D-deficient rats showed no significant changes in serum calcium concentration after parathyroidectomy or parathyroid extract administration. Vitamin D, lactose, and calcium all restored responsiveness to parathyroid hormone; serum calcium concentration decreased after parathyroidectomy and showed a dose-related increase in response to parathyroid extract. Hence, the unresponsiveness to parathyroid hormone in vitamin D deficiency may be due to a lack of calcium at a local site of action, presumably bone, rather than to cofactor. IntroductionThe observation that hypocalcemia can develop in vitamin D-deficient rats despite parathyroid hyperplasia has led to several studies of the relation between vitamin D and parathyroid hormone action. Harrison, Harrison, and Park (2) observed that the administration of parathyroid extract (PTE) to vitamin D-deficient, hypocalcemic rats at doses which were effective in normal animals resulted in little or no increase in serum calcium concentration. Rasmussen and coworkers (3)

25-hydroxycholecalciferol-enhanced bone maturation in the parathyroprivic state.

“…Unlike the vitamin D-deficient animal, however, the serum calciums of the PTX-calcium supplemented animals, although lower than normal, were never at the hypocalcemic levels which have been shown to decrease bone maturation (33). Rather, the 8.3 mg/100 ml serum calcium, which was maintained in this study (Table I), was comparable to the serum calcium concentration which Au and Raisz (34) found sufficient to maintain skeletal responsiveness in PTX rats. Thus the 250HD3 effect on bone in the present study cannot be solely a secondary reflection of the reversed hypocalcemia.…”

Calcium Release from the Skeletons of Rachitic Puppies

“…Au and Raisz (12) found that parenteral calcium did restore the response to parathyroid extract in rats. In puppies, complete restoration of the response was not achieved in rachitic animals despite a rise to near normal values for the serum calcium.…”

Abnormal sulfate metabolism in vitamin D-deficient rats.

“…Vitamin D-deficient diets supplemented with high calcium and lactose have been used previously to maintain normocalcemia in vitamin D-deficient rats (15,16). In all cases, protein was given in the form of casein, and the amount of inorganic sulfate in the diets was similar.…”

“…Alternatively, increased intestinal absorption of sulfate could occur in this group of rats by a mechanism independent of Na-SO 4 cotransport activity. In this regard, a lactose-induced enhancement of the passive (or diffusional) component of calcium transport has been suggested to explain the ability of lactose to increase intestinal calcium absorption (15,16). An analogous mechanism might be responsible for increasing intestinal sulfate uptake, thereby increasing serum sulfate concentrations.…”