VITAMIN-D DEFICIENCY, PANCREATIC AND SMALL INTESTINAL ENZYME DEVELOPMENT IN RATS

Maternal vitamin D deficiency has been shown to lead to reduced body weights in developing rat pups. To evaluate the effects of vitamin D deficiency alone both in dams and pups during the perinatal age on the ontogeny of gastrointestinal enzymes, female weanling rats (3 weeks of age) were divided into three groups. Groups I and III were fed a control (vitamin-D-replete) diet. Group II were fed a vitamin-D-deficient diet. Six weeks after they were mated with normal male rats while continuing on their respective diets until sacrifice. Only rats that delivered their pups on the same day from each group were brought into the study. Litter sizes of groups I and II were adjusted to 10, while group III was adjusted to 13 such that the rate of growth paralleled that of group II. At 19 days after birth, all dams and pups were sacrificed. There were no differences in the calcium and phosphorus contents in breast milk obtained from dams of each group. The serum calcium concentration of pups from group II (vitamin-D-deficient) was lower than the other groups. Body weights of pups from groups II and III were significantly lower than those of group I. The mucosal weight, total mucosal protein, mucosal DNA, sucrase, and maltase activities from groups II and III were similar, but lower than group I. Pancreatic weight, total pancreatic protein, DNA, amylase, and lipase activity from groups II and III were also similar, but lower than group I. Vitamin D deficiency was confirmed in both dams and pups from group II. This deficiency during gestation and lactation apparently affected the development of gastrointestinal enzymes. The effect was, however, similar to that due to an increase in litter size (group III). The results suggest that vitamin D deficiency in dams probably caused lower milk volume which resulted in a partial dietary restriction to the pups, thus affecting the development of their pancreatic and mucosal enzymes. The effects of vitamin D deficiency is, therefore, secondary.