One-year-old selectively parathyroidectomized rats showed a normalization of their plasma calcium level to above 4.1 mEq/l in 38% within 18 weeks on a normal dietary intake of calcium and inorganic phosphate but low in vitamin D. On a low level of dietary calcium, normalization did not occur in any of the parathyroidectomized animals. The conversion of 25-hydroxycholecalciferol into the active metabolite of vitamin D, 1,25-dihydroxycholecalciferol, by the kidneys was stimulated by a low dietary intake of calcium in intact animals and the accumulation of this metabolite was increased in small intestine mucosa. This adaptory increase in the level of intestinal 1,25-dihydroxycholecalciferol was not disturbed by selective parathyroidectomy, nor the synthesis by the kidneys. The synthesis reached a limit above which no further increase occurred despite the prevailing hypocalcemia possibly through an influence of the concomitant hyperphosphatemia. The renal synthesis and intestinal accumulation of 1,25-dihydroxycholecalciferol were directly related to the intestinal net absorption of dietary calcium, which we have reported on previously. Although increased, the endogenous level of 1,25-dihydroxycholecalciferol was too low to accomplish mobilization of skeletal calcium necessary for adaptation to a low calcium intake, as we have reported elsewhere. Thus, for adaptation skeletal calcium reserves must become mobilized through stimulated parathyroid activity with resulting osteoporosis. The parathyroids were found to have no direct regulatory influence upon the synthesis of 1,25-dihydroxycholecalciferol.