Table 1.

Serum levels of Ca and 25(OH)D₃ and in vivo conversion of [³H]25(OH)D₃ into [³H]1α,25(OH)₂D₃

Operation	Dietary vitamin D3, units g of diet	Treatment			Serum 25(OH)D3, ng/dl	Conversion of [3H]25(OH)D3 into [3H]1α,25(OH)2D3, % per 6 h	Amount of 1α,25(OH)2D3 synthesized from 25(OH)D3, pg/ml of serum per h
			Serum Ca level, mg/dl
			24 h	36 h
Sham	2.0	Vehicle	10.1  ±  0.1	9.9  ±  1.4	39.9  ±  1.4	0.21  ±  0.02	14.0
		CT	9.9  ±  0.2	6.3  ±  0.2	37.4  ±  2.4	2.30  ±  0.15	143.6
		PTH	12.3  ±  0.2	12.8  ±  0.4	34.9  ±  4.5	0.24  ±  0.02	13.9
TPTX	2.0	Vehicle	4.9  ±  0.4	5.2  ±  0.2	37.3  ±  7.9	0.15  ±  0.04	9.3
		PTH	10.3  ±  0.3	10.5  ±  0.2	35.1  ±  4.3	0.14  ±  0.02	8.3
		CT	5.4  ±  0.2	4.4  ±  0.2	31.3  ±  2.9	0.18  ±  0.03	9.4
		PTH + CT	9.9  ±  0.2	4.6  ±  0.1	38.9  ±  6.6	1.88  ±  0.11	122.0
		CaC12	10.3  ±  0.2	9.7  ±  0.2	32.8  ±  3.4	0.10  ±  0.04	5.6
		CaC12 + CT	10.1  ±  0.2	9.5  ±  0.1	32.5  ±  4.2	1.72  ±  0.23	94.3
Sham	0	Vehicle	—	4.5  ±  0.3	<2.0	13.58  ±  0.7	<4.5

Five-week-old rats, either sham-operated or TPTX, were fed a laboratory chow containing 2 units of vitamin D₃ per gram of diet. Either CaC1₂ or PTH was infused into TPTX rats at a rate of 25 μmol/h or 25 ng/h, respectively, for 36 h in total to induce normocalcemia. Twenty-four hours after the initiation of CaC1₂ or PTH infusion, CT (10 units per rat) or vehicle (0.5 μmol of sodium acetate per rat) was injected intramuscularly, and animals were killed 12 h later. [³H]25(OH)D₃ was injected intravenously 6 h after the CT injection. Data were obtained from five rats. Values are expressed as the means ± SE. Male weanling rats were maintained for 3 weeks on a vitamin D-deficient diet containing 0.03% calcium and 0.6% phosphorus.