Gastrointestinal calcium absorption in nephrolithiasis.
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To assess the effect of dietary lactose on the utilization of 40Ca and 45Ca, a one-day balance experiment was carried out. The urinary 45Ca excretion and 45Ca deposition in the femur were significantly higher in the 10% lactose diet group. In the second experiment, non-flushed lower small intestine was ligated in situ and calcium absorption was observed shortly after injecting lactose solution into the loop during the postprandial state. The estimated amounts of 40Ca and 45Ca absorbed and of 45Ca deposited in the femur were increased in the presence of lactose in the test solution. These results suggest that dietary lactose stimulates calcium utilization and also increases calcium absorption from the undisturbed small intestine containing digests.
The details of calcium flux during growth were examined in female rats. Twenty-eight 53-d-old rats were equally divided into 4 groups. Rats were given a purified diet (0.5% Ca and 0.35% Pi) throughout the experiment. Calcium balance and 45Ca kinetics studies using an open two-compartment model were performed over a 3-d period when rats were 60 (control), 74 , 88 and 116 d old. A simple calcium balance study, using the last group, was carried out at the age of 102 d. Compared with the control group, true intestinal calcium absorption was significantly increased at 74 d, but then decreased in a time-dependent manner up to 116 d. The apparent intestinal calcium absorption began to decrease at 88 d, and decreased further with age. An increase in urinary calcium output was observed at 74 and 88 d in phase with calcium excretion into the intestine, and both variables returned to the control level at 116 d. Calcium into bone was decreased at 74 and 116 d. Calcium from bone similarly changed with Vo+ at 74 d: however the highest value was observed at 88 d. Thereafter, Vo- reached the control level at 116 d. Calcium balance rapidly decreased at 88, 102 and 116 d, but still remained positive. Calcium intake remained steady until 102 d, but was significantly decreased at the end of the experiment. The changes in calcium flux with age can be summarized as follows: 1) bone turnover decreased, calcium excretion into the urine and feces began to increase, and true intestinal calcium absorption increased, 2) apparent intestinal calcium absorption decreased, while calcium from bone and calcium excretion into the urine and feces increased, and 3) calcium intake and calcium into bone decreased.
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Potassium depolarization of cultured muscle cells was employed to study cellular responses linked to calcium signaling. Events occurring after depolarization include i) A transient increase of the IP3 mass (2-10s); ii) A slow calcium transient (5 to 25s) that propagates as a low concentration wave along the myotube showing a distinct calcium transient at the level of cell nuclei. Due to the presence of IP3 receptors both in the SR (A-band region) and in the nuclear envelope, these two events appear to be related; iii) Phosphorylation of mitogen activated kinases (ERK 1/2) and of the transcription factor CREB (30 s-10 min), as well as expression of the early genes c-fos, c-jun and egr-1 mRNA (5-15 min). Several independent pieces of evidence, including results obtained using inhibitors specific for individual steps, allowed us to connect these in a sequential manner. As the same type of signaling cascade can be triggered by oxidants, neurotransmitters and hormones, the ensemble of results allows us to propose a general model to describe signaling events that link membrane stimulation to regulation of gene transcription in skeletal muscle cells.
3 cases of hypercalcemia are reported, among 14 tetraplegic patients with porphyria. The calciuria, the estimations of parathormone, calcitonin and the isotopic calcium balance studies, suggested in the two most serious cases, hypercalcemia due to immobilisation. The main factor seems to be the duration of the immobilisation. The predisposing role of renal failure and catecholamines is discussed.
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